Effects of Catalase Over-expression on Aging

A brief introduction led to the weakness of the elderly. According to the free radical theory of aging, it is caused by oxidative damage caused by ROS (reactive oxygen species). This article focuses partly on research supporting this theory, and it suggests that overexpression of human catalase in mitochondria can prolong the life span of mice. The specific paper in this article is overexpression of catalase-directed catalase by Samuel E. to extend mouse life span.

Overexpression of catalase reduces the increase in oxidative stress that occurs in mice as the mouse ages. Overexpressing mice showed no loss of sperm, testis embryo and supporting cells with aging in wild type mice. Oxidative stress in wild type mice typically induces oxidative DNA damage of spermatozoa as age (measured as 8-oxodG), but these lesions are significantly reduced in aged catalase overexpressing mice. In addition, these overexpressing mice showed no age-dependent littermate reduction for litter size. Catalase targeting catalase overexpression extends the life of the mouse

Many symptoms are associated with changes in catalase activity. There is evidence that moderate oxidative stress induces catalase expression in vascular cells, which can be beneficial to prevent further oxidative stress (Meilhac et al., 2000). Superoxide anion can inhibit catalase. In the leukocytes of Swiss-type ac type mastitis patients, the rate of dehydroascorbic acid reduction is 4 times as much as usual, indicating that the catalase protection function is supported by dehydroascorbic acid reductase. Increase in catalase activity was observed in experimental halothane hepatotoxicity, endotoxemia and hepatitis, hemolytic disease, liver disease, acute pancreatitis, muscular dystrophy etc (Goth, 1987).