Soil cadmium (Cd) contamination threatens plant growth and agricultural productivity. Hibiscus syriacus L., valued for its ornamental, edible, and medicinal properties, is widely cultivated in Cd-contaminated areas of southern China.This study aimed to evaluate the effectiveness of nano-zinc oxide (nZnO) in alleviating Cd toxicity in H. syriacus, examining plant phenotypes, physiological and biochemical responses, root ultrastructure, and the accumulation and distribution of Cd and Zn within the soil-H. syriacus system. Pot experiments included Cd treatment (100 mg/kg) and combined soil or foliar applications of nZnO (50 and 100 mg/L), with plants harvested after 45 days. Compared to Cd treatment alone, the combined application of nZnO significantly increased biomass in roots, stems, and leaves, improved photosynthetic performance, osmotic regulation, and antioxidant levels, and mitigated root cell damage; Cd concentrated mainly in roots, and nZnO reduced root Cd levels by 0.24 %-9.06 %. SEM-EDS observations revealed that Cd predominantly accumulated in the root epidermis and cortex, with Cd stress leading to increased levels and localized aggregation of Cd in the xylem. By contrast, nZnO treatment alleviated this disruption. Leaf application of 50 mg/L nZnO showed the best results. These findings highlight nZnO as a promising nano fertilizer for alleviating Cd stress in plants.

In recent years, there has been increasing interest in utilizing fish cell culture in vitro assays, as alternatives to whole fish assays, for assessing the toxicity of aquatic pollutants. The fish cell line RTL-W1, derived from rainbow trout (Oncorhynchus mykiss) liver, was shown to retain several tissue specific features and to respond to chemical insults similarly to fish in vivo. In our study, we investigated the toxicity of two metals silver and cadmium and two pesticides azoxystrobin and paraquat using a cytotoxicity assay that measures simultaneously cell metabolic activity and cell membrane integrity. Moreover, we developed a novel 'high-content imaging' approach to evaluate if mitochondria's surface area is a sensitive and specific indicator of mitochondria toxicity. Initially, the cytotoxicity assay was used to determine the chemicals' effective concentrations (EC50). Subsequently, we assessed the mitochondria surface area at different toxicity level (i.e., EC50, EC25 and EC10) to compare the sensitivity and specificity of this method. The EC50s measured by cell metabolic activity, for silver, cadmium, azoxystrobin and paraquat were 0.71, 29.05, 2.34 and 1260 μM, respectively. Mitochondria surface area was reduced by all chemicals at the EC50, and by silver and azoxystrobin at the EC10 and EC25; indicating that the latter chemicals affect mitochondria more specifically. In conclusion, our study demonstrated that mitochondrial surface area serves as a sensitive marker for chemicals inducing mitochondria toxicity in fish liver cells. Additionally, assays using RTL-W1 cells proved to be effective for detecting the hepatic cytotoxicity of environmental contaminants.

Environmental pollution severely affects ecological functions/health, and nondegradable pollutants such as heavy metals (HMs) cause significant damage to living organisms. Escherichia coli is one of the most studied life forms, and its response to oxidative stress is driven by a complex ensemble of mechanisms driven by transcriptomic-level adjustments. However, the magnitude of the physiological, metabolic, and biochemical alterations and their relationships with transcriptomic changes remain unclear. Studying the growth of E. coli in Cd-, Cu-, and Ni-polluted media at pH 5.0, we observed that (i) downregulation of the alkyl hydroperoxide complex, glutathione reductase, and glutathione S-transferase by Cd inhibited H2O2 degradation, and the accumulated H2O2 was respectively 2.7, 1.7, and 2.4 times greater than that in the control, Cu, and Ni treatments; (ii) Zn-associated resistance protein (ZraP) was the major scavenger of Cd, with a 140.7-fold increase in its expression; (iii) the P-type Cu+ transporter (CopA), multicopper oxidase (CueO), and heteromultimeric transport system (CusCBAF) controlled the excretion and detoxification of Cu; (iv) the Cd2+/Zn2+/Pb2+-exporting P-type ATPase (ZntA) and transcriptional activator ZntR were the major transporters of Ni; (v) Cd upregulated biofilm formation and synthesis of secondary metabolites more than Cu and Ni, which resulted in increased adsorption and improved tolerance; and (vi) the activity of superoxide dismutase in Cu-spiked cells was 153.2 %, 141.7 %, and 172.7 % higher and corresponded to 85.7 %, 524.5 %, and 491.5 % lower O2●⁻ in the control, Cd-, and Ni-spiked cells, respectively. This study reveals E. coli's preferential tolerance mechanisms to Cd rather than Cu and Ni and demonstrates mechanisms for its survival in highly polluted environments.

Cadmium (Cd) is a highly toxic heavy metal, and its detrimental effects on reproductive health pose a significant risk to the general population. Farnesol (FAR), a sesquiterpene alcohol, exhibits anti-inflammatory, antioxidant, and anticancer properties. This study investigated the protective effects of FAR against Cd-induced testicular toxicity, focusing on its antioxidant and anti-inflammatory mechanisms. Rats were randomly divided into four experimental groups: control, FAR (10 mg/kg), Cd (1.2 mg/kg), and Cd + FAR. Cd administration caused testicular tissue damage, altered hormone levels, oxidative stress and apoptosis, upregulated TLR4/NF-κB signaling and diminished antioxidants. FAR ameliorated gonadotropins and testosterone, prevented tissue damage, and attenuated oxidative stress. Additionally, FAR significantly attenuated the inflammatory response triggered by Cd, as evidenced by reduced levels of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and suppression of the TLR4/NF-κB signaling pathway. FAR inhibited testicular apoptosis by upregulating the anti-apoptotic protein Bcl-2 and downregulating the pro-apoptotic markers Bax and caspase-3. These results suggest that FAR mitigates Cd-induced testicular toxicity through upregulation of antioxidants, suppression of TLR4/NF-κB signaling, and inhibition of apoptotic pathways. Thus, FAR represents a promising therapeutic agent for protecting against Cd-induced reproductive damage.

Heavy metal contamination in the soil has become more serious due to the rapid development of the economy. Phytoremediation has evoked widespread curiosity in recent years due to its advantages in terms of being environmentally friendly and sustainable. However, there are few reports on the application of bamboo species in the field of phytoremediation, and a comprehensive overview of their potential for restoring contaminated soil by removing heavy metals is lacking. This paper incorporates existing research on bamboo species for the remediation of heavy metal-contaminated soils. It meticulously debates the physiological responses exhibited by bamboo species to heavy metal stress, encompassing growth and development responses, photosynthetic responses, and antioxidant system responses, among others. Furthermore, it elaborates on the capacity of bamboo for heavy metal accumulation and translocation, as well as their remarkable tolerance and detoxification mechanisms. This comprehensive analysis sheds light on the intricate interactions between bamboo and contaminated soil environments. Additionally, the paper summarizes various strategies for the remediation of heavy metal contamination using bamboo species. This review facilitates a more thorough exploration of the potential applications of bamboo species in the remediation of heavy metal-contaminated soils, offering a novel approach for soil environmental restoration.

Breast cancer (BC) is a multifactorial disease with unresolved etiology. Environmental pollutants, primarily trace metals, play a pivotal role in the pathophysiological cascade of malignant tumors, including BC. In this up-to-date review, we comprehensively and critically examined the relationship between cadmium (Cd) and BC. For this purpose, peer-reviewed studies from relevant databases (PubMed, SCOPUS, and Cochrane Library) over the last 40 years were retrieved and analyzed. We found that in vitro and in vivo studies strongly support the view that Cd has harmful effects on breast health. According to the human studies, we found that Cd could be responsible for the development and progression of malignant breast tumors due to markedly higher levels in clinical matrices of cases (whole blood, urine, breast tissue, keratin materials) than in clinical matrices of controls. Cadmium does not appear to affect BC density. In contrast, Cd has been found to have a detrimental effect on sex hormones, disrupting the balance of estrogen and androgen. We found that studies looking at dietary Cd intake and BC risk generally (without measuring urine or blood Cd) do not support the association between dietary Cd intake and BC risk. In notable contrast, studies looking at dietary Cd intake and BC risk by measuring Cd in urine or blood generally support this association. The effect of airborne Cd on BC risk was weak, but in favor of specific histological forms, primarily ER-/PR- invasive tubular breast carcinomas. Regardless of the intake route of Cd into the body, it can be concluded that Cd has a harmful effect on breast health. However, well-designed longitudinal, mechanistic, meta-analytic, and other studies are urgently needed to confirm the exact role of environmental Cd in breast carcinogenesis.

