Accurate diagnosis and treatment in poisoning cases necessitate the monitoring of diquat and paraquat concentrations. This study presents a competitive colloidal gold immunochromatographic assay (GICA) strip for qualitative detection, alongside hydrophilic interaction liquid chromatography with ultraviolet detection (HILIC-UV) for quantitative assessment. Both methods underwent rigorous validation. The GICA strip achieved a detection limit of 20 ng/mL and demonstrated no cross-reactivity with glyphosate, deltamethrin, or dichlorvos in spiked serum samples. A compliance rate of 100 % confirmed its repeatability, validated by ten quality control samples at a concentration of 200 ng/mL. HILIC-UV exhibited a detection limit of 0.2 μg/mL and excellent linearity for paraquat and diquat in serum and urine across a range of 0.2-6.4 μg/mL (r² > 0.99). Accuracy ranged from 86.4 % to 111.4 %, with relative standard deviation (RSD) below 10.8 %. Sigma metrics for quality control samples varied from 4.47 to 6.09, establishing a 1-3 s/2/3-2 s/R-4s internal quality control scheme (n = 3, r = 1). A total of 24 patient specimens were subjected to dual testing with HILIC-UV and GICA strips. Among these, 21 samples from 17 patients tested positive, while three patients with confirmed glyphosate, deltamethrin, and dichlorvos poisoning tested negative, indicating complete consistency. Of the positive results, 11 patients were diagnosed with paraquat poisoning, and six with diquat poisoning, both of which significantly impair liver, kidney, and coagulation functions. Integrating GICA for rapid qualitative assessment with HILIC-UV for quantitative analysis enhances the identification of diquat and paraquat poisoning, making it particularly suitable for emergency diagnostics.

Diquat is a widely used bipyridyl herbicide that is extensively applied in agricultural production and water management due to its high efficacy in weed control. However, its environmental persistence and the toxic effects it induces have raised widespread concern. Studies show that Diquat primarily enters the body through the digestive tract, leading to poisoning. The core mechanism of its toxicity involves reactive oxygen species (ROS)-induced oxidative stress, which not only directly damages the intestinal barrier function but also exacerbates inflammation and systemic toxicity by disrupting the balance of the gut microbiota and the normal production of metabolic products. This review systematically summarizes the physicochemical properties of Diquat, with a focus on analyzing the mechanisms by which it damages the gut tissue structure, barrier function, and microbiota after digestive tract exposure. The aim is to provide theoretical support for a deeper understanding of Diquat's toxic mechanisms and its digestive tract-centered toxic characteristics, laying a scientific foundation for the development of effective interventions and protective strategies against its toxicity.

We studied the case of a 22-year-old Pregnant woman who self-administered about 200 ml of diquat solution (200 g/L) during a suicide attempt. She developed vomiting, and was admitted to the emergency department of our hospital 5 h later. Based on symptoms, and elevated levels of myoglobin and creatine kinase, the patient was diagnosed with rhabdomyolysis, acute renal failure and toxic encephalopathy caused by diquat poisoning. Undergoing hemoperfusion and hemofiltration were administered immediately. Rhabdomyolysis, toxic encephalopathy, and abortion occurred successively in the pregnant woman. The patient was discharged from the hospital after 37 days of treatment with a Glasgow-Pittsburgh Cerebral Classification (CPC) score of grade 2.this was a case of diquat poisoning complicated with renal failure, rhabdomyolysis, and toxic encephalopathy in a pregnant, which would enrich the experience of diquat poisoning treatment.

