OBJECTIVE: To explore the mechanism of impairment and defense of oxidative stress in cavernous mitochondria of diabetic rats. METHODS: Adult male SD rats(n=42)were randomly divided into normal control group(n=10) and experimental group(n=32). The diabetic model rats induced by streptozotocin were randomly divided into diabetes group(n=13) and therapeutic group with reduced glutathione (GSH) treatment(n=12). Eight weeks later, erectile function was assessed by measuring the rise in intracavernous pressure (ICP) of the rats following cavernous nerve eletrostimulation before the rats were sacrificed. The levels of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) in cavernous tissue were detected. The masson staining was used to show the structure of the rat penis. Mitochondrial transmembrane potential was detected. RESULTS: A significant decrease in ICP was recorded in the diabetic rats [(50.80 ± 9.80)vs.(90.42 ± 7.02) mmHg,P<0.05], with improvement measured in the rats receiving GSH [(74.20 ± 5.69)vs.(50.80 ± 9.80)mmHg, P<0.05]. The levels of MDA increased remarkably [(6.15 ± 1.07)vs.(3.52 ± 0.94)mmol/g protein, P<0.01] and the activities of SOD decreased significantly[(73.34 ± 6.56)vs.(114.22 ± 6.34)U/mg protein, P<0.05)] in cavernous tissue of the diabetes group. Mitochondria transmembrane potential was decreased [(727.98 ± 68.33)vs.(1223.15 ± 222.92),P<0.01]. A remarkable decrease in MDA [(3.90 ± 0.96)vs.(6.15 ± 1.07)mmol/g protein, P<0.05] and increase in SOD[(95.74 ± 4.65)vs.(73.34 ± 6.56)U/mg protein,P<0.05] were observed in GSH treatment group. Meanwhile, the morphology changes of cavernous tissue and the decrease of mitochondria transmembrane potential were inhibited[(930.30 ± 48.36) vs.727.98 ± 68.33),P<0.05], in diabetic rats with GSH treatment. CONCLUSION: Hyperglycemia could cause oxidative stress in the cavernous tissue of diabetic rats and this impairment could contribute to diabetic erectile dysfunction; Oxidant treatment could attenuate oxidative stress by improving the function of mitochondria in cavernous tissue. Oxidative stress plays an important role in diabetic erectile dysfunction (DED) and our study might provide a new insight into the prevention and treatment of DED.
OBJECTIVE: To explore the mechanism of impairment and defense of oxidative stress in cavernous mitochondria of diabeticrats. METHODS: Adult male SD rats(n=42)were randomly divided into normal control group(n=10) and experimental group(n=32). The diabetic model rats induced by streptozotocin were randomly divided into diabetes group(n=13) and therapeutic group with reduced glutathione (GSH) treatment(n=12). Eight weeks later, erectile function was assessed by measuring the rise in intracavernous pressure (ICP) of the rats following cavernous nerve eletrostimulation before the rats were sacrificed. The levels of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) in cavernous tissue were detected. The masson staining was used to show the structure of the rat penis. Mitochondrial transmembrane potential was detected. RESULTS: A significant decrease in ICP was recorded in the diabeticrats [(50.80 ± 9.80)vs.(90.42 ± 7.02) mmHg,P<0.05], with improvement measured in the rats receiving GSH [(74.20 ± 5.69)vs.(50.80 ± 9.80)mmHg, P<0.05]. The levels of MDA increased remarkably [(6.15 ± 1.07)vs.(3.52 ± 0.94)mmol/g protein, P<0.01] and the activities of SOD decreased significantly[(73.34 ± 6.56)vs.(114.22 ± 6.34)U/mg protein, P<0.05)] in cavernous tissue of the diabetes group. Mitochondria transmembrane potential was decreased [(727.98 ± 68.33)vs.(1223.15 ± 222.92),P<0.01]. A remarkable decrease in MDA [(3.90 ± 0.96)vs.(6.15 ± 1.07)mmol/g protein, P<0.05] and increase in SOD[(95.74 ± 4.65)vs.(73.34 ± 6.56)U/mg protein,P<0.05] were observed in GSH treatment group. Meanwhile, the morphology changes of cavernous tissue and the decrease of mitochondria transmembrane potential were inhibited[(930.30 ± 48.36) vs.727.98 ± 68.33),P<0.05], in diabeticrats with GSH treatment. CONCLUSION:Hyperglycemia could cause oxidative stress in the cavernous tissue of diabeticrats and this impairment could contribute to diabetic erectile dysfunction; Oxidant treatment could attenuate oxidative stress by improving the function of mitochondria in cavernous tissue. Oxidative stress plays an important role in diabetic erectile dysfunction (DED) and our study might provide a new insight into the prevention and treatment of DED.