Effect of alpha-tocopherol supplementation on renal oxidative stress and Na+/K+ -adenosine triphosphatase in ethanol treated Wistar rats.

Ethanol intoxication resulted in high extent of lipid peroxidation, and reduction in antioxidant defenses (decreased GSH, GSH/GSSG ratio, and catalase, SOD and GPx activities) and (Na+/K+)-ATPase activity in kidney. Alpha-tocopherol treatment effectively protected kidney from ethanol induced oxidative challenge and improved renal (Na+/K+)-ATPase activity. Ethanol induced oxidative stress in the kidney and decreased (Na+/K+)-ATPase activity could be reversed by treatment with ascorbic acid.

Radio frequency electromagnetic radiation (RF-EMR) from GSM (0.9/1.8GHz) mobile phones induces oxidative stress and reduces sperm motility in rats.

INTRODUCTION: Mobile phones have become indispensable in the daily lives of men and women around the globe. As cell phone use has become more widespread, concerns have mounted regarding the potentially harmful effects of RF-EMR from these devices. OBJECTIVE: The present study was designed to evaluate the effects of RF-EMR from mobile phones on free radical metabolism and sperm quality. MATERIALS AND METHODS: Male albino Wistar rats (10-12 weeks old) were exposed to RF-EMR from an active GSM (0.9/1.8 GHz) mobile phone for 1 hour continuously per day for 28 days. Controls were exposed to a mobile phone without a battery for the same period. The phone was kept in a cage with a wooden bottom in order to address concerns that the effects of exposure to the phone could be due to heat emitted by the phone rather than to RF-EMR alone. Animals were sacrificed 24 hours after the last exposure and tissues of interest were harvested. RESULTS: One hour of exposure to the phone did not significantly change facial temperature in either group of rats. No significant difference was observed in total sperm count between controls and RF-EMR exposed groups. However, rats exposed to RF-EMR exhibited a significantly reduced percentage of motile sperm. Moreover, RF-EMR exposure resulted in a significant increase in lipid peroxidation and low GSH content in the testis and epididymis. CONCLUSION: Given the results of the present study, we speculate that RF-EMR from mobile phones negatively affects semen quality and may impair male fertility.

Radio frequency electromagnetic radiation (RF-EMR) from GSM (0.9/1.8GHz) mobile phones induces oxidative stress and reduces sperm motility in rats

INTRODUCTION: Mobile phones have become indispensable in the daily lives of men and women around the globe. As cell phone use has become more widespread, concerns have mounted regarding the potentially harmful effects of RF-EMR from these devices. OBJECTIVE: The present study was designed to evaluate the effects of RF-EMR from mobile phones on free radical metabolism and sperm quality. MATERIALS AND METHODS: Male albino Wistar rats (10-12 weeks old) were exposed to RF-EMR from an active GSM (0.9/1.8 GHz) mobile phone for 1 hour continuously per day for 28 days. Controls were exposed to a mobile phone without a battery for the same period. The phone was kept in a cage with a wooden bottom in order to address concerns that the effects of exposure to the phone could be due to heat emitted by the phone rather than to RF-EMR alone. Animals were sacrificed 24 hours after the last exposure and tissues of interest were harvested. RESULTS: One hour of exposure to the phone did not significantly change facial temperature in either group of rats. No significant difference was observed in total sperm count between controls and RF-EMR exposed groups. However, rats exposed to RF-EMR exhibited a significantly reduced percentage of motile sperm. Moreover, RF-EMR exposure resulted in a significant increase in lipid peroxidation and low GSH content in the testis and epididymis. CONCLUSION: Given the results of the present study, we speculate that RF-EMR from mobile phones negatively affects semen quality and may impair male fertility.

Effect of exogenous L-ornithine L-aspartate on ethanol induced testicular injury in Wistar rats.

To investigate reversibility of ethanol induced testicular injuries on treatment with L-ornithine-L-aspartate, male Wistar rats were treated with ethanol (1.6g/kg b.wt/day) and L-ornithine- L-aspartate (200mg/kg b.wt/ day) for 4 weeks. L-ornithine-L-aspartate effectively prevented the ethanol induced body and testes weight reduction; changes in testicular weight well correlated with body weight. Drug exhibited an ability to counteract ethanol induced oxidative challenge as it effectively reduced testicular TBARS and increased tissue ascorbic acid, GSH and activities of superoxide dismutase, catalase, GSH-Red and Se-GSH-Px. However the drug didn't show promising effect on inhibitory effect of ethanol on testicular D5, 3-beta and 17-beta HSD (hydroxy steroid dehydrogenase).

Role of reactive oxygen species and antioxidants on pathophysiology of male reproduction.

The excessive generation of reactive oxygen species (ROS) by abnormal spermatozoa and contaminating leukocytes has been defined as one of the few etiologies for male infertility. Administration of antioxidants in patients with 'male factor' infertility has begun to attract considerable interest. The main difficulty of such an approach is our incomplete understanding of the role of free radicals in normal and abnormal sperm function leading to male infertility. Mammalian spermatozoa membranes are very sensitive to free radical induced damage mediated by lipid peroxidation, as they are rich in polyunsaturated fatty acids. Limited endogenous mechanisms exist to reverse these damages. ROS attacks the fluidity of the sperm plasma membrane and the integrity of DNA in the sperm nucleus. ROS induced DNA damage accelerate the germ cell apoptosis. Unfortunately spermatozoa are unable to repair the damage induced by excessive ROS as they lack the cytoplasmic enzymes required to accomplish the repair. Assessment of such oxidative stress status (OSS) may help in the medical treatment. Treatment strategies must be directed toward lowering of ROS levels to keep only a small amount necessary to maintain normal cell function.