Diquat (DQ), a contact herbicide extensively utilized in both agricultural and nonagricultural domains, exhibits a high correlation with neuronal disorders. Nevertheless, the toxicity and underlying mechanisms associated with exposure to environmental concentrations of DQ remain ambiguous. Here, we report dose-dependent cellular neurotoxicity of DQ in Caenorhabditis elegans. First, DQ significantly compromised the development and brood size of worms, shortened the lifespan, and caused epidermal abnormalities. An unbiased transcriptomic analysis disclosed several pathways related to cell death and peroxisome homeostasis underlying this organismal-level toxicity. Moreover, exposure of DQ to C. elegans led to a notable increase of embryonic cell death. Concurrently, DQ exposure specifically caused the loss of dopamine neurons but not two other types of neurons in adulthood, which is in accordance with DQ-induced muscle-related defects such as pharyngeal pumping, body bends, and head thrashes. Mechanistically, DQ exposure induces the generation of reactive oxygen species (ROS) and enhances glutathione-related ROS scavenging pathway. Protein levels and activities of mitochondrial electron transport chain complexes were specifically impaired in the DQ-treated worms. Collectively, this study suggests an ROS-mediated cell death pathway involving the neuronal and behavioral toxicity of DQ, which offers a novel mitochondria-related perspective to elucidate the general toxicity caused by a widely distributed herbicide, DQ, at near-environment concentrations.

Chlorfenapyr, a broad-spectrum insecticide and acaricide of the pyrrole-class pesticides, can induce dizziness, fatigue, profuse sweating, and altered consciousness by interfering with cell energy metabolism. However, chlorfenapyr-related rhabdomyolysis has rarely been reported.

Patient 1 was a healthy 26-year-old man who ingested approximately 30 mL of chlorfenapyr. After gastric lavage, rehydration, diuresis, liver protection, and symptomatic treatment, he was discharged. However, he was readmitted 11 days later with rhabdomyolysis and acute kidney injury, and his blood tralopyril level was 187 μg/mL. Patient 2 was a 43-year-old man who consumed approximately 50 mL of chlorfenapyr without seeking medical care for 6 days. On day 7, his blood chlorfenapyr and tralopyril levels were 42 μg/mL and 542 μg/mL, respectively. Subsequently, the patient was diagnosed with rhabdomyolysis and brainstem injury.

Chlorfenapyr can disrupt cellular energy metabolism, leading to rhabdomyolysis and brainstem injury, and physical activity may trigger and accelerate rhabdomyolysis. The delayed damage caused by chlorfenapyr poisoning may be attributed to the gradual depletion of cellular energy and prolonged presence of its metabolites in the body.

This study aims to explore the clinical characteristics and prognostic factors in patients with diquat (DQ) poisoning and to develop a clinical risk assessment model to improve diagnosis and treatment strategies. Data from 60 patients with DQ poisoning, including basic characteristics, poisoning severity, and inflammatory response indicators, were collected. The plasma concentration of DQ was measured using liquid chromatography-mass spectrometry. The included patients were categorized into survival and death groups based on their 30-day outcomes. Fisher's exact test was used to identify statistically significant clinical indicators (p < .05), and logistic regression within a generalized linear model (GLM) framework was employed to analyze these indicators alongside the severity index of diquat poisoning (SIDP), followed by the construction of a prognostic model. The performance of the model was evaluated through receiver operating characteristic (ROC) analysis, and the accuracy of the model was assessed. Additionally, two independent sample Wilcoxon tests compared the clinical indicators between high-risk and low-risk groups. Fisher's exact test identified significant differences in variables such as oral drug dosage (ODD), time from poisoning to admission (TFPTA), state of consciousness (SOC), Glasgow Coma Scale (GCS), white blood cells (WBC), myoglobin (Myo), high-flow nasal cannula (HFNC), invasive mechanical ventilation (IMV), acute kidney injury (AKI), and acute lung injury (ALI) (p < .05) between the survival and death groups. The GLM-based risk assessment model demonstrated high predictive accuracy, with an area under the ROC curve (AUC) of 0.97 (SE 0.017, 95% CI 0.939-1.001), indicating potent prognostic capability. The Wilcoxon test revealed that ODD, Myo, SIDP, aspartate transferase (AST), creatine kinase (CK), hemoglobin (Hb), cardiac troponin (cTnT), and serum creatinine (Cr) levels were significantly higher in the high-risk group. The clinical risk assessment model effectively predicts the prognosis of patients with DQ poisoning, aiding clinicians in personalizing treatment strategies to improve patient outcomes.

This study aimed to explore the factors influencing pulmonary fibrosis in patients with acute diquat poisoning through logistic regression analysis.

