Review of the Protective Effects of Selenium against T-2 Toxin-Induced Toxicity.

The objective of the present study was to review the potential protective effects of Se against T-2 toxin-induced adverse effects in cartilage and other tissues as well as to discuss the potential molecular mechanisms by which Se counteracts T-2 toxicity. Laboratory studies demonstrate that Se attenuates T-2 toxin-induced chondrocyte death by inhibition of the mitochondrial pathway of apoptosis. Protective effects of Se against T-2 toxin-induced oxidative stress in chondrocytes are mediated by improvement of antioxidant selenoprotein expression, which is altered upon mycotoxin exposure. In addition to T-2 toxin-induced oxidative stress, Se treatment is associated with the inhibition of mycotoxin-induced chondrocyte ferroptosis. Along with prevention of chondrocyte damage, Se improves extracellular matrix (ECM) metabolism by the up-regulation of type II collagen and proteoglycans expression and inhibition of T-2 toxin-induced ECM degradation by matrix metalloproteinases. It is also noteworthy that part of the interactive effects between Se treatment and T-2 toxin exposure is mediated by epigenetic mechanisms, especially modulation of noncoding RNA expression. Recent evidence also shows that Se mitigates the toxic effects of the T-2 toxin in the liver, kidney, immune system, and other organs. Notably, a number of studies demonstrated that a Se deficiency aggravates the adverse effects of T-2 toxin exposure, supporting the notion of the protective effects of Se. However, the existing data were obtained in laboratory in vivo and in vitro models, and the potential therapeutic effects of Se supplementation in T-2 toxin-exposed human subjects have yet to be fully characterized.