Streptozotocin-induced diabetes increases apoptosis through JNK phosphorylation and Bax activation in rat testes.
Diabetic disease is known to suppress male reproductive activity in laboratory animals and humans. The present study was designed to evaluate whether streptozotocin-induced diabetes increases apoptotic cell death in rat testes through activation of the JNK and Bax pathway. Diabetes was induced by a single intravenous injection of streptozotocin (40 mg/kg) and testis samples were collected after 3 months. Compared with controls, body weight and testicular weight were lower in the diabetic group, and the apoptotic index in testicular germ cells was significantly increased. Expression of phospho-JNK and Bax was significantly increased in the diabetic group, and the level of activated caspase-3 was also increased, compared to that of controls. Our findings suggest that streptozotocin-induced diabetes increases apoptotic cell death in rat testes through phosphorylation of JNK and activation of Bax.
Koh
Phil-Ok
PO
Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 900 Gajwa-dong, Jinju 660-701, South Korea. pokoh@gsnu.ac.kr
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001835:Body Weight; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology*; D020287:In Situ Nick-End Labeling; D048670:MAP Kinase Kinase 4 / Q000378:metabolism*; D008297:Male; D009929:Organ Size; D010766:Phosphorylation; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013737:Testis / Q000033:anatomy & histology / Q000201:enzymology / Q000378:metabolism*; D051028:bcl-2-Associated X Protein / Q000378:metabolism*
D051028:bcl-2-Associated X Protein; D048670:MAP Kinase Kinase 4