Authors: Jérôme Lapointe Siegfried Hekimi
Publish Date: 2009/09/03
Volume: 67, Issue: 1, Pages: 1-8
Abstract
According to the widely acknowledged mitochondrial free radical theory of aging MFRTA the macromolecular damage that results from the production of toxic reactive oxygen species ROS during cellular respiration is the cause of aging However although it is clear that oxidative damage increases during aging the fundamental question regarding whether mitochondrial oxidative stress is in any way causal to the aging process remains unresolved An increasing number of studies on longlived vertebrate species mutants and transgenic animals have seriously challenged the pervasive MFRTA Here we describe some of these new results including those pertaining to the phenotype of the longlived Mclk1 +/− mice which appear irreconcilable with the MFRTA Thus we believe that it is reasonable to now consider the MFRTA as refuted and that it is time to use the insight gained by many years of testing this theory to develop new views as to the physiological causes of aging
Keywords: