Accelerated chronologic aging of S. cerevisiae induced by PUFA is associated to mitochondrial dysfunction, enhanced sensitivity to lipid peroxidation and ROS overproduction

Abstract

Correlative evidence from comparative studies has suggested that longevity in higher eucaryotes keeps an inverse correlation with the unsaturation degree of mitochondrial membranes. Since lipid peroxidation (LP) depends on the number of double bonds, it has been hypothesized that lower unsaturation degree of the membranes from longevous animals preserves mitochondrial function from the damage by ROS. To further test this hypothesis, we have studied if accelerated aging and impaired mitochondrial function by the incorporation of PUFA in the yeast is associated with increased sensitivity to LP and enhanced ROS production. When yeast incorporated C18:3 into mitochondrial membranes, it was observed accelerated aging along with increased ROS production, which was attributed to impairment in electron transfer between complex II and complex III. These effects were associated with a higher susceptibility to LP, although the cells become more resistant to this process at late stages of aging. These data confirm the observations made in higher eukaryotes about the primordial role of LP in the mitochondrial impairment associated to a lower longevity. This work was funded by a CONACYT (130638 to CCR) grant.