Desert shrubs play an important role in the stability of arid and fragile desert ecosystems. However, despite their significant ecological importance, limited research has been performed on shrub drought tolerance strategies at the morphological, physiological, and molecular levels. Therefore, this study focused on the typical desert shrub, Calligonum leucocladum, and analyzed its morphology, physiology, and protein expression under two different habitats: moist low-salt and arid low-salt. The results indicate that drought stress inhibited the growth of C. leucocladum, leading to significant reductions in its plant height, base diameter, and crown width by 14.93%, 49.57%, and 48.49%, respectively. Drought stress triggered a 30% decline in stomatal conductance, whereas homeostasis was observed in net photosynthesis, intercellular CO₂, and transpiration. The soluble sugar content significantly increased by 13.43%, while the starch, soluble protein, and proline content significantly decreased by 20.32%, 10.67%, and 55.61%, respectively. In addition, under drought stress, membrane peroxidation products, reactive oxygen species metabolites, and antioxidant enzyme activities significantly increased. Weighted gene co-expression network analysis revealed 40 proteins that were significantly enriched in the photosynthesis and oxidative phosphorylation pathways through KEGG enrichment analysis. In addition, C. leucocladum maintains photosynthetic homeostasis by enhancing PSII repair (PsbE, PsbL, PsbH) and electron transfer chain efficiency (PetD, nad 2, nad 9), thereby compensating for the insufficient carbon dioxide supply caused by stomatal limitation. This study integrated multidimensional data from morphology, physiology, and proteomics to reveal that C. leucocladum drives a coupled network of photosynthesis, antioxidant, and carbon metabolism through chloroplast translation reprogramming. It maintains photosynthetic homeostasis and osmotic balance under a 30% decrease in stomatal conductance, elucidating the cross-scale regulatory strategy of desert shrubs adapting to extreme drought.

Sea rice (Haidao 86) is a vital cultivar that could be cultivated in saline soil but is sensitive to heavy metal stress, and cadmium (Cd) stress in eastern coastal parts of China is frequently a great hazard. Nevertheless, there is a scarcity of research on the metabolic pathways involved in the detoxification of Cd stress in sea rice. Here, we added a kind of monoterpene hormone, (1S)-(-)-β-Pinene (βP), in Cd (100 mg/kg) stressed experiment to study its interaction with sea rice. Multiple Morphological traits were significantly rescued after the application of βP. Similarly, Cd alleviation by βP was also demonstrated in physio-chemical indicators. Cd contents in roots, leaves, grains, H2O2, and MDA contents have decreased by 28.1 %, 50.9 %, 51.4 %, 18.2 %, and 18.0 %, respectively, with the presence of βP compared to Cd alone. SOD, POD, CAT, and GPX activities were elevated by 17.1 %, 40.0 %, 12.4 %, and 22.5 %, respectively, and contents of GSH and APX were also significantly modulated after the supplementation of βP. Transmission electron microscopy also indicated that the Cd+βP group had intact cellular structure compared to the Cd group. Through metabolomic analysis, 27 and 31 differentially expressed metabolites (DEMs) were identified from CKvsCd and CdvsCd+βP. According to the results, carbohydrate metabolism (e.g. I-inositol, Gluconapoleiferin), phenylpropanoid (lignan, flavonoids) biosynthesis (e.g. Cyanidin, Leucoside), terpenoids, and alkaloids biosynthesis, were all significantly regulated with the presence of βP. Our study provided a detailed understanding of the mechanism behind Cd-stress tolerance and will aid in developing Cd tolerance in sea rice.

Reactive oxygen species (ROS), as redox messengers, play an important role in regulating plant growth, sensing biotic and abiotic stresses, and integrating different environmental signals. As the microenvironment of the interaction between root, soil and microorganism, the rhizosphere is the hotspot of ROS production and action. Root exudates are an important medium for communication between roots and the soil environment, and they have a significant regulatory effect on the production of ROS in the rhizosphere. At the same time, the formation of rhizosphere ROS is determined by the coupling of various biotic and abiotic factors, and it is also affected by environmental stresses such as temperature, humidity, and disease. This review summarizes how root exudates affect plant growth and induce plant defense mechanisms by regulating the generation and distribution of ROS. It also discusses the role of ROS in promoting the decomposition of soil organic matter, nutrient cycling, and pollutant degradation and transformation. In-depth study of the regulation mechanism of root exudates on ROS not only helps to reveal the molecular mechanism of plant adaptation to environmental stress but also provides theoretical support and practical guidance for sustainable agricultural development and ecological environment protection.

Rapid industrialization in China has led to widespread soil contamination, particularly with heavy metals like cadmium (Cd). This study investigates Cd accumulation and translocation in 12 commercial maize cultivars grown on contaminated soils. Initial soil Cd concentrations averaged 0.68 mg kg-1, exceeding safe limits for agricultural soils. Post-harvest results indicated that the soil Cd concentration decreased under all cultivars, with values ranging from 0.25 to 0.55 mg kg-1, indicating effective Cd uptake by maize. The bio-concentration factor (BCF) values indicated Cd accumulation, varying between 0.016 and 0.051, while translocation factor (TF) values ranged from 0.04 to 0.12. Cultivar C868 (pollution index (Pi) = 0.048, BCF = 0.016 and TF = 0.05) and C380 (Pi = 0.071, BCF = 0.023 and TF = 0.09) were the best cultivars on contaminated soils, which demonstrated reduced Cd uptake and limited translocation to grains. In addition, a strong positive correlation (r = 0.72, p < 0.05) was observed between soil Cd, Pi, BCF and TF, indicating that cultivars grown on high Pi soils, with higher Cd uptake and translocation result in higher accumulation of Cd in grains. The combined VNIR-PLSR model showed strong predictive performance for the prediction of Cd (R2 = 0.67 and RPD = 2.4). Spectral analysis revealed significant increases of reflectance at 450-500 and 600-700 nm associated with Cd absorption. Our findings indicated the capability of VNIR spectroscopy coupled with PLSR method as a reliable and efficient method for soil Cd assessment.

The level of protection by the seawater quality criteria (SWQC) of cadmium (Cd) on planktonic population remains unknown. Therefore, this study assessed the level of protection and safe exposure period of SWQC of cadmium for protection of marine life. The copepod Oithona similis exposed to the Cd at SWQC such as predicted no-effect concentration (PNEC, 0.6 μg/l), criterion continuous concentration (CCC, 1.2 μg/l), and criterion maximum concentration (CMC, 5 μg/l). The in-vivo assays with fluorescein diacetate (FDA) and 2,7-dichlorofluorescein diacetate (DC-FDA) revealed that the SWQCs are safe except for CMC for prolonged exposure. The population growth was higher at 5.4 folds in the control culture, with 4291 ± 134 ind/l, than the culture with CMC of Cd with 2403 ± 149 ind/l which is 2.7 fold growth. Protein content in copepod biomass increased between 3.27 mg/g in the control and 5.73 mg/g in CMC. Biomarker enzyme activities varied among the treatments, and higher expressions were found in CMC. Inhibition of in-vitro FDA and induced DC-FDA activities indicate the stress due to Cd toxicity. Overall, results reveal the SWQC of Cd is not safe for long-term exposure. The PNEC may ensure the protection for up to four days, CCC may be prescribed for one day, and CMC may be prescribed for one-hour exposure.

