KARAMI M, GHAZI-KHANSARI M, REZAYAT M, MINAEI B, ABDOLLAHI M, SABZEVARI O. *Correspondence: M. Ghazi-Khansari. Ph.D., Department ofPharmacology,. Med J Islam Repub Iran 2001; 15 (1) :55-60
URL:
http://mjiri.iums.ac.ir/article-1-826-en.html
the Departments of Pharmacology School of Medicine, Tehran University of Medical Sciences, Tehran, I.R. Iran , ircongpp@nrcgeb.ac.ir
Abstract: (5329 Views)
2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a by-product o f t he
trichlorophenol (herbicide) production and is also produced through a variety of
combustion processes. It appears that TCDD is a ubiquitous chemical, particularly
in industrialised countries, and the liver is the target organ of its toxicity. The
prominent hepatotoxic effect of TCDD is progressive centrilobular necrosis. The
isolated rat liver perfusion system approaches the normal physiology of the liver
and is ideal for studying biochemical alterations of the liver since hepatocytes are
easily exposed to various concentrations of chemicals with minimum neural-hormonal
effects. In this study, the liver was perfused with Krebs-Henseleit butfer
containing different concentrations of TCDD (0.3, 3, 20 and 30).lg/L). During the
perfusion many factors including gross liver appearance, bile formation, and aminotransferase
activities were assessed as indicators of liver viability. Consequently,
sections of liver tissue were examined for any histopathological changes. The
results showed that histopathological changes in liver tissues were related in a
dose-dependent manner to TCDD concentrations. In this instance doses of 20 and
30 ).lglL caused a significant (p<0.05) histopathological change in liver sections.
Liver necrosis and hemorrhage were also increased significantly in a dose-dependent
manner.