Induction of immunological, hormonal and histological alterations after sublethal exposure of chlorpyrifos in the freshwater fish, Pseudetroplus maculatus (Bloch, 1795).

The present study investigated the induction of immunological, hormonal and histological changes in the freshwater fish, Pseudetroplus maculatus after sublethal exposure of chlorpyrifos. Fish were exposed to chlorpyrifos at one-tenth (0.661µg/L) and one-fifth (1.32 µg/L) of LC50 value, for 15 and 30 d, along with the respective control group. Innate and adaptive immune responses of the fish against the toxicant exposure were measured using lysozyme, complement (ACH50) levels, phagocytic, nitroblue tetrazolium (NBT), myeloperoxidase (MPO), anti-protease and hemagglutination activities, and IgM concentration. The results revealed that sublethal exposure of chlorpyrifos caused significant (p < 0.05) reduction in lysozyme, ACH50, phagocytic, and anti-protease activities whereas there was significant (p < 0.05) increase in NBT, MPO and hemagglutination levels along with serum IgM concentration. Chlorpyrifos treatment showed significant (p < 0.05) decline in the serum levels of cortisol, thyroid, testosterone and estradiol hormones in duration- and concentration-dependent manner. The major histological lesions noted in liver includes necrosis, vacuolization, hepatocytic and cytoplasmic degeneration, while kidneys showed vacoules, necrosis and rupture in renal tubules and glomerulus, whereas spleen were found with melanomacrophage aggregation and necrosis. Similarly, testis showed remarkable changes like reduction in the number of spermatozoa and disintegrated seminiferous tubules while ovarian lesions include degenerated and empty follicles, few atretic oocytes, reduced size of follicles, and broken theca granulosa. The current findings revealed that the use of chlorpyrifos in domestic and agricultural purposes even at sublethal concentration could affect the non-target organisms including fish, and thereby alter the health status of aquatic ecosystems.

Fullerene C60 nanomaterial induced oxidative imbalance in gonads of the freshwater fish, Anabas testudineus (Bloch, 1792).

The engineered carbon nanomaterial, fullerene C60, with unique physicochemical properties, released into the aquatic environment is known to formulate high risk factor for the aquatic life. The present study was aimed to investigate fullerene C60 induced oxidative imbalance in ovary and testis of the freshwater fish, Anabas testudineus. The median lethal concentration (96 h-LC50) of fullerene C60 in Anabas testudineus was 50 mg/ L, and fish exposed to two sublethal concentrations i.e., 5 mg/ L and 10 mg/ L (one-tenth and one-fifth of LC50) for short-term (24, 48, 72 and 96 h) and long-term (7, 15, 30 and 60 d) durations. The antioxidant parameters such as the activities of superoxide dismutase (SOD), catalase, glutathione reductase, glutathione peroxidase, the levels of hydrogen peroxide generation and lipid peroxidation were analyzed along with histopathological alterations in gonadal tissues. Both sublethal concentrations of fullerene C60 caused significant (P < 0.05) decrease in the activities of antioxidant enzymes, whereas the levels of hydrogen peroxide generation and lipid peroxidation increased significantly (P < 0.05) in gonads. Fullerene exposure significantly (P < 0.05) increased the mucous deposition with significant (P < 0.05) reduction in the weights of gonads and gonado-somatic index. The histopathological analysis showed prominent alterations in testis and ovary of treated fishes when compared to the control groups. After 60 d of sublethal exposure of fullerene C60, fish were left in the toxicant-free water for another 60 d, in which the changes in the activities of the gonadal antioxidant enzymes and histological alterations were not completely recovered. Hence, from the present study, it was illustrated that fullerene C60 caused oxidative imbalance in the gonads, which may possibly affect the reproductive potential of the fish, Anabas testudineus.

Vitamin E prevents nonylphenol-induced oxidative stress in testis of rats.

In the present study we have investigated if administration of nonylphenol-induced oxidative stress in various subcellular fractions of adult rat testis and the effect of vitamin E on reactive oxygen species mediated nonylphenol toxicity. Male rats were administered orally with nonylphenol at 1, 10 and 100 microg/kg body weight per day for 45 days with and without supplementation of vitamin E (20 mg/kg body weight). In nonylphenol-treated rats the activities of antioxidant enzymes superoxide dismutase and glutathione reductase decreased significantly while the levels of lipid peroxidation increased significantly in the crude homogenate and in the mitochondrial and microsome-rich fractions of testis. Co-administration of nonylphenol and vitamin E did not cause changes in the activities of antioxidant enzymes in various subcellular fractions of rat testis. The results suggest that graded doses of nonylphenol elicit depletion of antioxidant defence system in rat testis, indicating nonylphenol induced oxidative stress in the testis of rats which could be reversed by the administration of vitamin E.

Effect of bisphenol A and co-administration of bisphenol A and vitamin C on epididymis of adult rats: a histological and biochemical study.