Cadmium, a ubiquitous environmental pollutant, has been linked to testicular damage, primarily through mechanisms such as oxidative stress and various forms of programmed cell death. Despite extensive studies on its toxic effects, the specific role of necroptosis in cadmium-induced reproductive toxicity remains unclear. In this study, we provide critical insights into how cadmium triggers necroptosis in Leydig cells, leading to testicular dysfunction. Using both in vitro and in vivo models, we demonstrated that cadmium exposure induces necroptotic cell death in Leydig cells, with significant involvement of the TNF-α/TNFR1 signaling pathway and reactive oxygen species (ROS) generation. Co-treatment with Nec-1, a specific necroptosis inhibitor, significantly reduced elevated ROS levels and suppressed TNF-α/TNFR1-induced necroptotic cell death, suggesting that ROS and the TNF-α/TNFR1 signaling pathway contribute to necroptosis activation in cadmium-induced Leydig cell injury. In conclusion, we demonstrate that necroptosis is a key driver of cadmium-induced testicular damage, suggesting that targeting necroptosis could offer novel therapeutic strategies for mitigating reproductive toxicity caused by heavy metals.

The present study aims to unlock the cross-protection mechanism of the diazotrophic cyanobacterium Anabaena sp. PCC 7120. Heat pre-treatment elicited a beneficial response against subsequent cadmium stress as revealed by integrated morphological, physiological, biochemical, transcript, and proteomics analyses under four sets of experimental conditions: control (C), heat (HS), cadmium (Cd), and heat + cadmium (HS + Cd). Outcomes of the present study suggested a better survival strategy shown by Anabaena sp. PCC 7120 under HS + Cd compared to Cd. According to comparative proteomics, protochlorophyllide reductase, CO2 hydration protein, and NAD(P)H quinone oxidoreductase work in concert to support the light and dark reactions of photosynthesis. Furthermore, in cross protection involvement of enzymes from pentose phosphate pathway and glycolysis for fulfilling cellular energy demand; antioxidants and antioxidant enzymes in scavenging ROS, cellular detoxification, and Cd chelation, chaperons and proteases in proper protein folding and synthesis; signaling and transporters to generate cross talk and Cd efflux were found. Increased accumulation of vegetative to heterocyst connection protein (FraH) in HS + Cd compared to Cd may be envisioned to manage better nitrogen fixation.

Cadmium (Cd) is a highly toxic heavy metal contaminant found in soil and water due to human activities such as mining and industrial discharge. Cd can accumulate in the body, leading to various health risks such as organ injuries, osteoporosis, renal dysfunction, Type 2 diabetes (T2DM), reproductive diseases, hypertension, cardiovascular diseases, and cancers. The gut is particularly sensitive to Cd toxicity as it acts as the primary barrier against orally ingested Cd. Even at low concentrations, Cd can cause oxidative stress, inflammation, and intestinal bleeding. Cd also disrupts the gut microbiota, affecting its structure, taxonomic composition, and metabolic functions. Cd exposure alters the structure of the gut microbial community, reducing diversity and upregulating certain phyla and genera. This disturbance can lead to physiological and metabolic imbalances, including disruptions in energy homeostasis, amino acid, lipid, nucleotide, and short-chain fatty acid (SCFAs) metabolism. The effects of Cd on the gut microbiota depend on the duration of exposure, the dose of Cd, and can vary based on sex and age. Cd-induced gut dysbiosis has been linked to various diseases, including diabetes, adiposity, atherosclerosis, liver damage, infections, cancer, and neurodegenerative diseases. Interventions targeting the gut microbiota, such as probiotics, specific diets, melatonin, selenium, vitamin D3, and certain compounds, have shown potential in reducing the health risks associated with Cd exposure. However, combined exposure to Cd and other toxicants, such as microplastics (MPs), heavy metals, and antibiotics, can amplify the toxicity and dysbiosis in the gut microbiota.

Cadmium is a widely distributed heavy metal found in the environment that poses serious hazards to human health. Dapagliflozin (DAPA), a sodium-glucose co-transporter 2 (SGLT-2) inhibitor, exhibited antioxidant, antiapoptotic, and anti-inflammatory properties. Our data assessed the effect of DAPA against Cd-triggered renal and testicular impairment in rats, as well as the underlying mechanisms. Cd (30 mg/kg) and DAPA (5 and 10 mg/kg) were administrated by oral gavage to rats and continued for 21 days. DAPA attenuated Cd-triggered renal and testicular injury as shown by diminishing serum creatinine, BUN, and urinary total protein concentration in addition to increasing creatinine clearance, urinary creatinine, and serum testosterone. Moreover, it diminished renal and testicular histopathological alterations induced by Cd. DAPA stimulated the impaired autophagy flux as seen by significantly elevating the p-AMPK/total AMPK, decreasing p-mTOR/total mTOR ratios, and diminishing p62 & LC3 protein levels. Additionally, DAPA significantly lowered MDA content, increased GSH level and SOD activity. Moreover, it augmented the cytoprotective Nrf2/HO-1 signaling pathway. Furthermore, it attenuated renal and testicular apoptotic cell death via decreasing caspase-3 expression. Conclusion: Boosting autophagic events and combating oxidative stress and apoptosis by DAPA were engaged in alleviating Cd-induced renal and testicular impairment. This was accomplished by modulating the AMPK/mTOR and enhancing the Nrf2/HO-1 pathways.

Rice (Oryza sativa L.) is a staple food in most Asian countries, although it serves as a significant carrier of cadmium (Cd) accumulation. Developing low-Cd accumulating rice varieties is crucial for minimizing Cd contamination in soil and rice grains while also mitigating harmful health consequences. In the present study examined the Cd accumulation and sub-cellular distribution of both high Cd (IR-50) and low Cd (White Ponni) rice varieties under Cd-treated hydroponic nutrient solutions. The results showed that under all Cd treatments, overall plant height, plant fresh and dry biomass reduced substantially in both rice varieties compared to the control. Both rice varieties accumulated more Cd in their roots than shoots, with IR-50 accumulating higher Cd levels. Iron (Fe) concentrations were higher in both roots and shoots of both rice varieties compared to other trace elements. Translocation factor (TF) values were < 1, indicating limited Cd translocation from roots to shoots. Cd was mainly distributed in the epidermis, cortex, and bulliform cells of both rice varieties roots, and shoots. The peroxidase (POD), catalase (CAT), and superoxide dismutase (SOD) enzymes activity significantly increased in both IR-50 and WP rice varieties when exposed to Cd treatment. The current study concluded that the IR-50 rice variety accumulated and distributed more Cd than the WP rice variety under different Cd treatments. As a result, WP exhibited higher Cd tolerance, while IR-50 became more susceptible to Cd stress.

Cadmium (Cd) pollution is a widespread threat to aquatic life, and ongoing freshwater acidification (FA) can be expected to interact with Cd compounds to disrupt freshwater ecosystems. However, the effects of FA on Cd biotoxicity remain unclear. Herein, the model ciliate Paramecium tetraurelia, a model unicellular eukaryotic organism, was used to explore the response to environmental relevant concentrations of Cd under acidification conditions. We show for the first time that exposure to acidified freshwater accelerated Cd bioaccumulation and enhanced Cd bioavailability in P. tetraurelia, suggesting the synergistic interaction of Cd and FA. The co-exposure greatly reduced the abundance and carbon biomass, altered lysosomal membrane stability, induced oxidative stress, and consumed more ATP in exposed ciliates. Transcriptome plasticity enabled P. tetraurelia to develop a Cd stress-adaptive transcriptional profile (upregulation of transport and detoxification and downregulation of energy metabolism) under acidification. With a concomitant inhibition in energy production, the exposed ciliates might have diverted the energy from growth and cell replication to compensate for the energetic cost from stress response and detoxification. Collectively, acidified freshwater could aggravate Cd toxicity, which, in turn, arouses the response strategy of ciliates to cope with stress, providing a mechanistic understanding of the interaction between freshwater acidification and Cd pollution in the basic trophic level ciliated protozoa in freshwater ecosystems.