A retrospective analysis was conducted on 68 cases of acute diquat poisoning due to suicidal intent admitted to our hospital from February 2020 to March 2023. Patients were divided into a combined group (28 cases with pulmonary fibrosis) and an acute diquat poisoning group (40 cases without). A healthy control group consisted of 40 individuals. General data were compared among the three groups, and laboratory indicators were analyzed. Single and multiple logistic regression analyses were performed to identify risk factors for pulmonary fibrosis.

There were no significant differences in gender, age, BMI, poisoning status, or treatment timing among the groups (P > 0.05). The combined group had significantly higher diquat ingestion dose, SIRS score, SOFA score, and APACHE II score compared to the poisoning group (P < 0.05). In the acute poisoning group, these scores were also higher than in the healthy controls (P < 0.05). Laboratory indicators, including Hb, PLT, ALP, DBil, ALB, BUN, Glu, BNP, and pH, showed no significant differences (P > 0.05). However, WBC, ALT, TBil, DBil, Cr, K+, Tn I, and Lac levels were significantly higher in the combined group compared to the acute poisoning group (P < 0.05). Logistic regression analysis identified factors influencing pulmonary fibrosis as diquat ingestion dose, K+, ALT, PaO2, Lac, and HCO3-.

The factors influencing pulmonary fibrosis in acute diquat poisoning include diquat ingestion dose, K+, ALT, PaO2, Lac, and HCO3-. These findings enhance understanding of pulmonary fibrosis pathogenesis and may inform clinical management for affected patients.

This study investigates the impact of diquat toxicity levels on in-hospital mortality rates among patients with acute diquat poisoning. It aims to clarify the relationship between diquat toxicity scores and the likelihood of death during hospitalization.

A retrospective cohort study was conducted on 98 individuals with acute diquat poisoning. Data on post-ingestion time, initial diquat plasma concentration, and clinical outcomes were systematically collected for all participants. The toxicity-index of diquat was calculated based on post-ingestion time and initial diquat plasma concentration. Logistic regression analysis was utilized to assess the association between the toxicity-index of diquat and in-hospital mortality rates, adjusting for potential confounding variables such as age, comorbidities, and treatment interventions.

The study found that the overall prevalence of in-hospital mortality was 34.7%, with 58.2% in males. The multivariable-adjusted regression coefficient for in-hospital mortality associated with the toxicity-index was 1.09, with a 95% confidence interval (CI) of 1.01-1.17. Subsequent exploratory subgroup analysis indicated that there were no significant interactions (all p values for interaction were >0.05).

The study found that higher diquat toxicity-index values correlate with increased in-hospital mortality in acute diquat poisoning cases, indicating that the toxicity-index could be a useful biomarker for assessing mortality risk.

This experiment aimed to investigate the effects of Quercetagetin (QG) on the growth performance, antioxidant capacity, and cecal microbiota of broilers. Two hundred and forty 21-day-old WOD168 broilers with similar body weights were randomly divided into five groups of six replicates each with eight chickens. The control group was fed a basal diet composed of corn and soybean meal, while the experimental groups received basal diets supplemented with 0, 10, 20, and 40 mg/kg QG, along with intraperitoneal injection of 20 mg/kg body weight Diquat (DQ). The experiment lasted for 21 days. The results showed that: (1) QG significantly alleviated the decrease in average daily feed intake and average daily gain induced by Diquat, reduced the elevation of serum ACTH content, and significantly increased GH content (P < 0.05); (2) QG supplementation significantly mitigated the decrease in serum CAT activity and duodenal GSH-Px activity induced by Diquat (P < 0.05), as well as the increase in MDA content (P < 0.05); additionally, QG significantly increased the gene expression levels of GSH-Px, Nrf2, and Keap1 (P < 0.05); (3) Alpha and Beta diversity analysis revealed that QG supplementation significantly increased the cecal microbial OTUs and Chao1 index of broilers (P < 0.05). At the phylum level, compared with the Diquat group, the LQG group significantly decreased the relative abundance of Firmicutes (P < 0.05) and significantly increased the relative abundance of Bacteroidota (P < 0.05). At the genus level, compared with the CON group, the Diquat group significantly decreased the abundance of Lactobacillus and Alistipes (P < 0.05), while QG supplementation significantly alleviated the decrease in the abundance of Lactobacillus and Alistipes (P < 0.05). In conclusion, the addition of an appropriate amount (20 mg/kg) of QG to the diet can promote the growth of broilers, enhance antioxidant capacity, and improve intestinal health.

