As life expectancy rises, the number of patients with age-related conditions grows. One of the most accepted theories to explain the mechanism of aging is the accumulation of oxidative damage over time. Oxidative stress, defined as the imbalance between reactive oxygen species production and the antioxidant defenses, can result in macromolecular damage of lipids, proteins, and DNA. Over time, this eventually leads to progressive loss of tissue and organ function, a main feature of aging. However, the factors affecting this complex process are still poorly understood. It has been suggested that sex and inherited exercise capacity are two defining factors in the bodys response to aging and its corresponding pathologies. Women live longer and develop many diseases with a 10-year delay compared to men. Similarly, high inherited exercise capacity has been associated with a higher life expectancy. Since the influence of the intrinsic (inherited) exercise capacity is hard to investigate in humans separately from the extrinsic form, a specifically bred rat model for high (HCR) and low (LCR) intrinsic aerobic running capacity was developed. In fact, HCRs showed to live almost one third longer than LCRs. We aimed to investigate the antioxidant defense system and oxidative damage markers in the context of aging, sex, low and high inherited exercise capacity. Heart, brain, and gastrocnemius muscle tissues of each female and male rats were tested in 4 different groups: young (4 months old), old (24 months old), HCRs & LCRs. Antioxidant capacity was evaluated through photometric measurements of the 3 most important antioxidant enzyme activities: superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). On the other hand, oxidative damage markers related to lipid peroxidation (4-hydroxynonenal: 4-HNE) and protein carbonylation (PCO) were quantified by western blots and spectrophotometric measurements, respectively.
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