The role of free radical in the pathogenesis of impotence in streptozotocin-induced diabetic rats

Abstract

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 dependant 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 90mg/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 μ M/mg protein, long-term control; 150.2 ± 9.8 μ M/mg protein). In the diabetic groups, it was more significantly decreased in the long-term diabetics (134.8 ± 11.3 μ M/mg protein) than in short-term diabetics (182.1 ± 18.8 μ M/mg protein). NIDDM causes erectile dysfunction, which slowly progresses. Oxidative stress to cavernous tissue may be a contributory factor in erectile dysfunction in diabetics.