ABSTRACT
The free radical aging hypothesis is one of many hypotheses that attempt to re duce the myriad observations about aging to a few simple causes or processes (1). The hypothesis is of the “ wear and repair” variety, where the major deterioration mechanism is conceptualized as stochastic and extrinsic to the genetic program ming of the organism. But the process can be modified by genes or by environ ment (2). The free radical aging hypothesis as adapted to mitochondrial processes can be considered as a version of the “rate of living” hypothesis, since both theories relate metabolic activity rates to aging (2). Free radicals and free radical initiated damaging reaction cascades are the inevitable by-product of aerobic res piration. Common physiology among animals means that a more or less fixed percentage of the electrons and oxygen slated for respiration will be diverted to radicals which will produce damage to the animal. Lethal senescence will eventu ally result from the cumulative damage. Small animals consume oxygen at higher rates per unit body mass and consequently live shorter lives. While rates of oxy gen consumption correlate well with much of the life span variation among spe cies, birds and bats are notable exceptions of animals that live longer than species of similar sizes (2).
