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Xiang Z, Mei H, Wang H, Yao X, Rao J, Zhang W, Xu A, Lu L. Cuproptosis and its potential role in musculoskeletal disease. Front Cell Dev Biol 2025; 13:1570131. [PMID: 40292330 PMCID: PMC12022686 DOI: 10.3389/fcell.2025.1570131] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/03/2025] [Accepted: 03/19/2025] [Indexed: 04/30/2025] Open
Abstract
Cuproptosis, a recently identified form of copper-dependent cell death, arises from intracellular copper dyshomeostasis. As an essential trace element, copper plays a critical role in bioenergetic metabolism, redox regulation, and synaptic transmission. However, excessive copper exerts cytotoxic effects through multiple pathways, including increased reactive oxygen species (ROS) production, apoptotic cascade activation, necrotic membrane rupture, inflammatory responses, and mitochondrial dysfunction. Distinct from other cell death mechanisms, cuproptosis is characterized by copper ion binding to acetylated mitochondrial respiratory chain proteins, leading to pathogenic protein aggregation, iron-sulfur cluster depletion, and cellular collapse. Emerging evidence underscores aberrant copper accumulation and resultant proteotoxic stress as pivotal contributors to the pathogenesis of multiple musculoskeletal pathologies, including osteoporosis, osteoarthritis, sarcopenia, osteosarcoma, intervertebral disc degeneration, spinal cord injury, and biofilm-associated orthopedic infections. Understanding the spatiotemporal regulation of cuproptosis may provide novel opportunities for advancing diagnostic and therapeutic approaches in orthopedic medicine. This review synthesizes current insights into the molecular mechanisms of cuproptosis, its pathogenic role in musculoskeletal diseases, and the potential for biomarker-driven therapeutic interventions.
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Affiliation(s)
- Ziyang Xiang
- Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China
| | - Huiling Mei
- Department of Rheumatology and Immunology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Honglin Wang
- Department of Orthopaedics Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Xiaoyue Yao
- Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China
| | - Ji Rao
- Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China
| | - Wentao Zhang
- Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China
| | - Aoshuang Xu
- Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
| | - Lin Lu
- Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China
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Liang R, Zhu H, Cao X, Zeng Y, You Y, Guo P, Zhang Q. Insufficient Muscle Development Level Associated with Serum Zinc, Manganese and Cobalt Levels in Children Aged 6 to 9 Years in Shenzhen, China. Biol Trace Elem Res 2024:10.1007/s12011-024-04458-0. [PMID: 39578349 DOI: 10.1007/s12011-024-04458-0] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/28/2024] [Accepted: 11/19/2024] [Indexed: 11/24/2024]
Abstract
Some trace elements have been found to be associated with muscle mass and muscle function; however, evidence in children is limited, and it remains unclear which trace elements are more relevant. We aimed to explore the association of levels of individual and combined essential trace elements and muscle development level (MDL) in young children. Muscle mass was measured by body composition analysis, and trace elements were determined by using inductively coupled plasma mass spectrometry (ICP-MS). Logistic regression, restricted cubic spline (RCS) and weighted quantile sum regression (WQS) were used to assess the individual and joint associations between trace element levels and MDL. We enrolled 2851 children: 1595 boys (55.9%) and mean age 7.1 years (range 6.8-7.3). The proportion of insufficient muscle mass in the whole body, limbs, upper and lower limbs was 1.9%, 6.5%, 44.9% and 4.6%, respectively. The odds of insufficient MDL decreased with the fourth versus first quartile of zinc (OR = 0.67, 95% CI: 0.51-0.89), manganese (OR = 0.80, 95% CI: 0.65-1.00), and cobalt (OR = 0.89, 95% CI: 0.81-0.99) and was increased with the fourth quartile of nickel (OR = 2.23, 95% CI: 1.72-2.89) and selenium (OR = 1.51, 95% CI: 1.14-1.98). The RCS yielded similar results, except for the discrepancy in high cobalt levels. The odds of insufficient MDL decreased with the combination of nine trace elements (OR = 0.84, 95% CI: 0.73-0.97), primarily zinc (weight = 0.297), manganese (weight = 0.198) and cobalt (weight = 0.173). Insufficient MDL in young children was mainly in upper limbs. Low levels of zinc, manganese, and cobalt, individually or combined, were significantly associated with risk of insufficient MDL. Further foods rich in zinc, manganese, and cobalt should be suggested to supplement in diet, and increase exercise of upper limbs to improve insufficient MDL in the young children should be needed.
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Affiliation(s)
- Rimei Liang
- Department of Preventive Medicine, Shantou University Medical College, No.22, Xinling Road, Shantou, 515041, Guangdong, People's Republic of China
| | - Haide Zhu
- Department of Preventive Medicine, Shantou University Medical College, No.22, Xinling Road, Shantou, 515041, Guangdong, People's Republic of China
| | - Xiongcheng Cao
- Department of Preventive Medicine, Shantou University Medical College, No.22, Xinling Road, Shantou, 515041, Guangdong, People's Republic of China
| | - Yuheng Zeng
- Department of Preventive Medicine, Shantou University Medical College, No.22, Xinling Road, Shantou, 515041, Guangdong, People's Republic of China
| | - Yingbin You
- Baoan Central Hospital of Shenzhen, No. 233, Xixiang Section, Guangshen Road, Baoan District, Shenzhen, 518102, Guangdong, People's Republic of China
| | - Pi Guo
- Department of Preventive Medicine, Shantou University Medical College, No.22, Xinling Road, Shantou, 515041, Guangdong, People's Republic of China
| | - Qingying Zhang
- Department of Preventive Medicine, Shantou University Medical College, No.22, Xinling Road, Shantou, 515041, Guangdong, People's Republic of China.