This study used 24 male rats to determine the protective effects of a new selenium molecule (glucose selenol) on cadmium (Cd) induced hepatic toxicity. The rats were randomly divided into four groups: control group, Cd group, Cd + 0.15 Se group, and Cd + 0.4 Se group. The results showed that glucose selenol supplementation alleviated the adverse impact of Cd on lipid metabolism, including decreased serum triacylglycerol and cholesterol levels. Transcriptome analysis revealed that, compared to the control group, Cd changed the expression of 1379 genes - discernibly affecting lipid metabolism pathways. Proteomic analysis primarily indicated alterations in lipid metabolism-related pathways. In conclusion, glucose selenol restored lipid metabolism disorders induced by Cd, thus rescuing hepatic damage. This integrated analysis identified the influence of glucose selenol on Cd-induced hepatic toxicity and provided its potential application prospects in alleviating the impact of heavy metal pollution, such as Cd, on human health.

Cadmium (Cd) and inorganic arsenic (As) compounds are considered to be among the major public health hazards. This is due to both the high intrinsic toxicity of these substances and the often difficult to avoid exposure of the general population through contaminated water and food. One proposed method to reduce the toxic effects of As and Cd on animals and humans is the use of selenium (Se). As discussed in our previous article, laboratory studies show that this micronutrient can have a beneficial effect on the detoxification of As and Cd in the body through the formation of non-toxic complexes with these elements, as well as through the antioxidant effects of selenoproteins. New data that have emerged in recent years allow for a clearer description of the interaction between Se and As and Se and Cd. Human studies show that optimal levels of Se can have a beneficial effect in reducing the toxic effects associated with exposure to As or Cd. However, as Se levels in the body increase, the protective effects of Se may be reversed. Recent laboratory studies confirm the antagonistic effects of medium doses of Se toward Cd and As through the formation of nontoxic complexes, antioxidant, anti-inflammatory effects, and induction of pro-survival pathways in cells. In conclusion, Se has a complex effect on As and Cd toxicity, with both benefits and potential risks, depending on the form of Se and its dose as a supplement or the status (level) of this micronutrient in the body.

Erythropoietin (EPO) is known for its role in hematopoiesis and also exhibits anti-inflammatory, anti-apoptotic, antioxidant, and cytoprotective properties. However, its clinical application is limited by hematopoietic side effects. ARA290, a non-hematopoietic derivative of EPO, selectively activates the innate repair receptor (IRR) and replicates these protective effects without the associated hematopoietic complications. Cadmium (Cd), a prevalent environmental toxin, causes neurotoxic damage through mechanisms such as oxidative stress, genotoxicity, apoptosis, and inflammation. This study explored ARA290's neuroprotective effects against cadmium-induced toxicity in PC12 cells, an in vitro model for neuronal health. PC12 cells pretreated with ARA290 showed significantly improved cell viability in the MTT assay, indicating reduced cytotoxicity. The comet assay revealed decreased DNA damage, suggesting reduced genotoxicity. ARA290 also alleviated oxidative stress, as evidenced by reduced levels of reactive oxygen species (ROS) and malondialdehyde (MDA), alongside increased glutathione (GSH), total antioxidant capacity (TAC), and superoxide dismutase (SOD) activities. A marker of apoptosis, TUNEL-positive cells, was significantly reduced. Additionally, ARA290 decreased inflammatory markers such as TNF alpha, IL1ß and IL 6. These findings demonstrate that ARA290, via IRR activation, provides robust neuroprotection against cadmium-induced toxicity, suggesting a multi-faceted protective mechanism. This highlights ARA290's potential therapeutic role in managing heavy metal-induced neurotoxicity and supports further research into its long-term effects and applications in other neurodegenerative diseases or conditions involving environmental toxins.

ARA290 as a Neuroprotective Agent: ARA290, a modified form of erythropoietin that doesn't affect blood production, shows promising neuroprotective effects. It helps counteract the harmful effects of cadmium exposure on nerve cells by reducing oxidative stress, inflammation, cell death, and DNA damage.Reducing Oxidative Stress: ARA290 plays a key role in lowering oxidative stress by cutting down on harmful molecules like reactive oxygen species (ROS) and malondialdehyde (MDA). At the same time, it boosts the body's natural antioxidant defenses, including glutathione (GSH), superoxide dismutase (SOD), and overall antioxidant capacity.Protecting DNA Integrity: By reducing DNA damage caused by cadmium, ARA290 helps preserve the genetic stability of nerve cells. This protective effect is evident in laboratory tests, where it lowers the extent of DNA damage seen in the comet assay.Fighting Inflammation and Cell Death: ARA290 also has strong anti-inflammatory and anti-apoptotic effects. It reduces levels of inflammation markers like TNF-α, IL-1β, and IL-6, and significantly cuts down on nerve cell death, as seen in fewer TUNEL-positive cells in experiments.A Therapeutic Promise: Overall, these findings underscore ARA290's ability to protect the nervous system through multiple pathways. This makes it a promising candidate for treating cadmium-induced nerve damage and potentially other neurodegenerative conditions.

Cadmium (Cd) is a serious environmental pollutant affecting various tissues/organs in broilers and compromising their immunological function and productivity. Therefore, the current study aimed to investigate Cd-induced immunotoxicity and potential immunoprotective effect of rutin nanoparticles (RNPs) in the bursal tissue of broilers. A total number of 150 chicks from the Hubbard breed were randomly divided into 5 groups. Group I was fed on standard basal diet (SD) with normal drinking water (DW), Group II received SD containing RNPs (50 mg/kg feed) with DW, Group III fed on SD and DW containing Cd (150 mg/L), Group IV co-treated with rutin-enforced SD (50 mg/kg diet) and DW containing Cd (150 mg/L), and finally, Group V co-supplemented with RNP-enhanced SD (50 mg/kg diet) DW containing Cd (150 mg/L). Productive performance, economic efficiency, oxidative biomarkers, histopathological changes, and the expression level of TLR-4, HSP-70, caspase 3, NF-κB, Bcl-2, and Bax were assessed in the BF tissue. Cd led to severe production and economic losses in exposed birds with a marked surge of oxidative biomarkers, pro-inflammatory cytokines, and histopathological changes in the bursal tissue which could be explained through upregulation of the Hsp70/TLR4/NF-κB molecular pathway in the BF tissue. Meanwhile, RNPs could alleviate most of these changes and prevail optimistic immunomodulatory properties which subsequently could enhance broilers' productivity when incorporated in their diets.

Anthropic activities have significantly elevated cadmium levels, making it a significant stressor in aquatic ecosystems. Present in high concentrations across water bodies, cadmium is known to bioaccumulate and biomagnify throughout the food chain. While the toxic effects of cadmium on the organs and tissues of aquatic species are well-documented, little is known about its impact on sensory systems crucial for survival. Consequently, this study investigated the impact of short-term exposure (96 h) to 25 µM cadmium chloride on the olfactory system of adult zebrafish. The research aimed to assess structural and functional changes in the zebrafish's olfactory lamellae, providing a deeper understanding of how cadmium affects the sense of smell in this aquatic species. After exposure, cyto-anatomical alterations in the lamellae were analysed using light microscopy and immunocytochemistry. They revealed severe lamellar edema, epithelial thickening, and an increased number of apoptotic and crypt cells. Rodlet and goblet cells also increased by 3.5- and 2.5-fold, respectively, compared to control lamellae, and collagen density in the lamina propria increased 1.7-fold. Cadmium upregulated metallothioneins and increased the number of PCNA-positive cells. The olfactory function was assessed through a behavioural odour recognition test, followed by a recovery phase in which zebrafish exposed to cadmium were placed in clean water for six days. The exposed fish performed poorly, failing to reach food in five consecutive trials. However, lamellar damage was reduced after the recovery period, and their performance improved, becoming comparable to the control group. These results suggest that cadmium disrupts the sense of smell, and that recovery is possible after short-term exposure. This evidence sheds light on aspects of animal survival that are often overlooked when assessing environmental pollution.