Severe diquat poisoning often leads to acute kidney injury, gastrointestinal injury, paralytic ileus, rhabdomyolysis, respiratory failure, refractory circulatory failure, and brainstem damage.

A previously healthy 38-year-old man was admitted to our hospital with anuria, mild abdominal distension, and calf pain after ingesting diquat (200 g/L) 100 mL approximately 13 h before presentation. His blood diquat concentration was 8.14 µg/L on admission. Gastrointestinal catharsis, haemoperfusion, and haemodiafiltration were performed. Subsequently, he developed marked abdominal distention, impaired consciousness, hypotension, and respiratory failure, leading to death.

Computed tomography revealed gas accumulation in the portal venous system and mesenteric vessels. Moreover, gastrointestinal pneumatosis was present. Computed tomography also revealed changes in the lung, brainstem, and calf muscles.

Diquat poisoning can result in acute kidney injury, hepatic injury, gastrointestinal injury, paralytic ileus, rhabdomyolysis, refractory circulatory failure, brainstem damage, and hepatic portal venous gas, all observed in this patient.

Since 2016, diquat has replaced paraquat in China, resulting in increased diquat poisoning cases. However, understanding of diquat poisoning is still limited. This study aimed to investigate the relationship between initial diquat plasma concentration, severity index, and in-hospital mortality in acute diquat poisoning cases.

This retrospective cohort study, conducted from January 2016 to July 2023 in a tertiary care hospital, used univariate logistic regression to examine the link between the initial diquat plasma concentration, severity index, and in-hospital mortality in acute diquat poisoned patients. A receiver operating characteristic curve assessed the predictive value of these parameters for prognosis.

Among the 87 participants, the median age was 32 years, 35 (40.2%) were female. The overall mortality rate was 37.9%. Logistic regression analysis revealed that the initial diquat plasma concentration and severity index were associated with increased in-hospital mortality. These factors also effectively predicted the prognosis of acute diquat poisoning, with an area under the receiver operating characteristic curve of 0.851 and an optimal diquat concentration threshold of 2.25 mg/L (sensitivity 90.9%, specificity 74.1%, P < 0.05) and an area under the receiver operating characteristic curve of 0.845 with an optimal cut-off value for the sevity index of 9.1 mg/L*min (sensitivity 97%, specificity 74.1%, P < 0.05).

Our results are limited by the retrospective design of this study. However, if validated, these results could impact management strategies, especially in East Asia. Further research is needed due to potential confounding factors.

The findings suggest that a higher initial plasma concentration and severity index in patients with acute diquat poisoning were correlated with higher in-hospital mortality. Prospective validation will confirm the predicative value of these findings.