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Zhang Z, Zhang Y, Liu M, Su H, He Y, Zheng Q, Xu Z, Tang J. Paternal preconception alcohol consumption increased Angiotensin II-mediated vasoconstriction in male offspring cerebral arteries via oxidative stress-AT1R pathway. Addict Biol 2024; 29:e13385. [PMID: 38488472 PMCID: PMC11061854 DOI: 10.1111/adb.13385] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/25/2023] [Revised: 12/25/2023] [Accepted: 02/13/2024] [Indexed: 03/19/2024]
Abstract
Alcohol consumption is popular worldwidely and closely associated with cardiovascular diseases. Influences of paternal preconception alcohol consumption on offspring cerebral arteries are largely unknown. Male rats were randomly given alcohol or water before being mated with alcohol-naive females to produce alcohol- and control-sired offspring. Middle cerebral artery (MCA) was tested with a Danish Myo Technology wire myograph, patch-clamp, IONOPTIX, immunofluorescence and quantitative PCR. Alcohol consumption enhanced angiotensin II (AngII)-mediated constriction in male offspring MCA mainly via AT1R. PD123,319 only augmented AngII-induced constriction in control offspring. AngII and Bay K8644 induced stronger intracellular calcium transient in vascular smooth muscle cells (VSMCs) from MCA of alcohol offspring. L-type voltage-dependent calcium channel (L-Ca2+ ) current at baseline and after AngII-stimulation was higher in VSMCs. Influence of large-conductance calcium-activated potassium channel (BKC a ) was lower. Caffeine induced stronger constriction and intracellular calcium release in alcohol offspring. Superoxide anion was higher in alcohol MCA than control. Tempol and thenoyltrifluoroacetone alleviated AngII-mediated contractions, while inhibition was significantly higher in alcohol group. The mitochondria were swollen in alcohol MCA. Despite lower Kcnma1 and Prkce expression, many genes expressions were higher in alcohol group. Hypoxia induced reactive oxygen species production and increased AT1R expression in control MCA and rat aorta smooth muscle cell line. In conclusion, this study firstly demonstrated paternal preconception alcohol potentiated AngII-mediated vasoconstriction in offspring MCA via ROS-AT1R. Alcohol consumption increased intracellular calcium via L-Ca2+ channel and endoplasmic reticulum and decreased BKCa function. The present study provided new information for male reproductive health and developmental origin of cerebrovascular diseases.
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Affiliation(s)
- Ze Zhang
- Institute for FetologyFirst Hospital of Soochow UniversitySuzhouChina
| | - Yumeng Zhang
- Institute for FetologyFirst Hospital of Soochow UniversitySuzhouChina
| | - Mingxing Liu
- Infection Management DepartmentFirst Hospital of Soochow UniversitySuzhouChina
| | - Hongyu Su
- Institute for FetologyFirst Hospital of Soochow UniversitySuzhouChina
| | - Yun He
- Taixing People's HospitalTaixingChina
| | - Qiutong Zheng
- Institute for FetologyFirst Hospital of Soochow UniversitySuzhouChina
| | - Zhice Xu
- Institute for FetologyFirst Hospital of Soochow UniversitySuzhouChina
- Wuxi Maternily and Child Health HospitalWuxiChina
| | - Jiaqi Tang
- Institute for FetologyFirst Hospital of Soochow UniversitySuzhouChina
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Effect of Pinoresinol and Vanillic Acid Isolated from Catalpa bignonioides on Mouse Myoblast Proliferation via the Akt/mTOR Signaling Pathway. Molecules 2022; 27:molecules27175397. [PMID: 36080161 PMCID: PMC9457826 DOI: 10.3390/molecules27175397] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/12/2022] [Revised: 08/19/2022] [Accepted: 08/20/2022] [Indexed: 11/17/2022] Open
Abstract
Growth and maintenance of skeletal muscle is essential for athletic performance and a healthy life. Stimulating the proliferation and differentiation of muscle cells may help prevent loss of muscle mass. To discover effective natural substances enabling to mitigate muscle loss without side effects, we evaluated muscle growth with several compounds extracted from Catalpa bignonioides Walt. Among these compounds, pinoresinol and vanillic acid increased C2C12, a mouse myoblast cell line, proliferation being the most without cytotoxicity. These substances activated the Akt/mammalian target of the rapamycin (mTOR) pathway, which positively regulates the proliferation of muscle cells. In addition, the results of in silico molecular docking study showed that they may bind to the active site of insulin-like growth factor 1 receptor (IGF-1R), which is an upstream of the Akt/mTOR pathway, indicating that both pinoresinol and vanillic acid stimulate myoblast proliferation through direct interaction with IGF-1R. These results suggest that pinoresinol and vanillic acid may be a natural supplement to improve the proliferation of skeletal muscle via IGF-1R/Akt/mTOR signaling and thus strengthen muscles.
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Viña J, Olaso-Gonzalez G, Arc-Chagnaud C, De la Rosa A, Gomez-Cabrera MC. Modulating Oxidant Levels to Promote Healthy Aging. Antioxid Redox Signal 2020; 33:570-579. [PMID: 32008355 DOI: 10.1089/ars.2020.8036] [Citation(s) in RCA: 16] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
Significance: Free radicals although originally thought of as damaging molecules, inevitable side effects of the utilization of oxygen by cells, are now considered as signals that by modifying, among others, the thiol-disulfide balance regulate many cell processes from metabolism to cell cycle. Recent Advances: This review discusses the importance of the modulation of the oxidant levels through physiological strategies such as physical exercise or genetic manipulations such as the overexpression of antioxidant enzymes, in the promotion of healthy aging. Critical Issues: We have divided the review into five different sections. In the first two sections of the article "Oxidants are signals" and "Exercise training is an antioxidant," we discuss the main sources of free radicals during muscle contraction and their role, as hormetic substances, in the regulation of two main muscle adaptations to exercise in skeletal muscle; that is, mitochondrial biogenesis and the endogenous antioxidant defense. In the third section of the review, we deal with "the energy collapse in aging." The increased rate of reactive oxygen species (ROS) production and the low rate of mitochondria biosynthesis in the old cells are examined. Finally, in the fourth and fifth sections entitled "Overexpression of antioxidants enzymes in healthy aging" and "Exercise, longevity, and frailty," we consider the importance of the potentiation of the cellular defenses in health span and in life span. Future Directions: A correct manipulation of the ROS generation, directing these species to their physiological signaling role and preventing their deleterious effects, would allow the promotion of healthy aging. Antioxid. Redox Signal. 33, 570-579.
