T2-TOXIN HEPATOTOXICITY IN THE IN SITU RAT LIVER MODEL

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DARAEI B.; GHAZI KHANSARI M.; RASEKH H.R.

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Journal: Iranian Journal of Pharmaceutical Research Year:2004 | Volume:3 | Issue:4 Page(s): 225-230

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Title

T2-TOXIN HEPATOTOXICITY IN THE IN SITU RAT LIVER MODEL

Author(s)

DARAEI B. | GHAZI KHANSARI M. | RASEKH H.R. | Issue Writer Certificate

Keywords

T-2 TOXIN

GLUTATHIONE

LIPID PEROXIDATION

MDA

AMINOTRANSFERASE ACTIVITY

IPRL

Abstract

T-2 TOXIN, a trichothecene mycotoxin, is considered to be one of the most toxic compounds that are produced byrilolds, 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.

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APA: Copy

GHAZI KHANSARI, M., DARAEI, B., & RASEKH, H.R.. (2004). T2-TOXIN HEPATOTOXICITY IN THE IN SITU RAT LIVER MODEL. IRANIAN JOURNAL OF PHARMACEUTICAL RESEARCH (IJPR), 3(4), 225-230. SID. https://sid.ir/paper/287513/en

Vancouver: Copy

GHAZI KHANSARI M., DARAEI B., RASEKH H.R.. T2-TOXIN HEPATOTOXICITY IN THE IN SITU RAT LIVER MODEL. IRANIAN JOURNAL OF PHARMACEUTICAL RESEARCH (IJPR)[Internet]. 2004;3(4):225-230. Available from: https://sid.ir/paper/287513/en

IEEE: Copy

M. GHAZI KHANSARI, B. DARAEI, and H.R. RASEKH, “T2-TOXIN HEPATOTOXICITY IN THE IN SITU RAT LIVER MODEL,” IRANIAN JOURNAL OF PHARMACEUTICAL RESEARCH (IJPR), vol. 3, no. 4, pp. 225–230, 2004, [Online]. Available: https://sid.ir/paper/287513/en

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