title: [Mechanisms of oxidative stress-induced damage and its protection in cavernous mitochondria of diabetic rats].
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Urology, The Affiliated Drum Tower Hospital of Nanjing University Medical College, Nanjing 210008, China.
authors.forename: Xiao-xin
authors.initials: XX
authors.lastname: Li
authors.forename: Xue-feng
authors.initials: XF
authors.lastname: Qiu
authors.forename: Wen
authors.initials: W
authors.lastname: Yu
authors.forename: Wei-dong
authors.initials: WD
authors.lastname: Zhu
authors.forename: Yun
authors.initials: Y
authors.lastname: Chen
authors.forename: Yu-tian
authors.initials: YT
authors.lastname: Dai
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000378:metabolism*; D007172:Erectile Dysfunction / Q000188:drug therapy* / Q000209:etiology; D005978:Glutathione / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D008928:Mitochondria / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology*; D010413:Penis / Q000378:metabolism / Q000503:physiopathology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D008315:Malondialdehyde; D013482:Superoxide Dismutase; D005978:Glutathione