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Affiliation(s)
- Jose Viña
- Freshage Research Group, Department of Physiology, Faculty of Medicine, University of Valencia and CIBERFES, Fundación Investigación Hospital Clínico Universitario/INCLIVA, Valencia, Spain
| | - Gloria Olaso-Gonzalez
- Freshage Research Group, Department of Physiology, Faculty of Medicine, University of Valencia and CIBERFES, Fundación Investigación Hospital Clínico Universitario/INCLIVA, Valencia, Spain
| | - Coralie Arc-Chagnaud
- Freshage Research Group, Department of Physiology, Faculty of Medicine, University of Valencia and CIBERFES, Fundación Investigación Hospital Clínico Universitario/INCLIVA, Valencia, Spain.,Université de Montpellier, INRA, UMR866 Dynamique Musculaire et Métabolisme, Montpellier, France
| | - Adrián De la Rosa
- Freshage Research Group, Department of Physiology, Faculty of Medicine, University of Valencia and CIBERFES, Fundación Investigación Hospital Clínico Universitario/INCLIVA, Valencia, Spain
| | - Mari Carmen Gomez-Cabrera
- Freshage Research Group, Department of Physiology, Faculty of Medicine, University of Valencia and CIBERFES, Fundación Investigación Hospital Clínico Universitario/INCLIVA, Valencia, Spain
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Response to exercise in older adults who take supplements of antioxidants and/or omega-3 polyunsaturated fatty acids: A systematic review. Biochem Pharmacol 2019; 173:113649. [PMID: 31586588 DOI: 10.1016/j.bcp.2019.113649] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/11/2019] [Accepted: 09/30/2019] [Indexed: 12/20/2022]
Abstract
BACKGROUND Nutrition is a key factor in determining exercise response. The aim of this review is to assess the response to exercise in older adults who take supplements of antioxidants and/or omega-3 polyunsaturated fatty acids. METHODS A systematic literature search was performed (June 2009- September 2019) in MEDLINE via Pubmed. The following search strategy was used with Boolean markers: ("omega-3 fatty acids" [Major] OR "antioxidants" [Major]) AND "exercise" AND "aged" [MesH]. Fourteen articles were finally included. RESULTS Exercise-induced free radical and inflammatory marker blood levels, but not changed the plasma total antioxidant capacity (TAC), after administration of antioxidant supplement. The oral administration of antioxidants produced null or negative effect on endothelial function, but the infusion into the brachial artery during rhythmic handgrip exercise produced a significant improvement in muscle blood flow, due to an on increase in the availability of nitric acid derived from the nitric oxide synthase. Aerobic exercise and antioxidant supplementation improved submaximal and maximal aerobic parameters, as well as mitochondrial density and mitochondria-regulated apoptotic signaling. Antioxidant supplementation, but not omega-3 PUFA, decreased pro-inflammatory marker levels and fat oxidation induced by exercise. Strength training decreased serum B12 concentration but combined with omega-3 PUFA or antioxidant supplementation, B12 levels were maintained. Antioxidant supplementation has protective effect after fatigue in isometric exercise but improved appendicular fat-free mass just combined with resistance exercise. Omega-3 fatty acid supplement combined with exercise increased lean mass in women, but not in men. Muscle damage induced by exercise is protected by antioxidant supplementation. CONCLUSIONS Older people who take antioxidant and/or omega-3 PUFA supplements showed improved exercise response, as well as lower muscle damage.
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Yanar K, Simsek B, Atukeren P, Aydin S, Cakatay U. Is D-Galactose a Useful Agent for Accelerated Aging Model of Gastrocnemius and Soleus Muscle of Sprague-Dawley Rats? Rejuvenation Res 2019; 22:521-528. [PMID: 31131732 DOI: 10.1089/rej.2019.2185] [Citation(s) in RCA: 19] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/11/2022] Open
Abstract
Elderly population and age-related diseases are on the rise. On the contrary, aging studies are technically hard to conduct, because they require elderly animals, the maintenance of which requires ample effort and is expensive. To tackle this problem, D-galactose is used to hasten the aging process in various tissues in rodent models and it has been shown to successfully mimic the oxidative alterations that take place in the natural aging process in various tissues both by our group and others. In the present study, the validity of D-galactose aging model in skeletal muscles was tested both on predominantly slow-twitch (soleus) and rather fast-twitch (gastrocnemius) muscle in male Sprague-Dawley rats and the results are compared with young littermate controls and naturally aged rats. Redox-related modifications in soleus and gastrocnemius were assessed by measurement of protein carbonyl groups, advanced oxidation protein products, lipid hydroperoxides, total thiol, and Cu, Zn-superoxide dismutase activities. In the present study, we provide biochemical evidence demonstrating that D-galactose-induced mimetic aging does result in oxidative stress-related redox alterations that are comparable with the alterations that occur in natural aging in soleus. On the contrary, in the D-galactose-induced mimetic aging of gastrocnemius, even though the oxidative stress markers were significantly increased, the endpoint redox homeostasis markers were not statistically comparable with the redox status of naturally aged group.
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Affiliation(s)
- Karolin Yanar
- Department of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey
| | - Bahadir Simsek
- Department of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey
| | - Pinar Atukeren
- Department of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey
| | - Seval Aydin
- Department of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey
| | - Ufuk Cakatay
- Department of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey
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Abstract
Purpose The aim of this study was to explore the role of miRNAs in the process of skeletal muscle aging. Materials and methods We analyzed the miRNA microarray datasets from 19 young and 17 old skeletal muscle samples by bioinformatic analysis. Differentially expressed miRNAs were identified, followed by function and pathway enrichment analysis. The expression of miRNAs were validated by real-time quantitative PCR (RT-qPCR) analysis. Results A total of 23 miRNAs were found to be differentially expressed in old muscle samples based on two platforms. Gene targets of upregulated miRNAs were significantly enriched in the oxytocin signaling pathway, AMP-activated protein kinase (AMPK) signaling pathway, and Notch signaling pathway. The target genes of downregulated miRNAs were significantly related to gap junction, salivary secretion, and estrogen signaling pathway. has-miR-19a and hsa-miR-34a were significant nodes in the miRNA regulatory network. has-miR-19a was closely related to the AMPK signaling pathway. hsa-miR-34a was closely related to cellular senescence and mitogen-activated protein kinase (MAPK) signaling pathway. PCR analysis showed that the expression of has-miR-34a-5p and has-miR-449b-5p was significantly higher in the patient group than in the control group, while no significant difference was observed in the expression of has-miR-19a-3p and has-miR-144-3p between the two groups. Furthermore, the expression of key target genes involved in cellular senescence (sirtuin 1 [SITRI]), MAPK signaling pathway (vascular endothelial growth factor A [VEGFA]), and AMPK signaling pathway (protein kinase AMP-activated catalytic subunit alpha 1 [PRKAA1] and 6-phosphofructo-2-kinase/fructose-2-,6-biphosphatase 3 [PFKFB3]) were significantly increased in patients with sarcopenia. Conclusion has-miR-19a and hsa-miR-34a may play regulatory roles in the aging process of skeletal muscles and may be candidate targets to prevent muscle aging. Further experimental validations are warranted.
