Co-administration of glutathione alleviates the toxic effects of 2,3,7,8 TCDF on the DNA integrity of sperm and in the testes of mice

This study aimed to investigate the toxic impact prompted in the testes of adult mice exposed to 2,3,7,8-tetrachlorodibenzofuran (TCDF). Four groups of 12 mice each were used in the present study. Group 1 mice were kept as control and administered corn oil only. Group 2 animals were given glutathione (GSH) in a dose of 100 mg/kg body weight by oral gavage twice a week. Group 3 was given TCDF orally twice per week, in a dose of 0.5 μg/kg body weight for 8 weeks. Group 4 was administered GSH orally in a dosage of 100 mg/kg body weight plus TCDF twice a week for 8 weeks. Animals were sacrificed after 2, 4, and 8 weeks of exposure, serum samples were collected for estimation of testosterone hormone, the testes were dissected and one part was used for estimation of superoxide dismutase (SOD), malondialdehyde (MDA), lactate dehydrogenase (LDH), and 3β–hydroxysteroid dehydrogenase. Another portion of the testis was kept in formalin for histopathological examination. The results showed that the activities of SOD were decreased while the levels of lipid peroxidation MDA were increased in the testicular tissues of the exposed mice. The serum testosterone level and the steroidogenic enzyme 3β–hydroxysteroid dehydrogenase activity of testicular homogenate were essentially decreased in TCDF-treated mice. A significant increment in the testicular LDH activity in testicular tissues was recorded in mice exposed to TCDF. The percentage of DNA chromatin disintegration was significantly increased in TCDF-treated mice. Histopathological changes were recorded in TCDF-exposed group as degenerative changes of the seminiferous tubules with formation of spermatid giant cells at 2 weeks in addition to exhaustion of germinal epithelium and detachment of the germ cells from the basal lamina at 4 and 8 weeks. Co-administration of GSH could reestablish MDA and LDH levels besides reduction in percentage of sperm DNA damage and improvement of the testicular tissue architecture.