Physical activity (PA) may be considered an alternative method to ameliorate the elevated mortality risks associated with cadmium exposure. In this prospective cohort study, a total of 20,253 participants (weighted mean age, 47.79 years), including 10,247 men (weighted prevalence: 50.1 %), aged 18 years or older, were selected from the National Health and Nutrition Examination Survey from 2007 to 2018. Multivariable Cox proportional hazards regression models were utilized to evaluate the associations between blood cadmium levels, PA, and the risks of mortality. Restricted cubic spline analyses were employed to investigate the nonlinear relationships between blood cadmium and PA levels and mortality risks. During a median follow-up of 7.6 years, a total of 2002 (9.89 %) all-cause deaths occurred, of which 581 (2.87 %) participants were due to cardiovascular disease (CVD) and 498 (2.46 %) died of cancer. J-shaped associations were observed for blood cadmium with risks of mortality (all Poverall < 0.001; all Pnonlinearity < 0.001). Blood cadmium and PA had multiplicative interactions on mortality risk (all Pinteraction < 0.05). Compared with the subgroup with the lowest quartile of blood cadmium and recommended PA, the combination of the highest quartile of blood cadmium and without recommended PA was associated with the highest risks of all-cause and cancer mortality, followed by those meeting recommended PA but in the highest quartile of blood cadmium (hazard ratios, 2.43; 95 % confidence interval, 1.95-3.02). Achieving recommended PA significantly attenuated the detrimental effects of blood cadmium on all-cause, CVD, and cancer mortality risks.

Heavy metals are naturally occurring components of the Earth's crust and persistent environmental pollutants. Human exposure to heavy metals occurs via various pathways, including inhalation of air/dust particles, ingesting contaminated water or soil, or through the food chain. Their bioaccumulation may lead to diverse toxic effects affecting different body tissues and organ systems. The toxicity of heavy metals depends on the properties of the given metal, dose, route, duration of exposure (acute or chronic), and  extent of bioaccumulation. The detrimental impacts of heavy metals on human health are largely linked to their capacity to interfere with antioxidant defense mechanisms, primarily through their interaction with intracellular glutathione (GSH) or sulfhydryl groups (R-SH) of antioxidant enzymes such as superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione reductase (GR), and other enzyme systems. Although arsenic (As) is believed to bind directly to critical thiols, alternative hydrogen peroxide production processes have also been postulated. Heavy metals are known to interfere with signaling pathways and affect a variety of cellular processes, including cell growth, proliferation, survival, metabolism, and apoptosis. For example, cadmium can affect the BLC-2 family of proteins involved in mitochondrial death via the overexpression of antiapoptotic Bcl-2 and the suppression of proapoptotic (BAX, BAK) mechanisms, thus increasing the resistance of various cells to undergo malignant transformation. Nuclear factor erythroid 2-related factor 2 (Nrf2) is an important regulator of antioxidant enzymes, the level of oxidative stress, and cellular resistance to oxidants and has been shown to act as a double-edged sword in response to arsenic-induced oxidative stress. Another mechanism of significant health threats and heavy metal (e.g., Pb) toxicity involves the substitution of essential metals (e.g., calcium (Ca), copper (Cu), and iron (Fe)) with structurally similar heavy metals (e.g., cadmium (Cd) and lead (Pb)) in the metal-binding sites of proteins. Displaced essential redox metals (copper, iron, manganese) from their natural metal-binding sites can catalyze the decomposition of hydrogen peroxide via the Fenton reaction and generate damaging ROS such as hydroxyl radicals, causing damage to lipids, proteins, and DNA. Conversely, some heavy metals, such as cadmium, can suppress the synthesis of nitric oxide radical (NO·), manifested by altered vasorelaxation and, consequently, blood pressure regulation. Pb-induced oxidative stress has been shown to be indirectly responsible for the depletion of nitric oxide due to its interaction with superoxide radical (O2·-), resulting in the formation of a potent biological oxidant, peroxynitrite (ONOO-). This review comprehensively discusses the mechanisms of heavy metal toxicity and their health effects. Aluminum (Al), cadmium (Cd), arsenic (As), mercury (Hg), lead (Pb), and chromium (Cr) and their roles in the development of gastrointestinal, pulmonary, kidney, reproductive, neurodegenerative (Alzheimer's and Parkinson's diseases), cardiovascular, and cancer (e.g. renal, lung, skin, stomach) diseases are discussed. A short account is devoted to the detoxification of heavy metals by chelation via the use of ethylenediaminetetraacetic acid (EDTA), dimercaprol (BAL), 2,3-dimercaptosuccinic acid (DMSA), 2,3-dimercapto-1-propane sulfonic acid (DMPS), and penicillamine chelators.

As a crucial organ of the female reproductive system, the ovary has both reproductive and endocrine functions. Oxidative stress refers to an increase in intracellular reactive oxygen species (ROS), which play a role in the normal physiological activity of the ovary. However, excessive ROS can cause damage to the ovary. With the advancement of human industrial activities, heavy metal pollution has become increasingly severe. Heavy metals cause oxidative stress through both direct and indirect mechanisms, leading to changes in signal transduction pathways that damage the ovaries. This review aims to outline the adverse effects of oxidative stress on the ovaries triggered by heavy metals such as copper, arsenic, cadmium, mercury, and lead. The detrimental effects of heavy metals on ovaries include follicular atresia and decreased estrogen production in experimental animals, and they also cause premature ovarian insufficiency in women. Additionally, this review discusses the role of antioxidants, provides some treatment methods, summarizes the limitations of current research, and offers perspectives for future research directions.

Cadmium (Cd) is a very poisonous pollutant in the environment that has harmful implications on the neurological system. While high fiber intake is beneficial for mental health, it remains unknown whether the recommended basis for dietary fiber intake (DFI) (14 g/1000 kcal per day) can alleviate Cd-induced depression.

The investigation employed data from the National Health and Nutrition Examination Survey (NHANES) conducted between the years 2005 and 2020. The research encompassed individuals who had information on blood Cd concentrations, two 24-hour dietary recalls, and depression diagnosis. We deployed weighted logistic regression analyses to estimate the association of exposure to Cd and DFI with depression risk.

The adjusted ORs (95% CI) for depression were 1.33 (95% CI: 1.08, 1.65) and 1.64 (95% CI: 1.38, 1.94) for the third and fourth quartiles of blood Cd concentrations, respectively (Ptrend < 0.001). Doubling DFI was connected with a 0.78-fold (95% CI: 0.71, 0.85) decrease in the risk of depression. Participants below recommended DFI levels had a greater depression risk with higher blood Cd concentrations: OR of 1.39 (95% CI: 1.11, 1.73) for the third and 1.67 (95% CI: 1.40, 1.98) for the fourth quartile. No significant association between Cd exposure and depression was perceived for participants meeting recommended DFI levels.

Higher blood Cd burden was associated with elevated depression risk, while recommended DFI could alleviate this effect. High-fiber dietary pattern may counteract the deleterious effect of environmental pollutants such as Cd on depression.

Not applicable.

The presence of heavy metals in water represents a risk to the life of all species on the planet. Phytoremediation is an effective alternative to remove heavy metals from contaminated aqueous environments. In the present research, Chenopodium album L. was examined for the remediation of waters contaminated with Cd, Pb, and Hg. Studies were carried out in waters containing each metal separately (monometallic aqueous systems) and in mixtures (trimetallic aqueous systems). First, the adaptation of Chenopodium album to different concentrations of Hoagland's nutrient solution (HNS) was evaluated, then, a phytotoxicity study was carried out to determine the appropriate concentrations of each metal to test the tolerance of the plant during the accumulation study, and finally, the bioaccumulation capacity of Chenopodium album for Cd, Pb, and Hg was evaluated. Chenopodium album showed tolerance to levels of 5 mg/L Hg and 10 mg/L Cd and Pb in 25% HNS. The bioaccumulation tests showed that Chenopodium album can remediate Cd, Pb, and Hg contaminated waters in both monometallic and trimetallic aqueous systems. These findings suggest important future applications in the food industry for the production of Chenopodium album as we demonstrate that this species adapts and grows in hydroponic media. In particular, the ability of Chenopodium album to adapt to extreme conditions could be exploited for further studies on phytoremediation of heavy metals in river water, irrigation water, wastewater, effluents, and mine tailings.