AIM: To study the effect of bisphenol A on the epididymis and epididymal sperm of rats and the possible amelioration action of co-administration with vitamin C. METHODS: Male Wistar rats were orally administered bisphenol A (0.2 microg x kg (-1) x day(-1), 2 microg x kg(-1) x day(-1) and 20 microg x kg(-1) x day(-1)) and 0.2 microg, 2 microg and 20 microg bisphenol A + 40 mg vitamin C x kg(-1) x day(-1) for 60 days. On day 61, rats were killed with anesthetic ether and sperm collected from epididymis were used or assessment of sperm count, motility and viability and biochemical studies. A 1 % homogenate of epididymis was prepared and used for biochemical estimations. Caput, corpus and cauda epididymis were fixed in Bouin's fixative for histological studies. RESULTS: Administration of bisphenol A caused a reduction in the epididymal sperm motility and count and the sperm viability remained unchanged. The activities of superoxide dismutase and glutathione peroxidase decreased, while the levels of lipid peroxidation increased in epididymal sperm and epididymis at all doses. Co-administration with vitamin C reversed the effect of bisphenol A-induced oxidative stress in epididymal sperm and epididymis. A complete degeneration of epididymal epithelium in caput, corpus and cauda regions with reduction in the number of sperms were observed at all doses of bisphenol A-treated rats. CONCLUSION: Bisphenol A induced oxidative stress in epididymis and caused degeneration of the epididymal epithelium of rats. Co-administration with vitamin C had a protective effect against the bisphenol A-induced toxicity in epididymal sperm and epididymis.

Bisphenol A induces reactive oxygen species generation in the liver of male rats.

Bisphenol A, an environmental contaminant, widely used as a monomer in polycarbonate plastics, has been shown to cause abnormalities in liver of rats and mice. The nature and mechanism of action of bisphenol A on liver is not clear. The aim of the present study was to investigate if bisphenol A induces oxidative stress in the liver of rats and if co-administration of vitamin C, an antioxidant, can prevent oxidative stress. Bisphenol A (0.2, 2.0 and 20 micro g/kg body weight per day) and bisphenol A+vitamin C (0.2, 2.0, 20 micro g+40 mg/kg body weight per day) was orally administered to rats for 30 days. After 24 h of the last treatment, rats were killed using overdose of anesthetic ether. Body weights of the animals and the weights of liver showed no significant changes. The activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase were decreased in mitochondrial and microsome-rich fractions of liver. The levels of hydrogen peroxide and lipid peroxidation increased in the treated rats when compared with the corresponding group of control animals. Activity of alanine transaminase, a marker enzyme of hepatic injury remained unchanged in the treated rats as compared with the corresponding control rats. Co-administration of bisphenol A and vitamin C showed no changes in the activities of superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase and in the levels of hydrogen peroxide and lipid peroxidation as compared with the corresponding control groups. The results indicated that bisphenol A induces oxidative stress in the liver of rats by decreasing the antioxidant enzymes. Co-administration of vitamin C reversed the effects of bisphenol A-induced oxidative stress in the liver of rats.

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 microg/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(2)O(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.

The effect of methoxychlor on the epididymal antioxidant system of adult rats.

Methoxychlor is widely used as a pesticide in many countries and has been shown to induce reproductive abnormalities in male rats, causing reduced fertility. The mechanism of action of methoxychlor on the male reproductive system is not clear. In the present study we investigated whether administration of methoxychlor induces oxidative stress in the epididymis and epididymal sperm of adult rats. Methoxychlor (50, 100, or 200 mg/kg body weight/day) was administered orally for 1, 4, or 7 days. The animals were killed using anesthetic ether 24 h after of the last treatment. Epididymal sperm were collected by cutting the epididymis into small pieces in Ham's F-12 medium at 35 degrees C. The body weight and weights of the testis, liver, and kidney did not show any significant changes in the methoxychlor-treated rats. The weight of the epididymis, seminal vesicles, and ventral prostate as well as epididymal sperm counts decreased after 50, 100, or 200 mg/kg/day for 7 days but remained unchanged after shorter courses of treatment. Epididymal sperm motility was decreased in a dose-dependent manner in the animals treated with methoxychlor for 4 or 7 days. The activities of the antioxidant enzymes superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase were decreased while the levels of hydrogen peroxide and lipid peroxidation were increased in the epididymal sperm as well as in the caput, corpus, and cauda epididymis after 4 or 7 days of treatment. The activities of superoxide dismutase decreased while the levels of lipid peroxidation increased in the liver but not in the kidney in all groups. Co-administration of the antioxidant vitamin E (20 mg/kg body weight/ day) to the 200 mg/kg/d methoxychlor-treated rats for 7 days prevented significant changes in the antioxidant systems in the epididymis and epididymal sperm and prevented alterations in sperm counts and motility. The results indicated that methoxychlor induces oxidative stress in the epididymis and epididymal sperm by decreasing antioxidant enzymes, possibly by inducing reactive oxygen species. In conclusion the adverse effect of methoxychlor on the male reproduction could be due to induction of oxidative stress.

The effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the antioxidant system in mitochondrial and microsomal fractions of rat testis.

The ability of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to induce oxidative stress in hepatic and some extrahepatic tissues of animals has been reported. The precise nature and mechanism of action of TCDD on the male reproductive system is not clear. In the present study, we have investigated the induction of oxidative stress in the testis of rat after exposure to low doses of TCDD. TCDD (1, 10, and 100 ng/kg body weight per day) was administered orally to the rat for 45 days. After 24 h of the last treatment the rats were killed using anesthetic ether. The weights of the testis, epididymis, seminal vesicles and ventral prostate decreased while the body weight remained unchanged in the rats administered with TCDD. Mitochondrial and microsomal fractions of the testis were obtained by the method of differential centrifugation. The activity of antioxidant enzymes such as superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase decreased significantly in the animals treated with TCDD in a dose-dependent manner in the mitochondrial and microsomal fractions of rat testis. The levels of hydrogen peroxide generation (H(2)O(2)) and lipid peroxidation increased in mitochondrial, and microsomal fractions of the testis. The results suggested that the low doses of TCDD elicit depletion of antioxidant enzymes and concomitant increase in the levels of H(2)O(2) and lipid peroxidation differentially in mitochondrial and microsomal fractions of rat testis. In conclusion the adverse effect of TCDD on male reproduction could be due to induction of oxidative stress.

Effect of lindane on antioxidant enzymes in epididymis and epididymal sperm of adult rats.

AIM: To find out the changes induced by lindane on the antioxidant enzymes in epididymis and epididymal sperm of adult rats. METHODS: Adult male rats were orally administered lindane at a dose of 5.0 mg/kg body weight per day for 30 days. At the end of the treatment, the rats were sacrificed. The epididymis was removed and weighed and sperm were collected for sperm count, motility and biochemical studies. A 1% homogenate of epididymis was prepared and used for biochemical estimations. RESULTS: In lindane-treated rats, there were significant reductions in the epididymal weight, epididymal sperm count and motility compared with the controls. Significant decreases in the superoxide dismutase (SOD), catalase, glutathione reductase and glutathione peroxidase activities and significant increases in the H2O2 generation and lipid peroxidation were also observed in the epididymis and epididymal sperm of lindane-treated rats. CONCLUSION: Lindane decreases the levels of antioxidant enzymes in the epididymis and epididymal sperm of adult rats thereby inducing oxidative stress.

Effect of lindane on testicular antioxidant system and steroidogenic enzymes in adult rats.

AIM: To find out the effect of lindane on testicular antioxidant system and testicular steroidogenesis in adult male rats. METHODS: Adult male rats were orally administered with lindane at a dose of 5.0 mg/kg body weight per day for 30 days. Twenty-four hours after the last treatment the rats were killed using anesthetic ether. Testes, epididymis, seminal vesicles and ventral prostate were removed and weighed. A 10% testicular homogenate was prepared and centrifuged at 4 degrees C. The supernatant was used for various biochemical estimations. RESULTS: The body weight and the weights of testes, epididymis, seminal vesicles and ventral prostate were reduced in lindane-treated rats. There was a significant decline in the activities of antioxidant enzymes superoxide dismutase (SOD), catalase and glutathione reductase while an increase in hydrogen peroxide (H2O2) generation was observed. The specific activities of testicular steroidogenic enzymes 3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase were decreased. The levels of DNA, RNA and protein were also decreased in lindane-treated rats. CONCLUSION: Lindane induces oxidative stress and decreases antioxidant enzymes in adult male rats.

Chronic effect of endosulfan on the testicular functions of rat.

AIM: To find out the toxic effect of endosulfan on the testicular function of pubertal rats. METHODS: Male rats of pubertal age were orally administered endosulfan at a dose of 1.0 mg/kg body weight for 30 days. Twenty-four hours after the last treatment, the rats were sacrificed and the testis, epididymis, seminal vesicles and ventral prostate were removed and weighed. A 10% testicular homogenate was prepared for biochemical estimations. RESULTS: In endosulfan-treated rats, there were a reduction in the body weight and the weights of testis and accessory sex organs, a decrease in the testicular lactate and pyruvate activities, and in the testicular DNA and RNA concentrations, whereas the testicular protein concentration was slightly increased; the specific activity of testicular steroidogenic enzyme, 3beta-OH-steroid dehydrogenase and the ascorbic acid level were decreased, which were correlated with a decrease in steroidogenesis. The lysosomal enzyme acid phosphatase and brush-border enzyme alkaline phosphatase activities were also decreased in the testis of treated rats. CONCLUSION: In pubertal rats, endosulfan treatment inhibits the testicular functions.