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Affiliation(s)
- Yan Zheng
- Department of Geriatrics, The First Hospital of Jilin University, Changchun 130021, Jilin, China,
| | - Jian Kong
- Department of Geriatrics, The First Hospital of Jilin University, Changchun 130021, Jilin, China,
| | - Qun Li
- Department of Thyroid Surgery, The First Hospital of Jilin University, Changchun 130021, Jilin, China
| | - Yan Wang
- Department of Geriatrics, The First Hospital of Jilin University, Changchun 130021, Jilin, China,
| | - Jie Li
- Department of Geriatrics, The First Hospital of Jilin University, Changchun 130021, Jilin, China,
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Brioche T, Pagano AF, Py G, Chopard A. Muscle wasting and aging: Experimental models, fatty infiltrations, and prevention. Mol Aspects Med 2016; 50:56-87. [PMID: 27106402 DOI: 10.1016/j.mam.2016.04.006] [Citation(s) in RCA: 80] [Impact Index Per Article: 8.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/19/2015] [Revised: 04/13/2016] [Accepted: 04/13/2016] [Indexed: 12/21/2022]
Abstract
Identification of cost-effective interventions to maintain muscle mass, muscle strength, and physical performance during muscle wasting and aging is an important public health challenge. It requires understanding of the cellular and molecular mechanisms involved. Muscle-deconditioning processes have been deciphered by means of several experimental models, bringing together the opportunities to devise comprehensive analysis of muscle wasting. Studies have increasingly recognized the importance of fatty infiltrations or intermuscular adipose tissue for the age-mediated loss of skeletal-muscle function and emphasized that this new important factor is closely linked to inactivity. The present review aims to address three main points. We first mainly focus on available experimental models involving cell, animal, or human experiments on muscle wasting. We next point out the role of intermuscular adipose tissue in muscle wasting and aging and try to highlight new findings concerning aging and muscle-resident mesenchymal stem cells called fibro/adipogenic progenitors by linking some cellular players implicated in both FAP fate modulation and advancing age. In the last part, we review the main data on the efficiency and molecular and cellular mechanisms by which exercise, replacement hormone therapies, and β-hydroxy-β-methylbutyrate prevent muscle wasting and sarcopenia. Finally, we will discuss a potential therapeutic target of sarcopenia: glucose 6-phosphate dehydrogenase.
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Affiliation(s)
- Thomas Brioche
- Université de Montpellier, INRA, UMR 866 Dynamique Musculaire et Métabolisme, Montpellier F-34060, France.
| | - Allan F Pagano
- Université de Montpellier, INRA, UMR 866 Dynamique Musculaire et Métabolisme, Montpellier F-34060, France
| | - Guillaume Py
- Université de Montpellier, INRA, UMR 866 Dynamique Musculaire et Métabolisme, Montpellier F-34060, France
| | - Angèle Chopard
- Université de Montpellier, INRA, UMR 866 Dynamique Musculaire et Métabolisme, Montpellier F-34060, France
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Bjørnsen T, Salvesen S, Berntsen S, Hetlelid KJ, Stea TH, Lohne-Seiler H, Rohde G, Haraldstad K, Raastad T, Køpp U, Haugeberg G, Mansoor MA, Bastani NE, Blomhoff R, Stølevik SB, Seynnes OR, Paulsen G. Vitamin C and E supplementation blunts increases in total lean body mass in elderly men after strength training. Scand J Med Sci Sports 2015; 26:755-63. [PMID: 26129928 DOI: 10.1111/sms.12506] [Citation(s) in RCA: 64] [Impact Index Per Article: 6.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 05/20/2015] [Indexed: 12/23/2022]
Abstract
The aim of this study was to investigate the effects of vitamin C and E supplementation on changes in muscle mass (lean mass and muscle thickness) and strength during 12 weeks of strength training in elderly men. Thirty-four elderly males (60-81 years) were randomized to either an antioxidant group (500 mg of vitamin C and 117.5 mg vitamin E before and after training) or a placebo group following the same strength training program (three sessions per week). Body composition was assessed with dual-energy X-ray absorptiometry and muscle thickness by ultrasound imaging. Muscle strength was measured as one-repetition maximum (1RM). Total lean mass increased by 3.9% (95% confidence intervals: 3.0, 5.2) and 1.4% (0, 5.4) in the placebo and antioxidant groups, respectively, revealing larger gains in the placebo group (P = 0.04). Similarly, the thickness of m. rectus femoris increased more in the placebo group [16.2% (12.8, 24.1)] than in the antioxidant group [10.9% (9.8, 13.5); P = 0.01]. Increases of lean mass in trunk and arms, and muscle thickness of elbow flexors, did not differ significantly between groups. With no group differences, 1RM improved in the range of 15-21% (P < 0.001). In conclusion, high-dosage vitamin C and E supplementation blunted certain muscular adaptations to strength training in elderly men.
