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Melatonin is a potent antioxidant agent that can scavenge oxy- and nitroradicals generated under hypoxic conditions in the brain. In this study, we investigated the effect of melatonin on protein oxidation and nitric oxide (NO) during hypoxia. Seven-day-old Sprague-Dawley newborn rats were divided into three groups. Hypoxic (n=9) and melatonin (n=11) groups were subjected to 2h of hypoxic exposure (a humidity mixture of gases consisting of 92% nitrogen and 8% oxygen). Melatonin (at a dose of 10mg/kg) was administrated 30 min before the onset hypoxia and then at 24th and 48th hours after the end of the hypoxic exposure. Control (n=10) and hypoxic groups received the isotonic sodium chloride according to the same schedule. The brain tissue concentration of advanced oxidation protein products (AOPP) and protein thiol (P-SH) was used as an index of protein oxidation. In our study, although AOPP and NO increased significantly, the levels of P-SH decreased in the hypoxic group. The level of AOPP was declined by melatonin treatment. However, perturbed thiol status could not be recovered by melatonin treatment. There was no relationship between the levels of NO and protein oxidation markers. These results indicate that exogenous melatonin could prevent AOPP, but that it is inadequate in recovering perturbed thiol status. Therefore, melatonin alone was observed to be an incomplete treatment to prevent protein oxidation in hypoxia-induced brain damage.

It has been reported that mental stress causes abnormality of spermiogram parameters. We investigated the effect of psychological stress on the L-arginine-nitric oxide (NO) pathway. Semen samples were collected from 29 healthy fourth semester medical students just before (stress) and 3 months after (non-stress) the final examinations. Psychological stress was measured by the State Anxiety Inventory questionnaire. After standard semen analysis, arginase activity and NO concentration were measured spectrophotometrically in the seminal plasma. Measurements were made in duplicate. During the stress period, sperm concentration (41.28 +/- 3.70 vs 77.62 +/- 7.13 x 10(6)/mL), rapid progressive motility of spermatozoa (8.79 +/- 1.66 vs 20.86 +/- 1.63%) and seminal plasma arginase activity (0.12 +/- 0.01 vs 0.22 +/- 0.01 U/mL) were significantly lower than in the non-stress situation, whereas seminal plasma NO (17.28 +/- 0.56 vs 10.02 +/- 0.49 micromol/L) was higher compared to the non-stress period (P0.001 for all). During stress there was a negative correlation between NO concentration and sperm concentration, the percentage of rapid progressive motility and arginase activity (r = -0.622, P0.01; r = -0.425, P0.05 and r = -0.445, P0.05, respectively). These results indicate that psychological stress causes an increase of NO level and a decrease of arginase activity in the L-arginine-NO pathway. Furthermore, poor sperm quality may be due to excessive production of NO under psychological stress. In the light of these results, we suggest that the arginine-NO pathway, together with arginase and NO synthase, are involved in semen quality under stress conditions.