Diquat dibromide (DQ) is a globally used herbicide in agriculture, and its overuse poses an important public health issue, including male reproductive toxicity in mammals. However, the effects and molecular mechanisms of DQ on testes are limited. In vivo experiments, mice were intraperitoneally injected with 8 or 10 mg/kg/ day of DQ for 28 days. It has been found that heme oxygenase-1 (HO-1) mediates DQ-induced ferroptosis in mouse spermatogonia, thereby damaging testicular development and spermatogenesis. Histopathologically, we found that DQ exposure caused seminiferous tubule disorders, reduced germ cells, and increased sperm malformation, in mice. Reactive oxygen species (ROS) staining of frozen section and transmission electron microscopy (TEM) displayed DQ promoted ROS generation and mitochondrial morphology alterations in mouse testes, suggesting that DQ treatment induced testicular oxidative stress. Subsequent RNA-sequencing further showed that DQ treatment might trigger ferroptosis pathway, attributed to disturbed glutathione metabolism and iron homeostasis in spermatogonia cells in vitro. Consistently, results of western blotting, measurements of MDA and ferrous iron, and ROS staining confirmed that DQ increased oxidative stress and lipid peroxidation, and accelerated ferrous iron accumulation both in vitro and in vivo. Moreover, inhibition of ferroptosis by deferoxamine (DFO) markedly ameliorated DQ-induced cell death and dysfunction. By RNA-sequencing, we found that the expression of HO-1 was significantly upregulated in DQ-treated spermatogonia, while ZnPP (a specific inhibitor of HO-1) blocked spermatogonia ferroptosis by balancing intracellular iron homeostasis. In mice, administration of the ferroptosis inhibitor ferrostatin-1 effectively restored the increase of HO-1 levels in the spermatogonia, prevented spermatogonia death, and alleviated the spermatogenesis disorders induced by DQ. Overall, these findings suggest that HO-1 mediates DQ-induced spermatogonia ferroptosis in mouse testes, and targeting HO-1 may be an effective protective strategy against male reproductive disorders induced by pesticides in agriculture.

The aim of this study was to develop and validate predictive models for assessing the risk of death in patients with acute diquat (DQ) poisoning using innovative machine learning techniques. Additionally, predictive models were evaluated through the application of SHapley Additive ExPlanations (SHAP). A total of 201 consecutive patients from the emergency departments of the First Hospital and Shengjing Hospital of China Medical University admitted for deliberate oral intake of DQ from February 2018 to August 2023 were analysed. The initial clinical data of the patients with acute DQ poisoning were collected. Machine learning methods such as logistic regression, random forest, support vector machine (SVM), and gradient boosting were applied to build the prediction models. The whole sample was split into a training set and a test set at a ratio of 8:2. The performances of these models were assessed in terms of discrimination, calibration, and clinical decision curve analysis (DCA). We also used the SHAP interpretation tool to provide an intuitive explanation of the risk of death in patients with DQ poisoning. Logistic regression, random forest, SVM, and gradient boosting models were established, and the areas under the receiver operating characteristic curves (AUCs) were 0.91, 0.98, 0.96 and 0.94, respectively. The net benefits were similar across all four models. The four machine learning models can be reliable tools for predicting death risk in patients with acute DQ poisoning. Their combination with SHAP provides explanations for individualized risk prediction, increasing the model transparency.

Diquat (DQ) poisoning can cause multiple organ damage, and the kidney is considered to be the main target organ. Increasing evidence shows that alleviating oxidative stress and inflammatory response has promising application prospects. Epigallocatechin gallate (EGCG) has potent antioxidant and anti-inflammatory effects. In this study, red blood cell membrane (RBCm)-camouflaged polylactic-co-glycolic acid (PLGA) nanoparticles (NPs) were synthesized to deliver EGCG (EGCG-RBCm/NPs) for renal injury induced by DQ. Human renal tubular epithelial cells (HK-2 cells) were stimulated with 600 μM DQ for 12 h and mice were intraperitoneally injected with 50 mg/kg b.w. DQ, followed by 20 mg/kg b.w./day EGCG or EGCG-RBCM/NPs for 3 days. The assessment of cellular vitality was carried out using the CCK-8 assay, while the quantification of reactive oxygen species (ROS) was performed through ROS specific probes. Apoptosis analysis was conducted by both flow cytometry and TUNEL staining methods. Pathological changes in renal tissue were observed. The expressions of NLRP3, IL-1β, IL-18, NFκB and Caspase1 were detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR), immunohistochemistry, immunofluorescence, and Western blot. The results showed that the DQ group had increased ROS expression, increased the level of oxidative stress, and increased apoptosis rate compared with the control group. Histopathological analysis of mice in the DQ group showed renal tubular injury and elevated levels of blood urea nitrogen (BUN), serum creatinine (SCr), kidney injury molecule-1 (KIM-1), and cystatin C (Cys C). Furthermore, the DQ group exhibited heightened expression of NLRP3, p-NFκB p65, Caspase1 p20, IL-1β, and IL-18. However, EGCG-RBCm/NPs treatment mitigated DQ-induced increases in ROS, apoptosis, and oxidative stress, as well as renal toxicity and decreases in renal biomarker levels. Meanwhile, the expression of the above proteins were significantly decreased, and the survival rate of mice was ultimately improved, with an effect better than that of the EGCG treatment group. In conclusion, EGCG-RBCm/NPs can improve oxidative stress, inflammation, and apoptosis induced by DQ. This effect is related to the NF-κB/NLRP3 inflammasome pathway. Overall, this study provides a new approach for treating renal injury induced by DQ.

