T2-Toxin Hepatotoxicity in the in situ Rat Liver Model

T-2 toxin, a trichothecene mycotoxin, is considered to be one of the most toxic compounds that are produced by molds, particularly the Fusarium species. Fusarium species have been recognized as a great agricultural problem. They occur worldwide on a variety of plant hosts and cereal grains. The aim of this study was to investigate T-2 toxin-induced liver injury using in situ perfused rat liver. The in situ perfused rat liver (IPRL) was chosen because it permits studies of liver function in a system that resembles normal physiology. Elevation of aminotransferase activities have shown to be a good indicator of hepatocellular damage. In addition, glutathione levels have also shown to be an indicator of liver damage through lipid peroxidation. Male Sprague-Dawley rats (6-8 weeks) weighing 250-300 g were used in this study. They were randomly divided into 5 groups of 3-4 rats per cage. In group 1, liver was perfused by Krebs-Henseleit buffer alone (Control).  Groups 2-5 received different concentration of T-2 toxin (4, 9, 21, 43 ρmol/L) in Krebs-Henseleit buffer and biochemical changes in the liver were examined within 2 h. There was a significant increase in both ALT and AST activity in all dose levels compared with the control group (p<0.01 and p<0.05). T-2 toxin treatment enhanced lipid peroxidation in the liver, as indicated by the increased MDA content in liver homogenates. The MDA level was maximal 2 h after the T-2 toxin challenge (p<0.01 and p<0.05). The results also show that T-2 toxin causes an increase in lipid peroxidation while causing a decrease in glutathione (GSH) content in bile secretion (p<0.01). This result suggests that both lipid peroxidation and glutathione (GSH) depletion play a role in T-2 toxin liver induced damages.