Effect of chronic ethanol administration on testicular antioxidant system and steroidogenic enzyme activity in rats.

In order to find out the effect of chronic ethanol administration on testicular antioxidant system and steroidogenic enzyme activity, male rats fed with ethanol 1.6g/kg body weight per day for four weeks were studied. Besides a drastic reduction in body and testis weight, there was decrease in ascorbic acid, reduced glutathione and activities of superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase in the testicular tissue of the treated animals. Simultaneously, there was increase in lipid peroxidation and glutathione S-transferase activity. Activities of 3 beta-hydroxy steroid dehydrogenase and 17 beta-hydroxy steroid dehydrogenase were also found decreased in the treated animals. The results indicate that chronic ethanol administration resulted in increase in oxidative stress and decrease in the activities of steroidogenic enzymes in the rat testes.

Evidence for oxidative stress in osteoarthritis.

Evidence of increased oxidative stress in patients of osteoarthritis in comparison with healthy control subjects was investigated by measuring the thiobarbituric acid reactive substances (TBARS), vitamin C, reduced glutathione (GSH) and the activities of superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) in erythrocytes. It was observed that osteoarthritis patients were more susceptible to oxidative damage than controls as evident from increased TBARS and decreased ascorbic acid, GSH, catalase and GPx in erythrocytes. Significant increase in SOD activity found in patients might be an adaptive response. With the understanding of the role of antioxidants in arthritis, it is becoming increasingly clear that these agents seem to be beneficial in osteoarthritis.

Role of oxidative stress in ethanol induced germ cell apoptosis - An experimental study in rats.

The study was undertaken to evaluate the possible involvement of oxidative stress in the pathogenesis of ethanol induced testicular atrophy in rats. Adult male rats were orally administered ethanol at a dose of 1.6 g/kg body weight/day for four weeks. Twenty-four hours after the last treatment the rats were sacrificed using anesthetic ether. Testes were removed and weighed. Apoptosis was studied by using the Feulgen reaction on 5 µ thin paraffin sections of testis. Testicular homogenate was prepared and centrifuged. The supernatant was used for the estimation of extent of lipid peroxidation and antioxidant defense status. There was significant reduction in body weight: and in testicular weight and diameter in ethanol treated rats. Extent of germ cell apoptosis was significantly high in ethanol treated rats. Ethanol treated rats showed significantly high tissue TBARS level and glutathione S-transferase activity; and low tissue ascorbic acid, reduced glutathione, superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase activities. Chronic ethanol administration resulted in high oxidative stress in the testes either due to increased extent of lipid peroxidation or due to decreased antioxidant defenses, and thereby induces germ cell apoptosis leading to testicular atrophy.

Effect of ascorbic acid, alpha-tocopherol, lecithin and L-ornithine-L-aspartate on ethanol induced hypoproteinemia and hyperlipidemia in rats.

We studied effect of exogenous ascorbic acid, alpha-tocopherol, lecithin and L-ornithine-L-aspartate on serum lipids and proteins in experimental hepatotoxic Wistar rats. Eleven groups (n = 6) of animals were used. Hepatotoxicity was induced by administering ethanol (1.6 g/kg/day) for 28 days. Both preventive and curative options were studied. Percentage increase in body weight was significantly lower in ethanol treated rats. Ethanol significantly (P<0.05) increased cholesterol, triglycerides and LDL, and decreased protein, albumin and A:G ratio in serum. Ascorbic acid, alpha-tocopherol, lecithin and L-ornithine-L-aspartate exhibited an ability to counteract the alcohol-induced changes in the body weight and biochemical parameters in preventive and therapeutic models in varying degree. Antioxidants showed better effect.

Effect of exogenous lecithin on ethanol-induced testicular injuries in Wistar rats.

Infertility is well-established harmful effect in chronic alcoholism and so far, there is no effective treatment for this condition. The study was conducted to determine the effects of lecithin, a known hepatoprotective on ethanol induced testicular injuries in male albino rats of Wistar strain. Five groups (n=6) of animals were used. Group I served as control. Group II received daily 1.6 g ethanol/kg body weight/day for 4 weeks orally. Group III received 1.6 g ethanol + 500 mg lecithin/kg body weight/day for four weeks orally. Group IV received 1.6 g ethanol/kg body weight for/day 4 weeks and followed by 500 mg lecithin/kg body weight/ day for four weeks orally. Group V received 1.6 g ethanol/kg body weight/ day orally for 4 weeks, followed by 4 weeks abstinence. Twenty-four hours after the last treatment the rats were sacrificed using anesthetic ether. Testes were removed and used for the estimation of extent of lipid peroxidation and tissue levels of antioxidants and steroidogenic enzymes. Lecithin protected testes from ethanol induced oxidative stress. However, the drug did not show any considerable effect on the activities of testicular delta5, 3beta-HSD and 17beta-HSD. In conclusion, ethanol induced oxidative stress can be reversed by treatment with lecithin. However the effect of lecithin on steroidogenesis was not promising.