Age and sex differences in human skeletal muscle: Role of reactive oxygen species

Abstract

Previous studies, conducted on experimental animals, have indicated that reactive oxygen species (ROS) are involved in the aging process. The objective of this work was to study the relationship between oxidative damage and human skeletal muscle aging, measuring the activity of the main antioxidant enzymes superoxide dismutase (total and MnSOD), glutathione peroxidase (GPx) and catalase in the skeletal muscle of men and women in the age groups: young (17-40 years), adult (41-65 years) and aged (66-91 years). We also measured glutathione and glutathione disulfide (GSH and GSSG) levels and the redox index; lipid peroxidation and protein carbonyl content. Total SOD activity was lower in the 66-91 year-old vs. the 17-40 year-old men; MnSOD activity was significantly greater in 66-91 year-old vs. 17-40 year-old women. GPx activity remained unchanged. The activity of catalase was lower in adults than in young men but higher in the aged. We observed no changes in GSH levels and significantly higher GSSG levels only in aged men vs. adult men, and a significant decrease in aged women vs. aged men. The protein carbonyl content increased significantly in the 41-65 and 66-91 year-old vs. the 17-40 year-old men. Finally, young women have lower lipid peroxidation levels than young men. Significantly higher lipid peroxidation levels were observed in aged men vs. both young and adult men, and the same trend was noticed for women. We conclude that oxidative damage may play a crucial role in the decline of functional activity in human skeletal muscle with normal aging in both sexes; and that men appear to be more subject to oxidative stress than women.

Evaluation of sex differences on mitochondrial bioenergetics and apoptosis in mice

“…The role of estrogens on glutathione metabolism seems clearer since it has been described that women or female rodents (rats or mice) have higher GSH (the reduced glutathione form) concentration than their male counterparts (Chen et al, 1998;2004: Pansarasa et al, 2000Wang et al, 2003). This can be relevant since it has been found that the concentration of oxidized glutathione can modulate ROS production of isolated complex I (Taylor et al, 2003).…”

Regional responses in antioxidant system to exercise training and dietary Vitamin E in aging rat brain

“…Will middle age and old brains respond to only dietary antioxidants or to only exercise training or to a combination of both in terms of improving their antioxidant defenses? The increase in LP with age in many tissues has been reported to occur concomitantly with increased DNA and protein oxidation, and mitochondrial OS in animal as well as human models [2,27,31]. Our results on statistically insignificant effect of either Vitamin E or exercise training on the accumulation of LF-like AFS in the CC as well as HC in the old is in accordance with that reported by Monji et al [23] for certain regions like HC and cerebellum A notable feature was that unsupplemented sedentary of 4, 8 and 12 mos of age showed significantly higher MDA and LF-like AFS in the CC than in the HC and this trend was not seen in the old.…”

Advanced Oxidation Protein Products in Aged with Dementia

“…The role of increased oxidative stress in the development of oxidative protein damage in aging is a subject of great interest [7,21,22] . Several lines of evidence implicate oxidative stress in neurodegeneration, particularly in AD which is a progressive dementia [1,23] .…”

“…The free radical theory of aging states that the reactive oxygen species (ROS) cause oxidative damage over the lifetime of the subject [6] . Central nervous system that is containing postmitotic cells which are liable to accumulate oxidative damage over time, is particularly vulnerable to oxidative stress and uses a large amount of oxygen [7] . Advanced glycation end products (AGEs), the products of nonenzymatic glycation and oxidation of proteins and lipids, accumulated in diverse biological settings, such as diabetes, inflammation, renal failure, aging, atherosclerosis, and neurodegenerative diseases (AD) [8,9] .…”