Phascolosoma esculenta is a unique aquatic invertebrate native to China, whose habitat is highly susceptible to environmental pollution, making it an ideal model for studying aquatic toxicology. Mitochondrial thioredoxin (Trx2), a key component of the Trx system, plays an essential role in scavenging reactive oxygen species (ROS), regulating mitochondrial membrane potential, and preventing ROS-induced oxidative stress and apoptosis. This study investigated the toxicity of cadmium (Cd) on P. esculenta and the role of P. esculenta Trx2 (PeTrx2) in Cd detoxification. The results showed that Cd stress altered the activities of T-SOD and CAT, as well as the contents of GSH and MDA in the intestine. After 96 h of exposure, histological damages such as vacuolization, cell necrosis, and mitophagy were observed. Suggesting that Cd stress caused oxidative damage in P. esculenta. Furthermore, with the prolongation of stress time, the expression level of intestinal PeTrx2 mRNA initially increased and then decreased. The recombinant PeTrx2 (rPeTrx2) protein displayed dose-dependent redox activity and antioxidant capacity and enhanced Cd tolerance of Escherichia coli. After RNA interference (RNAi) with PeTrx2, significant changes in the expression of apoptosis-related genes (Caspase-3, Bax, Bcl-2, and Bcl-XL) were observed. Proving that PeTrx2 rapidly responded to Cd stress and played a vital role in mitigating Cd-induced oxidative stress and apoptosis. Our study demonstrated that PeTrx2 is a key factor for P. esculenta to endure the toxicity of Cd, providing foundational data for further exploration of the molecular mechanisms underlying heavy metal resistance in P. esculenta.

Cadmium (Cd), a highly toxic heavy metal, profoundly impacts crop productivity. The bHLH-type transcription factors regulate plant stress responses, yet their involvement in maize's Cd stress response remains unclear. Here, we studied ZmbHLH105, a maize bHLH gene induced by Cd exposure. Overexpression of ZmbHLH105 in maize seedlings, which were treated with 1.0 mM CdCl2 for 7 days, increased endogenous ABA levels, decreased Cd accumulation, and enhanced Cd stress tolerance. ZmbHLH105 directly bound to promoter regions of two key ABA biosynthesis genes ZmNCED1/2, activating their transcription, thus boosting ABA levels and Cd tolerance. ZmbHLH105-overexpression promoted lignin synthesis, while ZmbHLH105-RNAi attenuated this effect. Exogenous ABA supplementation increased lignin content in Cd-stressed maize roots, suggesting ZmbHLH105-mediated Cd tolerance involves ABA-induced lignin deposition and cell wall thickening. Moreover, Cd transport-related gene expression was suppressed in ZmbHLH105 overexpression lines. Our findings demonstrate that ZmbHLH105 decreases Cd accumulation, improving Cd tolerance by enhancing ABA biosynthesis, increasing lignin deposition, thickening cell walls, and inhibiting Cd absorption in maize roots. This study unveils ZmbHLH105's mechanisms in Cd tolerance, highlighting its potential in breeding low Cd-accumulating crops for food and environment safety.

Cadmium (Cd) is a heavy metal environmental pollutant that can cause serious health problems. Cd can cause structural changes in the testes and exposure to this heavy metal is associated with the loss of sperms and male infertility. The role of oxidative stress and inflammation in Cd toxicity has been acknowledged. Diallyl disulfide (DADS), an organo-sulfur compound found in garlic, possesses antioxidant, anti-inflammatory, and cytoprotective effects. This study evaluated the protective effect of DADS against Cd reproductive toxicity in male rats, emphasizing the involvement of redox imbalance, TLR-4/NF-κB and JAK1/STAT3 signaling, and SIRT1.

DADS (10 mg/kg body weight) was administered orally to rats for 14 days and a single dose of Cd (1.2 mg/kg) was injected intraperitoneally on day 7. Blood and samples from the testes were collected for analysis.

Cd caused testicular injury manifested by multiple histopathological changes and loss of sperms from seminiferous tubules. Circulating levels of gonadotropins and testosterone were decreased in Cd-administered rats. DADS prevented Cd-induced testicular injury and ameliorated serum levels of gonadotropins and testosterone. Cd increased testicular reactive oxygen species (ROS) and malondialdehyde (MDA) and upregulated TLR-4, NF-κB, pro-inflammatory cytokines, JAK1 and STAT3 phosphorylation, Bax and caspase-3, while decreased antioxidants and Bcl-2. DADS effectively decreased ROS and MDA, downregulated TLR-4, NF-κB, JAK1, STAT3, pro-inflammatory cytokines and pro-apoptosis markers in Cd-administered rats. In addition, DADS enhanced antioxidants, Bcl-2, SIRT1 and cytoglobin in the testis of Cd-administered rats.

DADS prevents Cd-induced testicular injury by attenuating oxidative stress, apoptosis, and TLR-4/NF-κB and JAK1/STAT3 signaling, and upregulating SIRT1 and antioxidants.

Heavy metals are toxic environmental pollutants with serious health effects on humans and animals. Cadmium (Cd) is known for its serious nephrotoxic effect and its toxicity involves oxidative stress (OS) and inflammation. Diallyl disulfide (DADS), a main constituent of garlic, exhibites cytoprotective and antioxidant activities. This study investigated the effect of DADS on OS, inflammation, and fibrosis induced by Cd in rat kidney, pointing to the involvement of transforming growth factor-β (TGF-β)/Smad3 and nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling, and peroxisome proliferator-activated receptor gamma (PPARγ). Rats received DADS for 14 days and Cd on day 7 and blood and kidney samples were collected. Cd elevated serum creatinine, urea and uric acid, provoked kidney histopathological alterations and collagen deposition, increased kidney malondialdehyde (MDA) level, and decreased glutathione (GSH) and antioxidant enzymes. Nuclear factor-kappaB (NF-κB) p65, interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-1β, and CD68 were upregulated in Cd-administered rat kidney. DADS prevented kidney injury, mitigated OS, suppressed NF-κB, CD68 and pro-inflammatory mediators, and boosted antioxidants. DADS downregulated TGF-β1, Smad3 phosphorylation and Kelch-like ECH-associated protein-1 (Keap1), and increased Nrf2, HO-1, cytoglobin, and PPARγ. In conclusion, DADS protects the kidney against Cd toxicity by attenuating OS, inflammation, and TGF-β1/Smad3 signaling, and enhancement of Nrf2/HO-1 signaling, antioxidants, and PPARγ.

Abnormal biosynthesis of spliceosomes and ribosomes can lead to their dysfunction, which in turn disrupts protein synthesis and results in various diseases. While genetic factors have been extensively studied, our understanding of how environmental compounds interfere with spliceosome and ribosome biosynthesis remains limited. In the present study, we employed a Reduced Transcriptome Analysis (RTA) approach, integrating large-scale transcriptome data sets of zebrafish and compiling a specific zebrafish gene panel focusing on the spliceosome and ribosome, to elucidate the potential disruptors targeting their biosynthesis. Transcriptomic data sets for 118 environmental substances and 1400 related gene expression profiles were integrated resulting in 513 exposure signatures. Among these substances, several categories including PCB126, transition metals Lanthanum (La) and praseodymium (Pr), heavy metals Cd2+ and AgNO3 and atrazine were highlighted for inducing the significant transcriptional alterations. Furthermore, we found that the transcriptional patterns were distinct between categories, yet overlapping patterns were generally observed within each group. For instance, over 82 % differentially expressed ribosomal genes were shared between La and Pr within the equivalent concentration range. Additionally, transcriptional complexities were also evident across various organs and developmental stages of zebrafish, with notable differences in the inhibition of the transcription of various spliceosome subunits. Overall, our results provide novel insights into the understanding of the adverse effects of environmental compounds, thereby contributing to their environmental risk assessments.

