Protective Effects of Lactobacillus rhamnosus GG on Aflatoxins-Induced Toxicities in Male Albino Mice

The effects of sub-acute exposure (7 days) to aflatoxins and the potential protective effects of Lactobacillus rhamnosus GG ATCC53013 (LGG) were studied in male Albino mice. Four experimental groups were used, each comprising 30 mice; control group, LGG-treated group (1 × 1010 CFU), AFs-treated group (0.7 mg/kg b.w.), and a group given LGG two hours before AFs intoxication. The malondialdehyde (MDA), glutathione (GSH) levels and superoxide dismutase (SOD) activity were measured in liver and kidney tissues. Chromosomal aberrations in bone marrow and in spermatocytes, as well as mitotic and meiotic activities were performed to assess the genotoxicity; besides sperm parameters were evaluated. Results showed that AFs significantly elevated the tissue levels of MDA, whereas the levels of GSH as well as SOD activity were significantly decreased in liver and kidney. AFs increased significantly the frequencies of structural and numerical chromosome aberrations in bone marrow and spermatocytes. In addition, mitotic and meiotic activities of somatic and germ cells were declined significantly. Also, AFs caused a high significant reduction in cauda epididymal sperm count, sperm motility and significant increase sperm abnormalities, as compared to control. Mice received LGG before AFs gavage, showed a significant amelioration in oxidative status in both liver and kidney, by increasing the contents of GSH and SOD activity. Cytogenetic analyses revealed that LGG administration before AFs gavage significantly reduced frequencies chromosomal aberrations in bone marrow and spermatocytes, and recovered mitotic and meiotic activities as well. Moreover, gavage LGG before AFs intoxication caused significant recovery in all sperm parameters studied. In conclusion, LGG was found to be safe and successful agent counteracting the oxidative stress and protected against the genotoxicity induced by AFs, in addition to reduction in spermatotoxic alterations.