Conclusion:
Oxidative stress is known to impair immunological function, and functional decline in the immune system has been well characterized to occur during aging. C3 treatment reversed aging-associated alterations in the T-lymphocyte CD4+/CD8+ ratio and reversed age-related loss of B-cells as a percentage of total splenocytes.
Taken together, these data suggest that C3 decreases age-associated mitochondrial superoxide production and improves mitochondrial function, providing support for the mitochondrial theory of aging as one component of the aging process.
However, as discussed in detail by Beckman and Ames, changes in mitochondrial physiology may reflect more indirect processes (for example, changes in mitochondrial gene expression due to hormone status, inflammation, diet, activity) and may interact with other pathways linked to aging, such as insulin-dependent signaling or the sirtuins.
Because C3 has previously been shown to localize within mitochondria, to enhance survival of Sod2−/− mice and, as shown here, to regulate mitochondrial superoxide production by EPR and extend the lifespan of mice, we think it is likely that some of the actions of C3 in the current study are directly on mitochondria.
However, to what degree and howmitochondria contribute to aging remain important questions and are areas of future study that may provide valuable insights into the complex multifactorial process of aging.
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