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Affiliation(s)
- T Bjørnsen
- Department of Public Health, Sport and Nutrition, Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
| | - S Salvesen
- Department of Public Health, Sport and Nutrition, Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
| | - S Berntsen
- Department of Public Health, Sport and Nutrition, Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
| | - K J Hetlelid
- Department of Public Health, Sport and Nutrition, Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
| | - T H Stea
- Department of Public Health, Sport and Nutrition, Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
| | - H Lohne-Seiler
- Department of Public Health, Sport and Nutrition, Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
| | - G Rohde
- Department of Public Health, Sport and Nutrition, Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
| | - K Haraldstad
- Department of Public Health, Sport and Nutrition, Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
| | - T Raastad
- Department of Physical Performance, Norwegian School of Sport Sciences, Oslo, Norway
| | - U Køpp
- Southern Norway Hospital Trust, Agder, Norway
| | - G Haugeberg
- Department of Public Health, Sport and Nutrition, Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
| | - M A Mansoor
- Department of Public Health, Sport and Nutrition, Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
| | - N E Bastani
- Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway
| | - R Blomhoff
- Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.,Division of Cancer Medicine, Surgery and Transplantation, Oslo University Hospital, Oslo, Norway
| | - S B Stølevik
- Department of Public Health, Sport and Nutrition, Faculty of Health and Sport Sciences, University of Agder, Kristiansand, Norway
| | - O R Seynnes
- Department of Physical Performance, Norwegian School of Sport Sciences, Oslo, Norway
| | - G Paulsen
- Department of Physical Performance, Norwegian School of Sport Sciences, Oslo, Norway
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Special Needs Population: Care of the Geriatric Patient Population in the Perioperative Setting. AORN J 2015; 101:443-56; quiz 457-9. [DOI: 10.1016/j.aorn.2014.10.022] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/23/2014] [Accepted: 10/01/2014] [Indexed: 12/20/2022]
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12
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Stavropoulos-Kalinoglou A, Deli C, Kitas GD, Jamurtas AZ. Muscle wasting in rheumatoid arthritis: The role of oxidative stress. World J Rheumatol 2014; 4:44-53. [DOI: 10.5499/wjr.v4.i3.44] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/14/2014] [Revised: 09/01/2014] [Accepted: 09/24/2014] [Indexed: 02/06/2023] Open
Abstract
Rheumatoid arthritis (RA), the commonest inflammatory arthritis, is a debilitating disease leading to functional and social disability. In addition to the joints, RA affects several other tissues of the body including the muscle. RA patients have significantly less muscle mass compared to the general population. Several theories have been proposed to explain this. High grade inflammation, a central component in the pathophysiology of the disease, has long been proposed as the key driver of muscle wasting. More recent findings however, indicate that inflammation on its own cannot fully explain the high prevalence of muscle wasting in RA. Thus, the contribution of other potential confounders, such as nutrition and physical activity, has also been studied. Results indicate that they play a significant role in muscle wasting in RA, but again neither of these factors seems to be able to fully explain the condition. Oxidative stress is one of the major mechanisms thought to contribute to the development and progression of RA but its potential contribution to muscle wasting in these patients has received limited attention. Oxidative stress has been shown to promote muscle wasting in healthy populations and people with several chronic conditions. Moreover, all of the aforementioned potential contributors to muscle wasting in RA (i.e., inflammation, nutrition, and physical activity) may promote pro- or anti-oxidative mechanisms. This review aims to highlight the importance of oxidative stress as a driving mechanism for muscle wasting in RA and discusses potential interventions that may promote muscle regeneration via reduction in oxidative stress.
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Chen YL, Yang KC, Chang HH, Lee LT, Lu CW, Huang KC. Low serum selenium level is associated with low muscle mass in the community-dwelling elderly. J Am Med Dir Assoc 2014; 15:807-11. [PMID: 25112230 DOI: 10.1016/j.jamda.2014.06.014] [Citation(s) in RCA: 27] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/16/2013] [Revised: 06/14/2014] [Accepted: 06/19/2014] [Indexed: 11/16/2022]
Abstract
OBJECTIVES Elderly persons with low muscle mass (LMM) or sarcopenia are prone to frailty and functional decline. This study aimed to investigate the relationship between serum selenium level and skeletal muscle mass in community-dwelling elderly. DESIGN Cross-sectional observational study. SETTING AND PARTICIPANTS A total of 327 elderly Taipei citizens (mean age 71.5 ± 4.7 years) were recruited from the community. MEASUREMENTS Skeletal muscle mass was measured by bioelectrical impedance analysis. LMM was defined by low skeletal muscle index (SMI: muscle mass (kg)/[height (m)](2)). All participants were further divided into quartiles by serum selenium level and the risk for LMM among these quartiles was examined using multivariate logistic regression analyses. Estimated serum selenium levels for the LMM group vs the normal group and estimated SMI in the quartiles of serum selenium were computed by least square method in linear regression models. RESULTS The estimated mean (±standard deviation) of serum selenium level was significantly lower in the LMM group compared with the normal group after adjusting for confounders (1.01 ± 0.03 μmol/L vs 1.14 ± 0.02 μmol/L, P < .001). After adjusting for age, sex, lifestyle, and physical and metabolic factors, the odds ratios (95% confidence interval, P value) of LMM in the bottom, second, and third selenium quartile groups were 4.62 (95% CI 2.11-10.10, P < .001), 2.30 (95% CI 1.05-5.03, P < .05) and 1.51 (95% CI 0.66-3.46, P = .327), respectively, compared with the top quartile group of serum selenium level. The least square mean of SMI increased with the quartiles of serum selenium (P < .001). CONCLUSIONS This is the first study to demonstrate that low serum selenium is independently associated with low muscle mass in the elderly. The causality and underlying mechanism between selenium and low muscle mass or sarcopenia warrant further research.
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Affiliation(s)
- You-Ling Chen
- Department of Family Medicine, National Taiwan University Hospital, Taipei, Taiwan
| | - Kuen-Cheh Yang
- Department of Community and Family Medicine, National Taiwan University Hospital, Hsin-Chu Branch, Hsinchu, Taiwan
| | - Hao-Hsiang Chang
- Department of Family Medicine, National Taiwan University Hospital, Taipei, Taiwan
| | - Long-Teng Lee
- Department of Family Medicine, National Taiwan University Hospital, Taipei, Taiwan
| | - Chia-Wen Lu
- Department of Family Medicine, National Taiwan University Hospital, Taipei, Taiwan
| | - Kuo-Chin Huang
- Department of Family Medicine, National Taiwan University Hospital, Taipei, Taiwan; Department of Family Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan; Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan.
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Abstract
Aging physiology greatly impacts care delivery in the geriatric patient population. Consideration should be given to addressing the patient-specific needs regarding the systemic changes seen in the aging patient. Each major body system presents its own unique challenges to the critical care practitioner, and a comprehensive understanding of these changes is necessary to effectively care for this patient population. This article summarizes these changes and provides key points for the practitioner to consider when caring for the aging patient in the critical care arena.