The use of plant growth-promoting rhizobacteria (PGPR) for the bioremediation of heavy metal cadmium (Cd) and for enhancing plant growth in Cd-polluted soil is widely recognized as an effective approach. This study aimed to isolate Cd-resistant bacteria with plant growth-promoting (PGP) traits from the rhizosphere of vegetables subjected to metal contamination and to investigate the mechanisms associated with Cd adsorption as well as its impact on Cd uptake in lettuce. Six Cd-resistant bacterial strains were isolated from rhizosphere soil, among which the R27 strain exhibited the highest tolerance to Cd (minimum inhibitory concentration of 2000 mg/L) along with PGP traits, including phosphate solubilization (385.11 mg/L), the production of indole-3-acetic acid (IAA) (35.92 mg/L), and siderophore production (3.34 mg/L). Through a range of physiological, biochemical, and molecular assessments, the R27 strain was classified as Bacillus siamensis. This strain demonstrated notable efficiency in removing Cd2+ from the growth medium, achieving an efficacy of 80.1%. This removal was facilitated by cell surface adsorption through functional groups such as O-H, C=O, -CO-NH-, and C-O, alongside intracellular Cd accumulation, as evidenced by SEM, TEM, EDX, and FTIR analyses. Pot culture experiments indicated that R27 significantly promoted lettuce seedling growth and helped plants tolerate Cd stress, with the underlying mechanisms likely involving increased antioxidant activities for scavenging reactive oxygen species (ROS) induced by Cd stress, and reduced Cd2+ levels in lettuce seedlings to mitigate Cd2+ toxicity. These physiological changes were further supported by the down-regulation of genes associated with cadmium transport, including IRT1, Nramp1, HMA2, HMA4, ZIP4, and ZIP12, as well as the significantly reduced root bio-concentration factor (BCF) and translocation factor (TF). In summary, the R27 strain offers considerable potential in the bioremediation of Cd-polluted soils and can serve as a bio-fertilizer to enhance plant growth.

Cardiovascular diseases are a rampant public health threat. Environmental contaminants, such as Cadmium (Cd), a toxic metal, are risk factors for cardiovascular diseases. Given that human exposure to Cd is increasing, there is a need for therapies to ameliorate Cd toxicity. Selenium (Se), an essential trace element, has been proposed to rescue the effects of Cd toxicity, with mixed effects. Se's narrow therapeutic window necessitates precise dosing to avoid toxicity. Here, we assessed the effects of various waterborne Cd and Se concentrations and sequences on cardiac function using zebrafish (Danio rerio). We showed that Cd induced pericardial edemas and modified heart rates in zebrafish larvae in a concentration-dependent manner. To identify the therapeutic range of Se for Cd-induced cardiotoxicity, zebrafish embryos were treated with 0, 10, 50, 100, 150, or 200 μg/L Se for 1-4 days prior to exposure to 2.5 and 5 μg/L Cd. We found that a 50 µg/L Se pre-treatment before 2.5 μg/L Cd, but not 5 μg/L Cd, reduced the prevalence of pericardial edemas and ameliorated Cd-induced bradycardia in zebrafish. Zebrafish exposed to 10 and 50 μg/L of Se for up to 4 days showed typical heart morphology, whereas other Se-exposed and control fish presented pericardial edemas. Longer Se pre-treatment durations led to fewer incidences of pericardial edemas. Overall, this study highlights the importance of optimizing Se concentrations and pre-treatment periods to harness its protective effects against Cd-induced cardiotoxicity. These findings provide insights into potential therapeutic strategies for reducing Cd-related cardiovascular damage in humans.

Silver (Ag) and cadmium (Cd) are non-essential metals that, as a result of natural processes and human activities, reach the aquatic environment where they interact with biota inducing potential toxic effects. To determine the biological effects of these metals on the endobenthic bivalve Scrobicularia plana, specimens were exposed to Ag and Cd at two concentrations, 5 and 50 μg∙L-1, for 7 days in a controlled microcosm system. The levels of the metals were measured in the seawater, sediments and clam tissues. The possible toxic biological effects of Ag and Cd were studied using a battery of biochemical biomarkers that are responsive to oxidative stress: superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione-S-transferase (GST) activities, and metallothioneins (MTs) and lipid peroxidation (LPO) levels. Since both metals have been linked to oxidative stress, redox modifications to proteins were studied by differential isotopic labelling of the oxidised and reduced forms of cysteines (Cys). An accumulation of metals was observed in the digestive gland and gills following exposure, together with the activation of enzyme activities (SOD for the Cd exposure; SOD, CAT, GST, and GR for the Ag exposure). The MT and LPO levels (after individual exposure to Ag and Cd) increased, which suggests the existence of antioxidant and detoxification processes to mitigate the toxic oxidative effects of both metals. The redox proteomic analysis identified 771 Cys-containing peptides (out of 514 proteins), of which 195 and 226 changed after exposure to Ag and Cd, respectively. Bioinformatics analysis showed that exposure to metal affects relevant functional pathways and biological processes in S. plana, such as: "cellular respiration" (Ag), "metabolism of amino acids" and "synthesis and degradation of proteins" (Ag and Cd), "carbohydrate metabolism" and "oxidative stress" (Cd). The proteomic approach implemented here is a powerful complement to conventional biochemical biomarkers, since it evaluates changes at the protein level in a high-throughput unbiased manner, thus providing a general appraisal of the biological responses altered by exposure to the contaminants.

This study aimed to determine the protective role of l-ascorbic acid in a pregnant rat model of cadmium-induced toxicity. Cadmium is a toxic heavy metal that can seriously harm placenta and fetus tissue in pregnant women. Forty-two healthy female Wistar albino rats (250-300 g weight and 14-16 weeks) were randomly distributed into six equal groups (n = 7): control, cadmium 1 mg (CD1), cadmium 5 mg (CD5), ascorbic acid (AA), CD1+AA, CD5+AA. Cadmium was administered to pregnant rats by oral gavage every other day, and/or AA (200 mg) was administered every day. At the end of pregnancy (Day 21), blood, placenta, and fetuses were collected from rats. The results indicated that cadmium-induced oxidative stress by increasing the level of MDA and by decreasing the levels of GSH, SOD, and CAT activity in the serum of maternal. However, AA administration significantly decreased MDA levels and increased GSH levels, SOD, and CAT activity (p < 0.05). Cadmium (5 mg/kg) exposure significantly increased creatinine levels compared to AA and CD1+AA groups (p < 0.05). In addition, AA (200 mg/kg) significantly attenuated cadmium-induced histopathological alteration in the placental and fetal tissues. In conclusion, AA may prevent cadmium toxicity in maternal and fetal tissues, as it regulates oxidative imbalance in pregnant rat tissues and alleviates histopathological changes.

Cognitive impairment (CI) is a prodrome of many neurodegenerative diseases with complex and unclear pathogenesis. Metal exposure has been found to be associated with CI, but existing population studies are scarce and have the limitations of single outcome and ignoring mixed exposures. This cross-sectional study was conducted in Shanghai, China, enrolling 836 seniors aged over 60 years to investigate the relationship between combined metal exposure (Lead (Pb), cadmium (Cd), and mercury (Hg)) and CI in the elderly and the mediating effect of oxidative stress. It was found that there were significant differences in urinary Pb, Cd, Hg and blood Pb levels between the CI and normal groups. Urinary Pb and Cd levels were significantly negatively correlated with Montreal Cognitive Assessment (MoCA) score, amyloid β42 (Aβ42), and Aβ42/40, while urinary Cd, Hg and blood Hg were significantly positively correlated with phosphorylated tau protein (P-tau). Weighted quantile sum (WQS) regression indicated that combined metal exposure had a more significant effect on CI than individual exposure. Mediation modeling revealed that plasma superoxide dismutase (SOD) was involved in the effects of urinary Cd on Aβ42/40 and P-tau, with mediation effects accounting for 20 % of the total effect. This study emphasized the combined exposure to metals, and the results can help to properly understand the association between mixed metals exposure and CI in the elderly, as well as provide population data and theoretical basis for identifying early environmental risk factors and discovering potential mechanisms of CI.

