Oxidative Stress In Epididymal Sperm Research Articles

English

Reactive oxygen species (ROS) generation, induced by Bisphenol A (BPA) may cause mammalian sperm damage according to research findings. BPA is a known contaminant that with increased exposure in the body can exert both toxic and estrogenic effects in mammalians cells. The aim of this study was to evaluate the effect of BPA-induced oxidative stress in the liver on epididymal semen quality in adult rat. BPA was mixed in corn oil and intra-peritoneally administered for 20 days in dose dependent manner. After 24 h of the last treatment, rats were weighed, sacrificed and organs harvested for analysis. BPA caused a reduction in the epididymal semen quality and sperm count in a dose dependent manner. Sperm analyses results showed that there was oligozoospermia (E‚20 × 106 spermatozoids/ml) and asthenozoospermia (motility E‚50%) in the treatment group compared to the control groups. The levels malondialdehyde (MDA) and superoxide dismutase (SOD) increased significantly in the treatment group compared to the control group (P E‚ 0.05; P E‚ 0.01, respectively). While, the levels of glutathione peroxidase (GSH-Px) decreased in the treatment group compared to the control group (P E‚ 0.01). These results indicate that exposure of graded doses of BPA may elicit depletion of antioxidant system and induce oxidative stress in epididymal sperm of rat thereby decreasing sperm count and quality. These findings provide a possible toxicological evidence of an adverse effect of BPA on semen quality. Key words: Bisphenol A (BPA, 2, 2-bis (4-hidroxyphenyl) propane), semen quality, oxidative stress, sperm count, rat, reactive oxygen species (ROS).

Antioxidative effect of epichlorohydrin on rat cauda epididymal spermatozoa

The aim of the study was to evaluate the effect of epichlorohydrin (ECH) on the antioxidant system of rat cauda epididymal sperm. Fresh epididymides of adult male rats were obtained from JIPMER, (Pondicherry) were collected by chopping the epididymis in modified Ringer's phosphate solution (RPS medium). After several washings the sperm samples were equally dispersed in RPS medium and incubated with epichlorohydrin (25, 50 and 100 μmol) and ECH /ascorbate (50/100 μmol) with or without ECH (25, 50 and 100 μmol) for 3 h at 32oC. After incubation, the sperm motility and viability were assessed. An aliquot of sperm samples were homogenized and centrifuged and the supernatant used for biochemical studies. In ECH-incubated sperm and in sperm co-incubated with ECH and vitamin C, the sperm motility and viability showed no significant changes as compared to the corresponding controls. In ECH-incubated sperm the activity of superoxide dismutase, catalase, glutathione reductase, glutathione-Stransferase and glutathione peroxidase were significantly decreased while lipid peroxidation was significantly increased in a dose-dependent manner. Co-incubation of sperm with ECH and vitamin C showed no significant changes in the activity of superoxide dismutase, catalase, glutathione reductase and glutathione-S-transferase and glutathione peroxidase and in the level of lipid peroxidation. Epichlorohydrin induced oxidative stress in epididymal sperm of rat by decreasing the level of antioxidant enzymes. Co-incubation of sperm with ECH and vitamin C, a natural antioxidant, reversed the effect of ECH.

2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) induces oxidative stress in the epididymis and epididymal sperm of adult rats.

2,3,7,8-Tetrachlorodibenzo- p-dioxin (TCDD) is one of the most potent environmental contaminants, which has been shown to induce oxidative stress in testis and epididymal sperm of rats. However, the nature and mechanism of action of TCDD on the epididymis is not clear. The aim of the present study was to investigate whether induction of oxidative stress in epididymal sperm was direct effect of TCDD on epididymis. In the present studies, TCDD (0.1, 1.0 and 10 micro g/kg body weight per day) was administered orally to rats for 4 days. Twenty-four hours after the last treatment the animals were killed using anesthetic ether. Both epididymides were dissected out and epididymal sperm were collected by cutting the epididymides into small pieces in Ham's F-12 medium at 35 degrees C. The epididymal sperm and caput, corpus and cauda epididymides were homogenized and used for biochemical studies. Epididymal sperm counts did not decrease in the rats treated with TCDD. Administration of TCDD increased the production of reactive oxygen species such as hydrogen peroxide while the activities of antioxidant enzymes superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase were found to be decreased in the epididymal sperm as well as in cauda epididymides. Lipid peroxidation also increased in the epididymal sperm and in the various regions of the epididymides after exposure to TCDD. The results indicated that TCDD induces oxidative stress in the epididymis and epididymal sperm by decreasing the antioxidant enzymes through induction of reactive oxygen species. Thus, the adverse effects of TCDD on the epididymal sperm were due to direct effect of TCDD on epididymis.