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Affiliation(s)
- Mandi Walker
- Nursing Education and Research Department, University of Louisville Hospital, 530 South Jackson Street, Louisville, KY 40202, USA.
| | - Mark Spivak
- Nursing Education and Research Department, University of Louisville Hospital, 530 South Jackson Street, Louisville, KY 40202, USA
| | - Mary Sebastian
- Nursing Education and Research Department, University of Louisville Hospital, 530 South Jackson Street, Louisville, KY 40202, USA
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Larkin LM, Hanes MC, Kayupov E, Claflin DR, Faulkner JA, Brooks SV. Weakness of whole muscles in mice deficient in Cu, Zn superoxide dismutase is not explained by defects at the level of the contractile apparatus. AGE (DORDRECHT, NETHERLANDS) 2013; 35:1173-1181. [PMID: 22696118 PMCID: PMC3705120 DOI: 10.1007/s11357-012-9441-7] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Received: 10/21/2011] [Accepted: 05/21/2012] [Indexed: 06/01/2023]
Abstract
Mice deficient in Cu,Zn superoxide dismutase (Sod1 (-/-) mice) demonstrate elevated oxidative stress associated with rapid age-related declines in muscle mass and force. The decline in mass for muscles of Sod1 (-/-) mice is explained by a loss of muscle fibers, but the mechanism underlying the weakness is not clear. We hypothesized that the reduced maximum isometric force (F o) normalized by cross-sectional area (specific F o) for whole muscles of Sod1 (-/-) compared with wild-type (WT) mice is due to decreased specific F o of individual fibers. Force generation was measured for permeabilized fibers from muscles of Sod1 (-/-) and WT mice at 8 and 20 months of age. WT mice were also studied at 28 months to determine whether any deficits observed for fibers from Sod1 (-/-) mice were similar to those observed in old WT mice. No effects of genotype were observed for F o or specific F o at either 8 or 20 months, and no age-associated decrease in specific F o was observed for fibers from Sod1 (-/-) mice, whereas specific F o for fibers of WT mice decreased by 20 % by 28 months. Oxidative stress has also been associated with decreased maximum velocity of shortening (V max), and we found a 10 % lower V max for fibers from Sod1 (-/-) compared with WT mice at 20 months. We conclude that the low specific F o of muscles of Sod1 (-/-) mice is not explained by damage to contractile proteins. Moreover, the properties of fibers of Sod1 (-/-) mice do not recapitulate those observed with aging in WT animals.
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Affiliation(s)
- Lisa M. Larkin
- />Departments of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109-2200 USA
- />Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109 USA
| | - Michael C. Hanes
- />Departments of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109-2200 USA
| | - Erdan Kayupov
- />Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109 USA
| | - Dennis R. Claflin
- />Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109 USA
- />Surgery, Section of Plastic Surgery, University of Michigan, Ann Arbor, MI 48109 USA
| | - John A. Faulkner
- />Departments of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109-2200 USA
- />Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109 USA
| | - Susan V. Brooks
- />Departments of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109-2200 USA
- />Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109 USA
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Birds and longevity: does flight driven aerobicity provide an oxidative sink? Ageing Res Rev 2012; 11:242-53. [PMID: 22198369 DOI: 10.1016/j.arr.2011.12.002] [Citation(s) in RCA: 30] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/19/2011] [Revised: 11/28/2011] [Accepted: 12/06/2011] [Indexed: 12/25/2022]
Abstract
Birds generally age slower and live longer than similar sized mammals. For birds this occurs despite elevated blood glucose levels that for mammals would in part define them as diabetic. However these data were acquired in respiration states that have little resemblance to conditions in healthy tissues and mitochondrial RS production is probably minimal in healthy animals. Indeed mitochondria probably act as net consumers rather than producers of RS. Here we propose that (1) if mitochondria are antioxidant systems, the greater mitochondrial mass in athletic species, such as birds, is advantageous as it should provide a substantial sink for RS. (2) The intense drive for aerobic performance and decreased body density to facilitate flight may explain the relative insensitivity of birds to insulin, as well as depressed insulin levels and apparent sensitization to glucagon. Glucagon also associates with the sirtuin protein family, most of which are associated with caloric restriction regulated pathways, mitochondrial biogenesis and life span extension. (3) We note that telomeres, which appear to be unusually long in birds, bind Sirtuins 2 and 4 and therefore may stabilize and protect nuclear DNA. Ultimately these flight driven responses may suppress somatic growth and protect DNA from oxidative damage that would otherwise lead to ageing and non-viral cancers.
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Lanoix D, Lacasse AA, Reiter RJ, Vaillancourt C. Melatonin: the smart killer: the human trophoblast as a model. Mol Cell Endocrinol 2012; 348:1-11. [PMID: 21889572 DOI: 10.1016/j.mce.2011.08.025] [Citation(s) in RCA: 71] [Impact Index Per Article: 5.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/03/2011] [Accepted: 08/15/2011] [Indexed: 02/08/2023]
Abstract
Melatonin has both the ability to induce intrinsic apoptosis in tumor cells while it inhibits it in non-tumor cells. Melatonin kills tumor cells through induction of reactive oxygen species generation and activation of pro-apoptotic pathways. In contrast, melatonin promotes the survival of non-tumor cells due to its antioxidant properties and the inhibition of pro-apoptotic pathways. In primary human villous trophoblast, a known pseudo-tumorigenic tissue, melatonin promotes the survival through inhibition of the Bax/Bcl-2 pathway while in BeWo choriocarcinoma cell line melatonin induces permeabilization of the mitochondrial membrane leading to cellular death. These findings suggest that the trophoblast is a good model to study the differential effects of melatonin on the intrinsic apoptosis pathway. This review describes the differential effects of melatonin on the intrinsic apoptosis pathway in tumor and non-tumor cells and presents the trophoblast as a novel model system in which to study these effects of melatonin.
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Affiliation(s)
- Dave Lanoix
- INRS-Institut Armand-Frappier, Université du Québec, Laval, QC, Canada
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18
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Reactive oxygen species in skeletal muscle signaling. JOURNAL OF SIGNAL TRANSDUCTION 2011; 2012:982794. [PMID: 22175016 PMCID: PMC3235811 DOI: 10.1155/2012/982794] [Citation(s) in RCA: 266] [Impact Index Per Article: 19.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 06/30/2011] [Accepted: 08/25/2011] [Indexed: 12/13/2022]
Abstract
Generation of reactive oxygen species (ROS) is a ubiquitous phenomenon in eukaryotic cells' life. Up to the 1990s of the past century, ROS have been solely considered as toxic species resulting in oxidative stress, pathogenesis and aging. However, there is now clear evidence that ROS are not merely toxic species but also-within certain concentrations-useful signaling molecules regulating physiological processes. During intense skeletal muscle contractile activity myotubes' mitochondria generate high ROS flows: this renders skeletal muscle a tissue where ROS hold a particular relevance. According to their hormetic nature, in muscles ROS may trigger different signaling pathways leading to diverging responses, from adaptation to cell death. Whether a "positive" or "negative" response will prevail depends on many variables such as, among others, the site of ROS production, the persistence of ROS flow or target cells' antioxidant status. In this light, a specific threshold of physiological ROS concentrations above which ROS exert negative, toxic effects is hard to determine, and the concept of "physiologically compatible" levels of ROS would better fit with such a dynamic scenario. In this review these concepts will be discussed along with the most relevant signaling pathways triggered and/or affected by ROS in skeletal muscle.
