Spermidine protects cellular redox status and ionic homeostasis in D-galactose induced senescence and natural aging rat models.

Impaired redox homeostasis is an important hallmark of aging. Among various anti-aging interventions, caloric restriction mimetics (CRMs) are the most effective in promoting health and longevity. The potential role of spermidine (SPD) as a CRM in modulating oxidative stress and redox homeostasis during aging remains unclear. This study aimed to investigate the protective effect of SPD in D-galactose (D-gal) accelerated induced senescence model and naturally aged rats. Young male rats (4 months), D-gal induced (500 mg/kg b. w., subcutaneously) aging model and naturally aged (22 months) rats were supplemented with SPD (10 mg/kg b. w., orally) for 6 weeks. The results showed that SPD supplementation suppresses the age induced increase in reactive oxygen species, lipid peroxidation and protein oxidation. Additionally, it increases the level of antioxidants, plasma membrane redox system in erythrocytes and membrane. These results also indicate that membrane transporter activity is correlated with the susceptibility of the erythrocyte towards oxidative damage. We therefore present evidence that SPD improves redox status and membrane impairments in erythrocytes in experimental and naturally aging rat models, however, more research is required to recommend a potential therapeutic role for SPD as an anti-aging intervention strategy.