JOURNAL ARTICLE

[Mechanisms of oxidative stress-induced damage and its protection in cavernous mitochondria of diabetic rats]

Xiao-xin Li, Xue-feng Qiu, Wen Yu, Wei-dong Zhu, Yun Chen, Yu-tian Dai
Beijing da Xue Xue Bao. Yi Xue Ban, Journal of Peking University. Health Sciences 2011 April 18, 43 (2): 189-93
21503110

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.

Full Text Links

Find Full Text Links for this Article

Discussion

You are not logged in. Sign Up or Log In to join the discussion.

Related Papers

Remove bar
Read by QxMD icon Read
21503110
×

Save your favorite articles in one place with a free QxMD account.

×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"