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19
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Lira Ferrari GS, Bucalen Ferrari CK. Exercise modulation of total antioxidant capacity (TAC): towards a molecular signature of healthy aging. FRONTIERS IN LIFE SCIENCE 2011. [DOI: 10.1080/21553769.2011.635008] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 10/28/2022]
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Baraibar MA, Hyzewicz J, Rogowska-Wrzesinska A, Ladouce R, Roepstorff P, Mouly V, Friguet B. Oxidative stress-induced proteome alterations target different cellular pathways in human myoblasts. Free Radic Biol Med 2011; 51:1522-32. [PMID: 21810466 DOI: 10.1016/j.freeradbiomed.2011.06.032] [Citation(s) in RCA: 40] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/06/2011] [Revised: 06/27/2011] [Accepted: 06/27/2011] [Indexed: 11/20/2022]
Abstract
Although increased oxidative stress has been associated with the impairment of proliferation and function of adult human muscle stem cells, proteins either involved in the stress response or damaged by oxidation have not been identified. A parallel proteomics approach was performed for analyzing the protein expression profile as well as proteins preferentially oxidized upon hydrogen peroxide-induced oxidative stress. Fifteen proteins involved in the oxidative stress response were identified. Among them, protein spots identified as peroxiredoxins 1 and 6, glyceraldehyde-3-phosphate dehydrogenase, and α-enolase were shifted to a more acidic isoelectric point upon oxidative stress, indicating posttranslational modifications. Oxidized proteins were evidenced by immunodetection of derivatized carbonyl groups followed by identification by mass spectrometry. The carbonylated proteins identified are mainly cytosolic and involved in carbohydrate metabolism, cellular assembly, cellular homeostasis, and protein synthesis and degradation. Pathway analysis revealed skeletal and muscular disorders, cell death, and cancer-related as the main molecular networks altered. Interestingly, these pathways were focused on two distinct proteins: p53 for altered protein expression and huntingtin for increased protein carbonylation. This study emphasizes the importance of performing analysis addressing different aspects of the cellular proteome to have a more accurate view of their changes upon stress.
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Affiliation(s)
- Martin A Baraibar
- Laboratoire de Biologie Cellulaire du Vieillissement, UR4, Université Pierre et Marie Curie-Paris 6, 75252 Paris Cedex 05, France
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21
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Abstract
This article discusses various theories of aging and their relative plausibility related to the human aging process. Structural and physiologic changes of aging are discussed in detail by organ system. Each of the organ systems is discussed when applicable to the various theories of aging. Normal versus abnormal aging is discussed in the context of specific aging processes, with atypical presentations of disease and general links to life expectancy. Life expectancy and lifespan are discussed in the context of advances in medical science and the potential ultimate link to human life span.
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Affiliation(s)
- Charles A Cefalu
- Department of Medicine, Louisiana State University Health Sciences Center, 1542 Tulane Avenue, New Orleans, LA 70113, USA.
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22
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Saleh F, Behbehani A, Asfar S, Khan I, Ibrahim G. Abnormal blood levels of trace elements and metals, DNA damage, and breast cancer in the state of Kuwait. Biol Trace Elem Res 2011; 141:96-109. [PMID: 20495889 DOI: 10.1007/s12011-010-8724-z] [Citation(s) in RCA: 27] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/15/2010] [Accepted: 05/03/2010] [Indexed: 12/30/2022]
Abstract
This study aims at investigating the blood level of Cu, Zn, Se, and Cd in breast cancer patients and the association between such level and the frequency of micronucleated lymphocytes. Fifty stage I breast cancer patients were recruited for this study at the time of diagnosis and before receiving any treatment or surgery. The control group consisted of 150 normal females matched to the patients for age (± 5 years). The whole blood level of Cu, Zn, Se, and Cd was determined using spectrophotometry. The frequency of micronucleated lymphocytes in the blood was determined using the cytokinesis-block micronucleus assay. The level of Cu, Zn, and Se was significantly lower (p = 0.0006, <0.0001, and <0.0001, respectively) in breast cancer patients, as compared to controls. The level of Cd was significantly (p < 0.0001) higher in the patients, as compared to controls. The frequency of lymphocytes with one micronucleus was significantly (p < 0.0001) higher in the patients, as compared to controls. In breast cancer patients, the frequency of micronucleated lymphocytes showed different associations with different levels of these trace elements. High Cd, low Zn, low Se, and both high and low Cu levels were significantly associated with micronucleus formation in lymphocytes. A similar association was found in the normal control group only in relation to high Se and Cd levels. Breast cancer patients seem to have abnormal levels of Cu, Zn, Se, and Cd, and such abnormality is associated with micronucleus formation in lymphocytes.
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Affiliation(s)
- Farid Saleh
- Department of Anatomy, Faculty of Medicine, Health Science Centre, Kuwait University, P.O. Box 24923, Safat, 13110, Kuwait.
