Age-dependent changes of antioxidant activities and markers of free radical damage in human skeletal muscle

Pansarasa, Orietta; Bertorelli, Laura; Vecchiet, Jacopo; Felzani, Giorgio; Marzatico, Fulvio

doi:10.1016/s0891-5849(99)00108-2

Cited by 179 publications

(124 citation statements)

References 31 publications

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“…Once survived, such cells would have a survival advantage over normal cells with intact mitochondrial function because they may be able to endure endogenous or exogenous oxidative stress and avoid cancer surveillance by p53 or TRAIL (7). This suggestion is consistent with previous papers showing increased MnSOD and GPx expression in aged or senescent tissue (45)(46)(47) and also a recent paper showing the decreased apoptosis of aged cells to genotoxic stress (48). In cancer cells, most previous reports (49,50) showed low MnSOD expression.…”

Section: Discussionsupporting

confidence: 93%

Resistance of Mitochondrial DNA-depleted Cells against Cell Death

Park

Chang

Kim

et al. 2004

Journal of Biological Chemistry

169

134

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Section: Discussionsupporting

confidence: 93%

Resistance of Mitochondrial DNA-depleted Cells against Cell Death

Park

Chang

Kim

et al. 2004

Journal of Biological Chemistry

169

134

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“…In addition, lipid peroxidation is significantly higher in aged human skeletal muscle, which is indicative of oxidative stress (Mecocci et al. , 1999; Pansarasa et al. , 1999; Fanò et al.…”

Section: Introductionmentioning

confidence: 99%

Modulation of reactive oxygen species in skeletal muscle by myostatin is mediated through NF‐κB

et al. 2011

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SummaryAbnormal levels of reactive oxygen species (ROS) and inflammatory cytokines have been observed in the skeletal muscle during muscle wasting including sarcopenia. However, the mechanisms that signal ROS production and prolonged maintenance of ROS levels during muscle wasting are not fully understood. Here, we show that myostatin (Mstn) is a pro‐oxidant and signals the generation of ROS in muscle cells. Myostatin, a transforming growth factor‐β (TGF‐β) family member, has been shown to play an important role in skeletal muscle wasting by increasing protein degradation. Our results here show that Mstn induces oxidative stress by producing ROS in skeletal muscle cells through tumor necrosis factor‐α (TNF‐α) signaling via NF‐κB and NADPH oxidase. Aged Mstn null (Mstn−/−) muscles, which display reduced sarcopenia, also show an increased basal antioxidant enzyme (AOE) levels and lower NF‐κB levels indicating efficient scavenging of excess ROS. Additionally, our results indicate that both TNF‐α and hydrogen peroxide (H2O2) are potent inducers of Mstn and require NF‐κB signaling for Mstn induction. These results demonstrate that Mstn and TNF‐α are components of a feed forward loop in which Mstn triggers the generation of second messenger ROS, mediated by TNF‐α and NADPH oxidase, and the elevated TNF‐α in turn stimulates Mstn expression. Higher levels of Mstn in turn induce muscle wasting by activating proteasomal‐mediated catabolism of intracellular proteins. Thus, we propose that inhibition of ROS induced by Mstn could lead to reduced muscle wasting during sarcopenia.

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“…A large number of physiological parameters have been related to ROS production: age [29,39,76,77], caloric restriction [73], oxygen tension [8,78], exercise [79], seasonal variation [80].…”

Section: Bias Variances and Interferences In Ros Measurementsmentioning

confidence: 99%

Determination of mitochondrial reactive oxygen species: methodological aspects

Batandier

Fontaine

Kériel

et al. 2002

J Cellular Molecular Medi

139

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The generation of Reactive Oxygen Species (ROS) as by-products in mitochondria Electron Transport Chain (ETC) has long been admitted as the cost of aerobic energy metabolism with oxidative damages as consequence. The purpose of this methodological review is to present some of the most widespread methods of ROS generation and to underline the limitations as well as some problems, identified with some experiments as examples, in the interpretation of such results. There is now no doubt that besides their pejorative role, ROS are involved in a variety of cellular processes for the continuous adaptation of the cell to its environment. Because ROS metabolism is a complex area (low production, instability of species, efficient antioxidant defense system, several places of production…) bias, variances and limitations in ROS measurements must be recognized in order to avoid artefactual conclusions, and especially to improve our understanding of physiological and pathophysiological mechanisms of such phenomenon.

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Age-dependent changes of antioxidant activities and markers of free radical damage in human skeletal muscle

Cited by 179 publications

References 31 publications

Resistance of Mitochondrial DNA-depleted Cells against Cell Death

Resistance of Mitochondrial DNA-depleted Cells against Cell Death

Modulation of reactive oxygen species in skeletal muscle by myostatin is mediated through NF‐κB

Determination of mitochondrial reactive oxygen species: methodological aspects

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