The role of free radical in the pathogenesis of impotence in streptozotocin-induced diabetic rats.
Diabetes is the most common cause of erectile dysfunction (ED). Oxidative stress has been suggested to be a contributory factor in vascular complications of diabetes in various organs. In the present study, we investigated whether oxidative stress is associated with erectile function in non-insulin dependent diabetes mellitus (NIDDM) rats. Fifty-four Sprague-Dawley rats were the subjects of this study. In each rat, NIDDM was induced by an intraperitoneal injection of 90 mg/Kg of streptozotocin on the second day after birth. Based on the diabetic period, they were classified into either short-term or long-term diabetics (avg. 22 weeks, n=18 and avg. 38 weeks, n=20), respectively, and their age-matched controls (n=16). To evaluate the erectile function in each rat, the intracavernous pressure, and latency to maximal pressure, following cavernous nerve stimulation (frequency: 1 Hz, intensity: 3 - 6 V, pulse width: 1 msec, pulse duration: 1 min.) was analyzed. To evaluate both oxidative stress from reactive oxygen species, and antioxidant function as a defense against them, total malondialdehyde and glutathione levels were measured in the corpus cavernosum of the penis, using a spectrophotometric assay. The intracavernous pressure following cavernous nerve stimulation was significantly lower in the long-term (49.8 +/- 9.4 cmH2O) than the short-term diabetics (75.9 +/- 14.8 cm H2O), and markedly decreased in the diabetic rats, compared with their age-matched controls (long-term controls; 60.7 +/- 17.2 cmH2O, short-term controls; 95.2 +/- 20.4 cmH2O). The malondialdehyde content in the corpus cavernosum was markedly increased in the diabetics (2.13 +/- 0.27 nM/mg protein) compared to the controls (1.48 +/- 0.22 nM/mg protein). Furthermore, the glutathione level was significantly decreased in the diabetics, compared to age-matched controls (short-term control; 218.3 +/- 25.6 microM/mg protein, long-term control; 150.2 +/- 9.8 microM/mg protein). In the diabetic groups, it was more significantly decreased in the long-term diabetics (134.8 +/- 11.3 microM/mg protein) than in short-term diabetics (182.1 +/- 18.8 microM/mg protein). NIDDM causes erectile dysfunction, which slowly progresses. Oxidative stress to cavernous tissue may be a contributory factor in erectile dysfunction in diabetics.
Ryu
Ji-Kan
JK
Department of Urology, Inha University College of Medicine, 7-206 3rd St., Sinhung-dong, Jung-gu, Incheon 400-103, Korea. jksuh@inha.ac.kr
Kim
Dae-Joong
DJ
Lee
Taek
T
Kang
Yun-Seog
YS
Yoon
Sang-Min
SM
Suh
Jun-Kyu
JK
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D007172:Erectile Dysfunction / Q000209:etiology*; D005260:Female; D005609:Free Radicals; D005978:Glutathione / Q000032:analysis; D015227:Lipid Peroxidation; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013311:Streptozocin
D005609:Free Radicals; D013311:Streptozocin; D005978:Glutathione