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Gómez-Pérez Y, Gianotti M, Proenza AM, Lladó I. Age-Related Decline of Skeletal Muscle Insulin Sensitivity in Rats: Effect of Sex and Muscle Type. Rejuvenation Res 2011; 14:153-61. [DOI: 10.1089/rej.2010.1107] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/09/2023] Open
Affiliation(s)
- Yolanda Gómez-Pérez
- Grup de Metabolisme Energètic i Nutrició, Departament de Biologia Fonamental i Ciències de la Salut, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, Palma de Mallorca, Illes Balears, Spain
- Ciber Fisiopatología Obesidad y Nutrición (CB06/03), Instituto de Salud Carlos III, Madrid, Spain
| | - Magdalena Gianotti
- Grup de Metabolisme Energètic i Nutrició, Departament de Biologia Fonamental i Ciències de la Salut, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, Palma de Mallorca, Illes Balears, Spain
- Ciber Fisiopatología Obesidad y Nutrición (CB06/03), Instituto de Salud Carlos III, Madrid, Spain
| | - Ana M. Proenza
- Grup de Metabolisme Energètic i Nutrició, Departament de Biologia Fonamental i Ciències de la Salut, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, Palma de Mallorca, Illes Balears, Spain
- Ciber Fisiopatología Obesidad y Nutrición (CB06/03), Instituto de Salud Carlos III, Madrid, Spain
| | - Isabel Lladó
- Grup de Metabolisme Energètic i Nutrició, Departament de Biologia Fonamental i Ciències de la Salut, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, Palma de Mallorca, Illes Balears, Spain
- Ciber Fisiopatología Obesidad y Nutrición (CB06/03), Instituto de Salud Carlos III, Madrid, Spain
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Chen Z, Lu M, Zhuang G, Wang H. Enhanced Bacterial Biosensor for Fast and Sensitive Detection of Oxidatively DNA Damaging Agents. Anal Chem 2011; 83:3248-51. [DOI: 10.1021/ac200426x] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/29/2022]
Affiliation(s)
- Zhilan Chen
- State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Shuangqing Road 18, Haidian District, Beijing, China
| | - Meiling Lu
- State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Shuangqing Road 18, Haidian District, Beijing, China
| | - Guoqiang Zhuang
- State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Shuangqing Road 18, Haidian District, Beijing, China
| | - Hailin Wang
- State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Shuangqing Road 18, Haidian District, Beijing, China
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Luin E, Giniatullin R, Sciancalepore M. Effects of H₂O₂ on electrical membrane properties of skeletal myotubes. Free Radic Biol Med 2011; 50:337-44. [PMID: 21109001 DOI: 10.1016/j.freeradbiomed.2010.11.015] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/18/2010] [Revised: 10/08/2010] [Accepted: 11/11/2010] [Indexed: 12/20/2022]
Abstract
Reactive oxygen species (ROS), normally generated in skeletal muscles, could control excitability of muscle fibers through redox modulation of membrane ion channels. However, the mechanisms of ROS action remain largely unknown. To investigate the action of ROS on electrical properties of muscle cells, patch-clamp recordings were performed after application of hydrogen peroxide (H₂O₂) to skeletal myotubes. H₂O₂ facilitated sodium spikes after a hyperpolarizing current pulse, by decreasing the latency for spike initiation. Importantly, the antioxidant N-acetylcysteine induced the opposite effect, suggesting the redox control of muscle excitability. The effect of H₂O₂ was abolished in the presence of catalase. The kinetics of sodium channels were not affected by H₂O₂. However, the fast inward rectifier K(+) (K(IR)) currents, activated by hyperpolarization, were reduced by H₂O₂, similar to the action of the potassium channel blockers Ba(2+) and Cs(+). The block of the outward tail current contributing to K(IR) deactivation can explain the shorter latency for spike initiation. We propose that the K(IR) current is an important target for ROS action in myotubes. Our data would thus suggest that ROS are involved in the control of the excitability of myotubes and, possibly, in the oscillatory behavior critical for the plasticity of developing muscle cells.
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Affiliation(s)
- Elisa Luin
- Department of Physiology and Pharmacology, University La Sapienza, Rome, Italy
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Stimulation of mechano-growth factor expression by second messengers. Arch Biochem Biophys 2010; 507:323-31. [PMID: 21192914 DOI: 10.1016/j.abb.2010.12.028] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/06/2010] [Revised: 12/17/2010] [Accepted: 12/22/2010] [Indexed: 11/23/2022]
Abstract
The effect of second messengers on the expression of mechano-growth factor (MGF) synthesis by myoblasts and differentiated myotubes in culture was investigated. cAMP stimulates MGF expression both in murine and human cells. CNG- and HCN-channel blockers slightly activated MGF synthesis, while an activator of Epac protein had no effect. It is assumed that cAMP activates MGF synthesis via protein kinase A. Phorbol ester (PMA) activates MGF synthesis in human myoblasts and myotubes only. The expression of another splice form of IGF-1 gene, IGF-1Ea, was also stimulated in human cells by db-cAMP and PMA and in murine cells by db-cAMP only. Stimulation of MGF expression in human cells by db-cAMP and PMA demonstrated different time dependences but showed additivity when the compounds were applied in a combination. Inhibitors specific to protein kinase A did not affect PMA-mediated activation, while inhibitors specific to protein kinase C did not affect db-cAMP-mediated process. Ca²+ ionophore and ROS inductor strongly inhibited synthesis of the growth factor. PGE2 known as physiological stimulator of cAMP synthesis was shown to stimulate MGF expression both in murine and human cells. Implication of protein kinase A and protein kinase C in MGF synthesis stimulation and a cross-talk between two signaling systems is discussed.
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27
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Whey protein precludes lipid and protein oxidation and improves body weight gain in resistance-exercised rats. Eur J Nutr 2010; 50:331-9. [PMID: 21046124 DOI: 10.1007/s00394-010-0141-8] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/04/2010] [Accepted: 10/21/2010] [Indexed: 12/25/2022]
Abstract
BACKGROUND Resistance exercise such as weight-lifting (WL) increases oxidation products in plasma, but less is known regarding the effect of WL on oxidative damage to tissues. Dietary compounds are known to improve antioxidant defences. Whey protein (WP) is a source of protein in a variety of sport supplements and can enhance physical performance. AIM To evaluate the effect of WL on biomarkers of lipid and protein oxidation, on liver antioxidants and on muscle growth in the absence or presence of WP in rats. METHODS Thirty-two male Fisher rats were randomly assigned to sedentary or exercise-trained groups and were fed with control or WP diets. The WL programme consisted of inducing the animals to perform sets of jumps with weights attached to the chest. After 8 weeks, arteriovenous blood samples, abdominal fat, liver and gastrocnemius muscle were collected for analysis. RESULTS WP precludes WL-mediated increases in muscle protein carbonyl content and maintains low levels of TBARS in exercised and sedentary animals. WL reduced liver CAT activity, whereas WP increased hepatic glutathione content. In addition, WL plus WP generated higher body and muscle weight than exercise without WP. CONCLUSIONS These data suggest that WP improves antioxidant defences, which contribute to the reduction of lipid and protein oxidation as well as body and muscle weight gain in resistance-exercised rats.
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28
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Proteasome and oxidative phoshorylation changes may explain why aging is a risk factor for neurodegenerative disorders. J Proteomics 2010; 73:2230-8. [DOI: 10.1016/j.jprot.2010.08.008] [Citation(s) in RCA: 29] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/12/2010] [Revised: 08/24/2010] [Accepted: 08/25/2010] [Indexed: 01/17/2023]
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