Oxygen free radicals resulting from metabolic processes and environmental toxins continuously produce brain damage contributing to degenerative diseases, including Alzheimer's disease, schizophrenia, and memory and learning dysfunctions. Our investigations of C57BL/6 mice indicate that aging involves (i) increased capacity for Superoxide and hydrogen peroxide generation by brain mitochondria; (ii) increased activity of the antioxidant enzymes Superoxide dismutase, catalase, and glutathione peroxidase; (iii) increased DNA damage; and (iv) regionally specific increases in oxidatively modified proteins. Reduction in daily caloric intake prevents the oxidative damage during aging. It promotes longevity and retards progression of a wide variety of age-associated biological changes. It also results in preservation or improvement in selected cognitive and sensorimotor functions of aged mice and rats. The concurrent modulation of brain oxidant generation by optimization of caloric intake and the prevention of oxidative damage by antioxidant administration offer a novel approach to retard degenerative diseases.
|Number of pages||1|
|Journal||Proceedings of the Western Pharmacology Society|
|State||Published - 1 Dec 1998|