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Objective: To explore the mechanism of impairment and defence of oxidative stress in cavernous tissue of diabetic rats.Methods: Adult male SD rats were randomly divided into normal control group and experimental group,which included diabetes group induced by STZ and therapeutic group with GHS treatment.Eight weeks later,erectile function was assessed by measuring the rise in intracavernous pressure(ICP)of the rats following cavernous nerve electrostimulation before sacrificed.The levels of malondialdehyde(MDA)and the activities of superoxide dismutase(SOD)in cavernous tissue were detected.The morphology of mitochondria in cavernous tissue was observed with transmission electron microscope and mitochondrial transmembrane potential was detected.Results: A significant decrease in ICP was recorded in the diabetic rats,with improvement measured in the rats receiving GSH.The levels of MDA increased remarkably and the activities of SOD decreased significantly in cavernous tissue of the diabetes group.The degeneration of mitochondria in the endothelia and smooth muscle cells of penis was observed,following with the reduction of mitochondria,and mitochondria transmembrane potential was decreased.A remarkable decrease in MDA and increase in SOD was observed in GSH treatment group.Meanwhile,the morphology changes of mitochondria were ameliorated and the decrease of mitochondria transmembrane potential was inhibited,in diabetic rats with GSH treatment.Conclusions: Hyperglycemia could cause oxidative stress in the cavernous tissue of diabetic rats and this impairment could contribute to diabetic erectile dysfunction(DMED);oxidant treatment could attenuate oxidative stress by improving the function of mitochondria in cavernous tissue.Oxidative stress plays an important role in DMED and our study might provide a new insight for the prevention and treatment of DMED.