AIMTo investigate the chronic cardioprotection of testosterone against ischemia/reperfusion injury and acute effect against H2O2-stress injury.

METHODSThe vas deferens were ligated bilaterally and the testes removed from male Sprague-Dawley rats, and testosterone propionate was supplemented every day. Eight weeks after gonadectomy, all the hearts were mounted on a Langendorff apparatus to assess the level of lactate dehydrogenase (LDH) in the coronary effluent and the infarct size. Isolated adult ventricular myocytes were obtained by enzymatic dissociation, in which H2O2-stress injury model was copied. The myocyte contraction was determined, and mitochondrial reactive oxygen species (ROS) production was measured by loading with fluorescent probe DCFH-DA.

RESULTSIn gonadectomy model, pretreatment with testosterone propionate significantly decreases the LDH release and the infarct size. In the isolated myocytes model, testosterone attenuated the decreases of +/- dL/dtmax and dL which produced by H2O2-stress, and prevented the production of ROS induced by H2O2-stress. Co-treatment with atractyloside or 5-HD attenuated the effect of testosterone.

CONCLUSIONThe findings show the chronic cardioprotection of testosterone against ischemia/reperfusion injury and acute effect against H2O2-stress injury via opening of mitoK(ATP) channel or/and the inhibiting mitochondrial permeability transition pore.