Posibles mecanismos por los que las mujeres viven más ue los varones

Abstract

AbstractTo elucidate the molecular mechanisms enabling females to live longer than males, we investigated differences in mitochondrial oxidative stress between both sexes. Mitochondria are a major source of free radicals in cells. Those from female rats generate half the amount of peroxides than those from males. This does not occur in ovariectomized animals. Oestrogen replacement therapy prevents the effect of ovariectomy. Mitochondria from females have higher levels of reduced glutathione than those from males. Again, those from ovariectomized rats have similar levels to males, while oestrogen therapy prevents the fall in glutathione levels that occurs in ovariectomized animals. All these differences are due to greater expression of the antioxidant enzymes Mn-superoxide dismutase and glutathione peroxidase in females than in males. Females behave as double transgenics overexpressing superoxide dismutase and glutathione peroxidase, conferring protection against free radical mediated damage in ageing. We also determined 16S rRNA expression, a marker of ageing associated with oxidative stress, and found that it was higher in mitochondria from females than in those from males of the same chronological age. Thus, it is as if males have a greater biological age than females of the same chronological age. In conclusion, experimental data support the existence of a biological basis for the differences in longevity found between males and females. These differences cannot entirely be explained by sociological factors.