Age‐ and Muscle‐Specific Oxidative Stress Management Strategies in a Long‐Lived Diver, the Weddell Seal

• Published in: The FASEB Journal
• Main Authors: Allen, Kaitlin, Hindle, Allyson, Vázquez‐Medina, José Pablo, Lawler, John M., Mellish, Jo‐Ann E., Horning, Markus
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wiley 2018
• Subjects: Weddell; Weddell Seal; Weddell Seals
• Online Access: http://dx.doi.org/10.1096/fasebj.2018.32.1_supplement.861.5

The free radical theory of aging purports that the accumulation of cellular oxidative damage leads to aging. While this process is not expected to manifest in wild populations, which can suffer from early predation or injury‐induced mortality, physically active long‐lived mammals are a model in which cellular aging may occur. Air breathing divers such as seals experience repeated bouts of ischemia‐reperfusion, potentially exposing their tissues to oxidative stress and thus damage and accelerated aging. We have previously demonstrated that skeletal muscle cellular morphology “ages” in Weddell seals without a corresponding decrease in diving behavior. This suggests stress response may protect against oxidative damage and functional impairment, providing insight into mechanisms for managing oxidative stress. We studied whether muscular senescence might arise from oxidative damage by comparing muscle from old (age 17–27 years) and young (age 9–16 years) cohorts of adult Weddell seals. Muscle biopsies were collected from healthy, active, non‐reproductive seals and frozen in liquid nitrogen. Apoptosis was examined with a cell‐death ELISA, while markers of oxidative damage to lipids (FOX assay) and proteins (4‐HNE western blot) were contrasted with antioxidant profiles (kinetic activity assays or western blots). These variables were statistically compared between age cohorts with an ANOVA model that included animal sex and biopsy site as cofactors. Old seals exhibited a 43% increase (p = 0.002) in apoptosis over young animals. Lipid peroxidation and oxidative protein damage, however, did not differ with age, suggesting that apoptotic differences were not due to oxidative stress. We also assessed antioxidant profiles and found that glutathione peroxidase (GPx) activity was 22% higher in the old cohort (p = 0.026). GPx reduces lipid hydroperoxides; this enhanced antioxidant protection may limit lipid peroxidation and downstream protein modification in old seals. The locomotory (longissimus dorsi, LD) and maneuvering ...