Free radical generation by skeletal muscle of adult and old mice: effect of contractile activity

Vasilaki, Aphrodite; Mansouri, Abdellah; Remmen, Holly Van; Meulen, J. H. van der; Larkin, Lisa M.; Richardson, Arlan; McArdle, Anne; Faulkner, John A.; Jackson, Malcolm J.

doi:10.1111/j.1474-9726.2006.00198.x

Cited by 187 publications

(206 citation statements)

References 47 publications

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“…Consistent with a role of mitochondria as a contributor to age‐related muscle redox changes, reports have shown that isolated213, 236 and intact mitochondria21 in skeletal muscle fibres exhibit an age‐dependent increase in H 2 O 2 generation. Considerable evidence has shown that age‐related mitochondrial oxidative damage can alter mitochondrial integrity and function in ageing skeletal muscle.…”

Section: Non‐enzymatic Key Antioxidants That Contribute To the Maintementioning

confidence: 54%

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

Sakellariou

Lightfoot

Earl

et al. 2017

J cachexia sarcopenia muscle

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Skeletal muscle is a major site of metabolic activity and is the most abundant tissue in the human body. Age‐related muscle atrophy (sarcopenia) and weakness, characterized by progressive loss of lean muscle mass and function, is a major contributor to morbidity and has a profound effect on the quality of life of older people. With a continuously growing older population (estimated 2 billion of people aged >60 by 2050), demand for medical and social care due to functional deficits, associated with neuromuscular ageing, will inevitably increase. Despite the importance of this ‘epidemic’ problem, the primary biochemical and molecular mechanisms underlying age‐related deficits in neuromuscular integrity and function have not been fully determined. Skeletal muscle generates reactive oxygen and nitrogen species (RONS) from a variety of subcellular sources, and age‐associated oxidative damage has been suggested to be a major factor contributing to the initiation and progression of muscle atrophy inherent with ageing. RONS can modulate a variety of intracellular signal transduction processes, and disruption of these events over time due to altered redox control has been proposed as an underlying mechanism of ageing. The role of oxidants in ageing has been extensively examined in different model organisms that have undergone genetic manipulations with inconsistent findings. Transgenic and knockout rodent studies have provided insight into the function of RONS regulatory systems in neuromuscular ageing. This review summarizes almost 30 years of research in the field of redox homeostasis and muscle ageing, providing a detailed discussion of the experimental approaches that have been undertaken in murine models to examine the role of redox regulation in age‐related muscle atrophy and weakness.

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Section: Non‐enzymatic Key Antioxidants That Contribute To the Maintementioning

confidence: 54%

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

Sakellariou

Lightfoot

Earl

et al. 2017

J cachexia sarcopenia muscle

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“…The automated glutathione recycling assay described by Anderson (2002), modified for use on a 96-well plate reader (Benchmark, Biorad, UK), was used to measure total and oxidised gastrocnemius glutathione content as described previously (Vasilaki et al 2006). Protein thiol and malonaldehyde contents of the muscle were measured as previously described (Di Monte et al 1984).…”

Section: Measurement Of Muscle Mass and Calculation Of Csamentioning

confidence: 99%

Absence of insulin signalling in skeletal muscle is associated with reduced muscle mass and function: evidence for decreased protein synthesis and not increased degradation

O’Neill

Wilding

Kahn

et al. 2010

AGE

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Loss of skeletal muscle mass and function is observed in many insulin-resistant disease states such as diabetes, cancer cachexia, renal failure and ageing although the mechanisms for this remain unclear. We hypothesised that impaired insulin signalling results in reduced muscle mass and function and that this decrease in muscle mass and function is due to both increased production of atrogenes and aberrant reactive oxygen species (ROS) generation. Maximum tetanic force of the extensor digitorum longus of muscle insulin receptor knockout (MIRKO) and lox/lox control mice was measured in situ. Muscles were removed for the measurement of mass, histological examination and ROS production. Activation of insulin signalling pathways, markers of muscle atrophy and indices of protein synthesis were determined in a separate group of MIRKO and lox/lox mice 15 min following treatment with insulin. Muscles from MIRKO mice had 36% lower maximum tetanic force generation compared with muscles of lox/lox mice. Muscle fibres of MIRKO mice were significantly smaller than those of lox/lox mice with no apparent structural abnormalities. Muscles from MIRKO mice demonstrated absent phosphorylation of AKT in response to exogenous insulin along with a failure to phosphorylate ribosomal S6 compared with lox/lox mice. Atrogin-1 and MuRF1 relative mRNA expression in muscles from MIRKO mice were decreased compared with muscles from lox/ lox mice following insulin treatment. There were no differences in markers of reactive oxygen species damage between muscles from MIRKO mice and lox/lox mice. These data support the hypothesis that the absence of insulin signalling contributes to reduced muscle mass and function though decreased protein synthesis rather than proteasomal atrophic pathways.

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“…The total glutathione concentration in liver was measured according to Anderson (1996) along with modification for use with a 96‐well plate reader (Vasilaki et al., 2006) and expressed in nmol per mg protein. In both analyses, protein content was measured with the Lowry method with Peterson modification (Lowry et al., 1951; Peterson, 1977).…”

Section: Methodsmentioning

confidence: 99%

Oxidative damage and antioxidant defense are assay and tissue‐dependent both in captive and wild‐caught bank voles (Myodes glareolus) before and after reproduction

Ołdakowski

Taylor

2018

Ecology and Evolution

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Reproduction is costly and life‐history theory predicts that current parental investment will result in lower survival or decreased future reproduction. The physiological mechanisms mediating the link between reproduction and survival are still under debate and elevated oxidative damage during reproduction has been proposed as a plausible candidate. Previous studies of oxidative stress during reproduction in animals under natural conditions have been restricted to analyses of blood. Herein, we measured the level of oxidative damage to lipids (tiobarbituric‐acid‐reactive substances) and proteins (carbonyls) in the liver, kidneys, heart and skeletal muscles in free‐living bank vole females from spring and autumn generations, before and after reproduction. Antioxidant defense in the liver and kidneys was also determined. We expected oxidative damage to tissues and hypothesized that the damage would be more uniform between tissues in wild animals compared to those breeding under laboratory conditions. Considering all combinations of markers/tissues/generations, oxidative damage in females did not differ before and after reproduction in 12 comparisons, was lower after reproduction in three comparisons, and was higher after breeding in one comparison. The total glutathione was significantly increased after reproduction only in the liver of the autumn generation and there was no change in catalase activity. Our results confirm—for the first time in the field—previous observations from laboratory studies that there is no simple link between oxidative stress and reproduction and that patterns depend on the tissue and marker being studied. Overall, however, our study does not support the hypothesis that the cost of reproduction in bank voles is mediated by oxidative stress in these tissues.

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Free radical generation by skeletal muscle of adult and old mice: effect of contractile activity

Cited by 187 publications

References 47 publications

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

Absence of insulin signalling in skeletal muscle is associated with reduced muscle mass and function: evidence for decreased protein synthesis and not increased degradation

Oxidative damage and antioxidant defense are assay and tissue‐dependent both in captive and wild‐caught bank voles (Myodes glareolus) before and after reproduction

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