Diquat (DQ) poisoning is a severe medical condition associated with life-threatening implications and multiorgan dysfunction. Despite its clinical significance, the precise underlying mechanism remains inadequately understood. This study elucidates that DQ induces instability in the mitochondrial genome of endothelial cells, resulting in the accumulation of Z-form DNA. This process activates Z-DNA binding protein 1 (ZBP1), which then interacts with receptor-interacting protein kinase 3 (RIPK3), ultimately leading to RIPK3-dependent necroptotic and ferroptotic signaling cascades. Specific deletion of either Zbp1 or Ripk3 in endothelial cells simultaneously inhibits both necroptosis and ferroptosis. This dual inhibition significantly reduces organ damage and lowers mortality rate. Notably, our investigation reveals that RIPK3 has a dual role. It not only phosphorylates MLKL to induce necroptosis but also phosphorylates FSP1 to inhibit its enzymatic activity, promoting ferroptosis. The study further shows that deletion of mixed lineage kinase domain-like (Mlkl) and the augmentation of ferroptosis suppressor protein 1 (FSP1)-dependent non-canonical vitamin K cycling can provide partial protection against DQ-induced organ damage. Combining Mlkl deletion with vitamin K treatment demonstrates a heightened efficacy in ameliorating multiorgan damage and lethality induced by DQ. Taken together, this study identifies ZBP1 as a crucial sensor for DQ-induced mitochondrial Z-form DNA, initiating RIPK3-dependent necroptosis and ferroptosis. These findings suggest that targeting the ZBP1/RIPK3-dependent necroptotic and ferroptotic pathways could be a promising approach for drug interventions aimed at mitigating the adverse consequences of DQ poisoning.

Sugarcane workers are exposed to potentially hazardous agrochemicals, including pesticides, heavy metals, and silica. Such occupational exposures present health risks and have been implicated in a high rate of kidney disease seen in these workers.

To investigate potential biomarkers and mechanisms that could explain chronic kidney disease (CKD) among this worker population, paired urine samples were collected from sugarcane cutters at the beginning and end of a harvest season in Guatemala. Workers were then separated into 2 groups, namely those with or without kidney function decline (KFD) across the harvest season. Urine samples from these 2 groups underwent elemental analysis and untargeted metabolomics.

Urine profiles demonstrated increases in silicon, certain pesticides, and phosphorus levels in all workers, whereas heavy metals remained low. The KFD group had a reduction in estimated glomerular filtration rate (eGFR) across the harvest season; however, kidney injury marker 1 did not significantly change. Cross-harvest metabolomic analysis found trends of fatty acid accumulation, perturbed amino acid metabolism, presence of pesticides, and other known signs of impaired kidney function.

Silica and certain pesticides were significantly elevated in the urine of sugarcane workers with or without KFD. Future work should determine whether long-term occupational exposure to silica and pesticides across multiple seasons contributes to CKD in these workers. Overall, these results confirmed that multiple exposures are occurring in sugarcane workers and may provide insight into early warning signs of kidney injury and may help explain the increased incidence of CKD among agricultural workers.

