Abstract
T-2 toxin is a member of a class of mycotoxins produced by a variety of Fusarium species under appropriate temperature and humidity conditions and is a common contaminant in food and feedstuffs of cereal origin. Selenium is an indispensable element in animals, regulates a variety of biological functions of the body, and can antagonize metal and mycotoxin poisoning to a certain extent. However, the effect of selenium on kidney injury induced by T-2 toxin has not been reported. In this study, 50 New Zealand rabbits were divided into 5 groups (the control group, T-2 toxin group, low-dose Se + T-2 toxin group, medium-dose Se + T-2 toxin group, and high-dose Se + T-2 toxin group). Rabbits were examined after oral administration of different doses of selenomethionine (SeMet) for 21days and after perfusion with 0.4mg/kg T-2 toxin (or the same dose of olive oil in the control group) for 5days. We found that T-2 toxin induced kidney function damage and increased the levels of ROS and the contents of inflammatory factors. Renal structure was pathologically damaged. However, we found that after pretreatment with 0.2mg/kg SeMet, oxidative stress, the inflammatory response, and pathological damage induced by T-2 toxin were attenuated. The results indicate that a low dose (0.2mg/kg) of SeMet effectively reversed T-2 toxin-induced kidney injury in rabbits.
Published Version
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