Protective effect of vitamin E against carbendazim-induced testicular toxicity-histopathological evidences and reduced residue levels in testis and serum.

The fungicide Carbendazim Methyl-2-benzimidazole carbamate (MBC) is known to produce male reproductive toxicity. The present study has been undertaken to investigate the impact of vitamin E, an antioxidant against the testicular toxicity induced by MBC. HPLC analysis showed that the amount of MBC in testis and serum was 57.40 +/- 3.38 nmol/g and 14.10 +/- 0.84 nmol/ml, respectively, in rats treated with carbendazim + vitamin-E, which were significantly lower than that of rats treated with carbendazim alone (240 +/- 15.60 nmol/g and 318.70 +/- 22.52 nmol/ml, respectively). MBC treatment significantly decreased the testicular weight while co-administration of vitamin-E registered normal testicular weight. Histomorphometric analysis revealed a significant decrease (P < 0.05) in the diameter of the seminiferous tubules and lumen in MBC-treated rats compared to control whereas they remained normal in vitamin E + MBC-treated rats. Leydig cells appeared dispersed and hypertrophic after MBC treatment. Various histopathological changes were observed in testis of rats treated with MBC whereas these changes were absent in vitamin-E + MBC-treated rat testis. In conclusion protection against MBC-induced toxicity was observed with co-administration of vitamin E with MBC.

Modulation of antioxidant defense system by the environmental fungicide carbendazim in Leydig cells of rats.

Carbendazim (methyl-2-benzimidazole carbamate, MBC) a metabolite of benomyl is one of the most widespread environmental contaminant of major concern to human and animal reproductive health. The present investigation was undertaken to study the impact of carbendazim exposure on Leydig cell functions. Adult albino male rats of the Wistar strain were administered with carbendazim (25 mg/(kg (body weight)/day)) orally for 48 days. The control animals received vehicle (corn oil) alone. Another group of rats were treated with carbendazim and the same was withdrawn for a further period of 48 days. After the treatment period, rats were euthanized and blood was collected for the assay of serum hormones such as luteinizing hormone (LH), prolactin (PRL), testosterone and estradiol. Testes were immediately removed and Leydig cells were isolated in aseptic condition. Purified Leydig cells were used for quantification of steroidogenic enzymes such as 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-hydroxysteroid dehydrogenase (17beta-HSD). Leydig cellular enzymatic antioxidants superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), gamma-glutamyl transpeptidase (gamma-GT), glucose-6-phosphate dehydrogenase (G6PDH) and non-enzymatic antioxidants such as reduced glutathione (GSH), alpha-tocopherol (vitamin E), ascorbic acid (vitamin C) and beta-carotene (vitamin A) were assayed. Lipid peroxidation (LPO) and reactive oxygen species (ROS) were also quantified. Carbendazim exposure had no effect on body weight, serum LH and prolactin. However, testis weight, serum testosterone and estradiol were significantly decreased. In addition to this, Leydig cellular activities of steroidogenic enzymes such as 3beta-HSD, 17beta-HSD, antioxidant enzymes SOD, CAT, GPx, GR, GST, gamma-GT, G-6-PDH and non-enzymatic antioxidants such as GSH, vitamins E, C and A were significantly diminished, whereas LPO and ROS were markedly elevated. All these above-mentioned parameters from the animals after withdrawal of MBC treatment were similar to those of the control group. Thus, the present study suggests that chronic low dose treatment of MBC is capable of inducing reproductive toxicity through increased oxidative stress, but is transient and reversible upon withdrawal of treatment.