The transition from paraquat (PQ) to diquat (DQ), both organic dication herbicides, in China has led to significant increases in the number of acute DQ poisoning cases. Case studies have shown that acute DQ poisoning resulted in injury to the central nervous system (CNS), but the mechanism underlying the injury remains to be explored. The present study aimed to investigate how DQ influenced purinergic signaling between astrocytes and microglia and whether extracellular ATP (eATP) was involved in promoting neuroinflammation induced by acute DQ toxicity through the activation of the P2X4/NLRP3 signaling pathway. We constructed a rat model of acute DQ toxicity to observe the pathological changes in hippocampal tissues after DQ exposure and measure the expression levels of IL-1β and TNF-α in the hippocampal tissue. We also established an in vitro co-culture model of C6 astrocytes and BV-2 microglia using transwell chambers, measured the amount of eATP secreted into C6 astrocytes after DQ treatment, and assessed the inflammatory response and changes in the P2X4/NLRP3 signaling pathway in BV-2 microglia. The results showed that the neurons in the hippocampal tissue of rats exhibited loose arrangement, nuclear consolidation, and necrosis after DQ exposure, and IL-1β and TNF-α levels were signification higher in the hippocampal tissue after DQ exposure. DQ exposure to the co-cultured cells induced an increase in ATP secretion from C6 astrocytes as well as a significant increase of P2X4, NLRP3, IL-1β, and IL-18 expression in BV-2 microglia. In contrast, pretreatment of C6 astrocytes with apyrase (an ATP hydrolase) resulted in a significant decrease of P2X4, NLRP3, IL-1β, and IL-18 expression in BV-2 microglia. Furthermore, inhibition of P2X4 expression in BV-2 microglia by transfection with si-P2X4 effectively reversed the increase of NLRP3, IL-1β, and IL-18 in BV-2 microglia induced by DQ when co-cultured with C6 astrocytes. These results indicate that astrocytes can activate the P2X4/NLRP3 signaling pathway in microglia through the DQ-induced extracellular release of ATP to promote neuroinflammation in rat hippocampal tissue.

Poisoned patients often suffer damage to multiple systems, and those experiencing central nervous system disorders present more severe conditions, prolonged hospital stays, and increased mortality rates. We aimed to assess the efficacy of rehabilitation interventions for patients with toxic encephalopathy.

This retrospective, observational, comparative cohort study was performed at the teaching hospital affiliated of Nanjing Medical University, from October 2020 to December 2022. Patients who met the diagnostic criteria for toxic encephalopathy and exclusion criteria were included, and patients were divided into three subgroups according to Glasgow Coma Scale (GCS). Demographic and clinical characteristics were collected. The effect of the rehabilitation intervention on patients were assessed in the improvement of consciousness status (Glasgow Coma Scale [GCS] score), muscle strength and movement and swallowing function (Fugl-Meyer Assessment [FMA] scale, Water Swallow Test [WST], and Standardized Swallowing Assessment [SSA]). Subgroup analysis was based on different toxic species.

Out of the 464 patients with toxic encephalopathy, 184 cases received rehabilitation treatments. For the severe toxic encephalopathy patients, patients without rehabilitation intervention have a 2.21 times higher risk of death compared to patients with rehabilitation intervention (Hazard ratio [HR]=2.21). Subgroup analysis revealed that rehabilitation intervention significantly increased the survival rate of patients with pesticide poisoning (P=0.02), while no significant improvement was observed in patients with drug/biological agent poisoning (P=0.44). After rehabilitation intervention, significant improvement in GCS and FMA were observed in severe patients with toxic encephalopathy (P<0.01).

Active rehabilitation intervention for patients exposed to poisons that can potentially cause toxic encephalopathy may improve the prognosis and reduce the mortality rate in clinical practice.

This study aims to explore the evaluation of lactic acid (Lac) and neutrophil gelatinase-associated lipocalin (NGAL) on the condition and prognosis of patients with diquat (DQ) poisoning.

A total of 79 cases of DQ poisoning treated in one hospital from January 2019 through February 2023 were included: 10 cases of mild poisoning, 49 cases of moderate to severe poisoning, and 20 cases of fulminant poisoning. According to the Kidney Disease: Improving Global Outcomes-acute kidney injury (KDIGO-AKI) criteria, the patients were divided into 60 cases in the AKI group and 19 cases in the non-acute kidney injury (NAKI) group. According to the AKI diagnostic indicators, AKI patients were divided into Grade I, Grade II, and Grade III. According to prognosis, the patients were divided into survivor group and non-survivor group. During the same period, 30 healthy subjects were selected as the healthy group. The changes of blood Lac, NGAL, cystatin C (CysC), and serum creatinine (Scr) levels of patients were detected, the 28-day survival of patients was recorded, and the correlation between blood Lac, NGAL levels, and renal injury grade in patients with AKI caused by DQ poisoning was analyzed. The receiver operator characteristic (ROC) curve was used to evaluate the predictive value and prognostic value of Lac, NGAL, and their combination in patients with AKI caused by DQ poisoning.

