Testosterone alleviates mitochondrial ROS accumulation and mitochondria-mediated apoptosis in the gastric mucosa of orchiectomized rats

The effects of testosterone propionate (TP) on the oxidative stress and mitochondrial function, as well as on mitochondria associated apoptotic signaling, were analyzed in the gastric mucosa in orchiectomized male rats. The present study showed that testosterone deficiency triggered apoptosis by damaging the mitochondrial function (ROS overload generation, membrane potential loss, ATP depletion, etc.), increasing both the release of mitochondrial cytochrome c (Cyt c) and the Bax/Bcl-2 ratio, and activating caspase-9 and caspase-3. Supplements of testosterone propionate to castrated male rats ameliorated mitochondrial function and confirmed the involvement of the mitochondrial pathway in the gastric mucosa. These results suggest that testosterone could maintain the mitochondrial function of the gastric mucosa and mediate mitochondria-associated apoptotic signaling.