Protective Effect of Organic Selenium on Oxidative Damage and Inflammatory Reaction of Rabbit Kidney Induced by T-2 Toxin

T-2 toxin is a member of a class of mycotoxins produced by a variety ofFusariumspecies 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 21 days and after perfusion with 0.4 mg/kg T-2 toxin (or the same dose of olive oil in the control group) for 5 days. 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 0.2 mg/kg SeMet, oxidative stress, the inflammatory response, and pathological damage induced by T-2 toxin were attenuated. The results indicate that a low dose (0.2 mg/kg) of SeMet effectively reversed T-2 toxin-induced kidney injury in rabbits.

Automated summary

T-2 toxin, a common contaminant in food, induced kidney injury in rabbits, characterized by increased oxidative stress and inflammation. However, pretreatment with a low dose of SeMet effectively reversed these effects, suggesting a potential protective role of selenium against T-2 toxin-induced kidney damage.