Induction of oxidative stress by bisphenol A in the epididymal sperm of rats

Bisphenol A has been shown to affect the reproduction of male rats and mice. However, the mechanism of action of bisphenol A on the epididymal sperm is not elucidated. The present study was undertaken to evaluate the effect of bisphenol A on the antioxidant system of rat epididymal sperm. Bisphenol A was administered orally to male rats at the dose levels of 0.2, 2 and 20 μg/Kg body weight per day for 45 days. After 24 h of the last treatment, rats were weighed and killed using anesthetic ether. The body weight of treated rats did not show significant change as compared with the corresponding control groups. In bisphenol A-treated rats there was a significant decrease in the weight of the testis and epididymis; the weight of ventral prostate increased significantly whereas there was no significant change in the weight of seminal vesicles as compared with the corresponding group of control animals. Sperm collected from the epididymis were used for sperm count and biochemical estimations. Administration of bisphenol A caused a reduction in the epididymal sperm motility and sperm count in a dose-dependent manner. The activities of superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase were decreased while the levels of H 2O 2 and lipid peroxidation increased significantly in the treated rats as compared with the corresponding group of control animals. The results suggested that graded doses of bisphenol A elicit depletion of antioxidant defence system and induce oxidative stress in epididymal sperm of rats. In conclusion, the adverse effect of bisphenol A on male reproduction may be due to induction of oxidative stress in sperm.

Effect of nonylphenol on the antioxidant system in epididymal sperm of rats

Nonylphenol, an environmental contaminant, has been shown to induce reproductive abnormalities in male rats. The nature and mechanism of action of nonylphenol on the epididymal sperm has not been elucidated. In the present study we have sought to investigate whether administration of nonylphenol induces oxidative stress in rat epididymal sperm. Nonylphenol was administered orally to male rats at 1, 10 and 100 microg/kg body weight per day for 45 days. Twenty-four hours after the last treatment, rats were weighed and killed using anaesthetic ether. The body weight of the animals treated with nonylphenol did not show any significant change. The weights of the testes and epididymides decreased significantly whereas the weights of seminal vesicles and ventral prostate remained unchanged at all doses of nonylphenol in treated rats. Epididymal sperm were collected by cutting the epididymides into small pieces in Ham's F-12 medium at 32 degrees C. Administration of nonylphenol decreased the epididymal sperm counts in a dose-dependent manner. The activities of antioxidant enzymes superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase decreased significantly while the levels of H(2)O(2) generation and lipid peroxidation increased significantly in the animals treated with nonylphenol when expressed in terms of milligram protein and milligram DNA. The activity of alpha-glucosidase, a negative control against antioxidant enzymes, in the sperm of nonylphenol-treated rats did not show any significant change at any of the doses. The results suggest that graded doses of nonylphenol elicit depletion of antioxidant defence system in sperm, indicating nonylphenol-induced oxidative stress in the epididymal sperm of rats.

Induction of oxidative stress in rat epididymal sperm after exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

The ability of 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) to induce oxidative stress in various tissues of animals has been reported. The nature and mechanism of action of TCDD on the antioxidant system of sperm has not been studied. In the present study we have sought to investigate whether TCDD induces oxidative stress in the epididymal sperm of rats. Subchronic doses of TCDD (1, 10, and 100 ng/kg body weight per day) were administered orally to male Wistar strain rats for 45 days. After 24 h of the last treatment the rats were killed using diethyl ether. The epididymides were removed and cleared from the adhering tissues. Epididymal sperm were collected by cutting the epididymides into small pieces in Ham's F12 medium, and counted using a hemocytometer. The epididymal sperm counts in the TCDD-treated groups decreased in a dose-dependent manner from the control value of 8.2+/-0.14 x 10(8) to 5.31+/-0.15 x 10(8). Since a positive correlation (r=0.95; n=24) was observed between sperm count and DNA content of the epididymal sperm, DNA content was routinely used as an indicator of sperm count, and the results were expressed in terms of both protein and DNA. There was a significant decline in the activities of superoxide dismutase (40+/-2.17 to 27.1+/-0.76/mg protein and 32.41 to 18.07+/-0.76/mg DNA), catalase (2.49+/-0.13 to 2.03+/-0.05/mg protein and 2.01+/-0.05 to 1.35+/-0.05/mg DNA), glutathione reductase (71.2+/-3.87 to 48+/-1.79/mg protein and 57.58+/-1.52 to 31.94/mg DNA) and glutathione peroxidase (22.4+/-1.43 to 16.9+/-1.57/mg protein and 18.08+/-0.61 to 11.38+/-1.22/mg DNA) while there were increases in the levels of hydrogen peroxide (20.8+/-1.96 to 55.3+/-0.88/ mg protein and 16.18+/-1.88 to 36.87+/-0.88/ mg DNA) and lipid peroxidation (2.17+/-0.2 to 6.08/mg protein and 1.75+/-0.12 to 4.05+/-0.12/mg DNA) in the epididymal sperm. The results suggest that graded doses of TCDD elicit depletion of antioxidant defense system in sperm, indicating TCDD-induced oxidative stress in the epididymal sperm. In conclusion, the adverse effect on male reproduction in TCDD-treated rats may be due to the induction of oxidative stress in sperm.