There were significant differences in AKI grade, Lac, NGAL, CysC, and Scr levels among different degrees of poisoning groups (P < .05). There were significant differences in the levels of Lac, NGAL, CysC, and Scr among patients with different AKI grades (P < .05). The levels of Lac, NGAL, CysC, and Scr in the survivor group were significantly lower than those in the non-survivor group (P < .05). The blood Lac and NGAL levels were positively correlated with AKI grades in patients with DQ poisoning (r = 0.752, 0.836; P = .000, .000). The combined detection of blood Lac and NGAL had higher predictive value for AKI and assessed value for death in DQ poisoning than either of them alone.

The combined detection of Lac and NGAL have a certain clinical value in AKI grading and evaluating AKI prognosis caused by DQ poisoning.

With the withdrawal of paraquat from the market, diquat is widely used, so the treatment of diquat poisoning has become one of the focuses of emergency poisoning diagnosis and treatment.

We studied the case of a 17-year-old male patient who drank 200 mL (20 g/100 mL) of diquat solution two hours before arriving at the hospital. Despite the use of treatments such as gastric lavage, hemoperfusion, continuous hemodialysis, glucocorticoids, and organ support, the patient's condition rapidly progressed to multiorgan failure, and he died 23.5 h after admission.

We summarized the clinical characteristics and treatment strategies of diquat poisoning through this case and performed a literature review to provide a basis and direction for clinical treatment.

Introduction: Diquat poisoning leads to kidney injury, hepatotoxicity, rhabdomyolysis, gastrointestinal hemorrhage, and respiratory failure. Diquat has high mortality and no specific antidote. The pathology of acute kidney injury caused by diquat poisoning has been mainly investigated in animal studies and autopsies, and typically shows renal tubular necrosis. To our knowledge, antemortem renal biopsy has not been reported in humans.Case reports: Two males and one female presented following deliberate diquat self-poisoning. Their main clinical manifestations were abdominal pain, nausea, and emesis. All developed acute kidney injury. Kidney biopsy was performed in two cases which showed acute tubular necrosis with renal interstitial edema and multifocal inflammatory cell infiltration. Treatments given included gastric lavage, catharsis, early hemoperfusion combined with continuous kidney replacement therapy or hemodialysis, administration of glucocorticoids, and antioxidant therapy. All patients survived.Discussion: Despite potentially lethal ingestions three patients survived oral diquat poisoning with intensive supportive care. No clear relationship can be made between any of the therapies given and patient outcome.Conclusions: Kidney biopsy in these patients confirmed proximal renal tubular injury was the major pathological finding although interstitial injury was also present. The role of therapies that address renal pathology requires further study.

The widespread use of diquat as a substitute for paraquat has led to an increase in poisoning deaths. A successful case of diquat poisoning complicated with rhabdomyolysis and shock was lacking. A 13-year-old previously healthy girl ingested 40 ml of diquat solution in a suicide attempt. The concentration of diquat in serum was 436.2 ug/L at 10 h after poisoning. The clinical course was characterized by progressive multi-organ dysfunction, particularly rhabdomyolysis and shock. The main treatments included intensive hemoperfusion combined with continuous renal replacement therapy (CRRT), drainage, and activated carbon adsorption. Meanwhile, accurate dilatation under the model of pulse indicator continuous cardiac output (PICCO) was essential for the successful treatment of shock. The serum concentration of diquat declined to 20 ug/L after 96 h of treatments. The patient was discharged from the hospital after 3 weeks of treatment without obvious symptoms. So far, this was the first successful case of diquat poisoning complicated with rhabdomyolysis and shock, which would enrich the experience of diquat poisoning treatment.