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 rmol/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.