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.
Ethanol is a testicular toxin and it causes fertility abnormalities with low sperm count and impaired sperm motility in men. The present study was designed to investigate plasma testosterone level and hypothalamic pituitary gonadal (HPG) axis function in alcoholic men and also effect of ethanol on systemic oxidative stress. Forty six male alcohol abusers in the age group 20-40 years were selected. Fifty five, males in the same age group served as control. Alcohol abusers had significantly low plasma testosterone with low luteinizing hormone and follicle stimulating hormone. In addition they had significantly high thiobarbituric acid reactive substances (TBARS), superoxide dismutase and glutathione S-transferase, and low glutathione, ascorbic acid, catalase, glutathione reductase and glutathione peroxidase. Moreover, serum testosterone level in alcoholics negatively correlated with duration of alcohol abuse, and TBARS. Duration dependent decreased serum testosterone level in alcohol abusers might be due to 1) increased oxidative stress which can damage Leydig and supporting Sertoli cells and 2) impaired HPG axis.
In view of association of diabetes mellitus and male infertility, present study was designed to investigate the functional status of hypothalamic pituitary gonadal (HPG) axis in diabetic men. Thirty-five diabetic men (BMI 22.24±0.21) in the age group 20-40 (30.6±4.7) years were selected. Twenty-five healthy men (BMI 23.85±0.25), in the same age group (29.5±4.8) served as control. Blood samples were collected for hormonal and biochemical estimations. Diabetic men had significantly low serum testosterone with low LH and FSH, hypercholesterolemia, hypertriglyceridemia, hypoalbuminemia and increased oxidative stress. Low serum testosterone in diabetic men was accompanied by low LH and FSH; the inability of the pituitary gland to respond appropriately to a decline in testosterone implying central effect of high serum glucose on the interaction between the nervous and endocrine system. Nutritional deficiency, increased oxidative stress and increased aromatase activity due to excessive body fat might have also contributed to low serum testosterone.
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 alpha tocopherol 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 1.6g ethanol/kg body weight/day for 4 weeks orally. Group III received 1.6g ethanol+80mg alpha tocopherol/kg body weight/day for four weeks orally. Group IV received 1.6g ethanol/kg body weight for/day 4 weeks and followed by 80mg alpha tocopherol/kg body weight/day for four weeks orally. Group V received 1.6g ethanol/kg body weight/day orally for 4 weeks, followed by 4 weeks abstinence. Twently-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. Alpha tocopherol treatment increased the activities of testicularΔ(5), 3β-HSD. Moreover, the treatment was also associated with significant decrease in testicular oxidative stress. Ethanol-induced oxidative stress and decreased steroidogenesis can be reversed by treatment with alpha tocopherol.