How Antioxidants Might Help

+ See all authors and affiliations

Science  04 Dec 2009:
Vol. 326, Issue 5958, pp. 1321
DOI: 10.1126/science.326.5958.1321-b

Most studies of mammalian aging eventually lead to the mitochondrion, the energy-producing organelle. A prevailing hypothesis has been that damaging byproducts of mitochondrial respiration, called reactive oxygen species (ROS), accumulate as we age and cause mitochondrial dysfunction, which manifests at the organismal level as age-related disorders. Yet this hypothesis is at odds with growing evidence that an increase in the biogenesis of mitochondria can have beneficial anti-aging effects. Illustrating this dilemma are two studies of mice in which genetic manipulations altered mitochondrial function. For mice deficient in the proapoptotic protein Bak, Someya et al. found that mitochondria actively contribute to age-related hearing loss by mediating the death of cochlear cells in the ear. The death of these cells was triggered by oxidative stress and could be suppressed by antioxidants. Independently, Wenz et al. found that increased muscle expression of peroxisome proliferator–activated receptor-γ coactivator α (PGC-1α), a protein that up-regulates mitochondrial biogenesis, not only prevented age-associated loss of muscle mass, but also had beneficial effects on whole-body metabolism. Why the salutary effects of increased mitochondrial biogenesis are not counteracted by a parallel increase in damaging ROS remains unclear, but could involve increased turnover of the “older” ROS-damaged organelles.

Proc. Natl. Acad. Sci. U.S.A. 106, 19432; 10.1073/pnas.0911570106 (2009).

Navigate This Article