Cadmium crosses the blood-brain barrier inducing damage to neurons. Cell impairment is predominantly linked to oxidative stress and glutathione (GSH) depletion. On the other hand, several reports have described an increase of GSH levels in neuronal cells after CdCl2 exposure. Therefore, the aim of the present report was to investigate the relation between changes in GSH levels and mitochondrial damage in neuronal cells after CdCl2 treatment. To characterize neuronal impairment after CdCl2 treatment (0-200 μM) for 1-48 h, we used the SH-SY5Y cell line. We analyzed GSH metabolism and determined mitochondrial activity using high-resolution respirometry. CdCl2 treatment induced both the decreases and increases of GSH levels in SH-SY5Y cells. GSH concentration was significantly increased in cells incubated with up to 50 μM CdCl2 but only 100 μM CdCl2 induced GSH depletion linked to increased ROS production. The overexpression of proteins involved in GSH synthesis increased in response to 50 and 100 μM CdCl2 after 6 h. Finally, strong mitochondrial impairment was detected even in 50 μM CdCl2 treated cells after 24 h. We conclude that a significant decrease in mitochondrial activity can be observed in 50 μM CdCl2 even without the occurrence of GSH depletion in SH-SY5Y cells.

Shrimp are non-negligible victims of cadmium (Cd) contamination, and there is still a lack of strategies for mitigating Cd toxicity in shrimp. Bacillus cereus, with its significant heavy metal (HM) tolerance and chelating effects, is a representative beneficial bacterium to be investigated for mitigating the toxicity of Cd exposure. This study revealed the effects and potential mechanisms of B. cereus in mitigating chronic Cd toxicity in shrimp by analyzing growth performance, hepatopancreatic Cd accumulation, pathology, as well as comprehensive hepatopancreatic transcriptomics and metabolomics in Litopenaeus vannamei. The results showed that shrimp's growth inhibition, hepatopancreatic Cd accumulation and physiological structure damage in B. cereus+chronic Cd group were effectively alleviated compared with the chronic Cd treatment group. The pathways related to amino acid metabolism, glycolipid metabolism, immune response, and antioxidant stress were significantly activated in the B. cereus+chronic Cd group, including glycolysis, pentose phosphate pathway, oxidative phosphorylation, biosynthesis of amino acids, and biosynthesis of unsaturated fatty acids pathways. The key differentially expressed genes (e.g., macrophage migration inhibitory factor, glycine cleavage system H protein, glycine dehydrogenase, phosphoglucomutase-2, asparaginase, ATP synthase subunit, cytochrome c, and 4-hydroxyphenylpyruvate dioxygenase) and metabolites (e.g., L-leucine, D-ribose, gluconic acid, 6-Phosphogluconic acid, sedoheptulose 7-phosphate, 1-Kestose, glyceric acid, arachidic acid, prostaglandins, 12-Keto-tetrahydro-leukotriene B4, and gamma-glutamylcysteine) associated with the above pathways were significantly altered. This study demonstrated that B. cereus is an effective mitigator for the treatment of chronic Cd poisoning in shrimp. B. cereus may play a role in alleviating the toxicity of Cd by enhancing the antioxidant performance, immune defense ability, metabolic stability, and energy demand regulation of shrimp. The study provides reference materials for the study of B. cereus in alleviating Cd toxicity of shrimp and broadens the application of probiotics in treating HM toxicity.

This study evaluated the efficacy of Azadirachta indica ethosomal nanovesicle against Eimeria tenella infection in broiler chicks. Azadirachta indica ethanolic extract was screened phtochemically and analyzed active components of the extracts using high‑performance liquid chromatography (HPLC). Azadirachta indica ethosomal nanovesicle was synthesized and characterized by zeta potential and scanning electron microscope. Broiler chicks were allocated into seven groups. Control group. The second group administered nanosized ethosomal vesicles (1 mL/kg b.wt.). The third group administered Azadirachta indica nanovesicles (30 mg/kg b.wt.) from 10th day of age. Fourth group was infected with E. tenella at a dose of 1 mL containing 40000 oocyst/ chick at 14th day of age. The fifth group administered Azadirachta indica nanovesicle (30 mg/kg b.wt.) from 10th day of age and infected with E. tenella as fourth group. The sixth group infected with E. tenella as the fourth group and treated with Azadirachta indica nanovesicle (30 mg/kg b.wt. for 4 days after clinical signs appearance. The seventh group infected with E. tenella as the fourth group and treated with diclazuril group (1 mL/4 L of water) for 2 successive days. Coccidiosis significantly decreased body weight, feed intake, reduced glutathione (GSH) level while increased feed conversion ratio, oocyst count, malonaldehyde (MDA) and nitric oxide (NO) serum levels, protein expression of interleukin-1 beta (IL-1β), interleukin 6 (IL-6), BAX and Caspase 3, in cecal tissue and induced cecal tissue injury. However, administration of coccidiosis chicks Azadirachta indica nanovesicle enhanced body weight, and serum GSH. While decreased feed intake, feed conversion ratio, oocyst count, MDA, and NO serum levels, and protein expression of IL-1β, IL-6, BAX, and caspase 3 in cecal tissues and ameliorated cecal tissue damage. This study indicated that, A. indica ethosomal nanovesicle had potent anticoccidial properties.

Heavy metals are environmental pollutants that can harm animals and humans even at low concentrations. Cadmium (Cd) is known for its serious health effects on different organs and its toxicity is associated with oxidative stress (OS) and inflammation. Farnesol (FAR), a sesquiterpene alcohol found in many vegetables and fruits, possesses promising anti-inflammatory and antioxidant activities. This study evaluated the effect of FAR on Cd-induced kidney injury, pinpointing its effect of the redox status, inflammation, fibrosis and necroptosis. Rats in this study received FAR for 14 days and Cd on day 7. Elevated serum creatinine, urea and uric acid, and several kidney histopathological alterations were observed in Cd-administered rats. Cd increased MDA, decreased antioxidants, downregulated PPARγ and upregulated NF-κB p65, IL-6, TNF-α, and IL-1β. Necroptosis mediators (RIP1, RIP3, MLKL, and caspase-8) and α-SMA were upregulated, and collagen deposition was increased in Cd-administered rats. FAR ameliorated kidney injury markers and tissue damage, attenuated OS, suppressed NF-κB and inflammatory mediators, and enhanced antioxidants. In addition, FAR suppressed RIP1, RIP3, MLKL, caspase-8, and α-SMA, and enhanced kidney cytoglobin and PPARγ. In conclusion, FAR protects against Cd nephrotoxicity by suppressing OS, inflammatory response and necroptosis, effects associated with enhanced antioxidants, cytoglobin, and PPARγ.

Cadmium (Cd) is a widely distributed pollutant that adversely affects plants' metabolism and productivity. Phytohormones play a vital role in the acclimation of plants to metal stress. On the other hand, phytohormones trigger systemic resistances, including systemic acquired resistance (SAR) and induced systemic resistance (ISR), in plants in response to biotic interactions. The present study aimed to investigate the possible induction of SAR and ISR pathways in relation to the hormonal alteration of barley seedlings in response to Cd stress. Barley seedlings were exposed to 1.5 mg g-1 Cd in the soil for three days. The nutrient content, oxidative status, phytohormones profile, and expression of genes involved in SAR and ISR pathways of barley seedlings were examined. Cd accumulation resulted in a reduction in the nutrient content of barley seedlings. The specific activity of superoxide dismutase and the hydrogen peroxide content significantly increased in response to Cd toxicity. Abscisic acid, jasmonic acid, and ethylene content increased under Cd exposure. Cd treatment resulted in the upregulation of NPR1, PR3, and PR13 genes in SAR pathways. The transcripts of PAL1 and LOX2.2 genes in the ISR pathway were also significantly increased in response to Cd treatment. These findings suggest that hormonal-activated systemic resistances are involved in the response of barley to Cd stress.