Özet:

Ethanol and benzo(a)pyrene cause an increase in lipid peroxidation either by producing the reactive oxygen species or decreasing the level of endogenous antioxidant enzymes that leads to cellular damage and cellular dysfunction. The aim of this study was to investigate both physiological and histological changes in liver tissue after administration of benzo(a)pyrene and ethanol Male Sprague Dawley rats were divided into four groups. Group I was control group. Group II treated with benzo(a)pyrene, group III treated with benzo(a)pyrene plus ethanol and group IV was given ethanol. Superoxide dismutase (SOD), alanin aminotransferase (ALT), aspartat aminotransferase (AST) , gamma-glutamyl transferase (GGT), glutathione (GSH), malondialdehyde (MDA) levels as well as histological examination were evaluated to demonstrate the liver response following administration of benzo(a)pyrene and ethanol separately and together. SOD activities of the liver tissue in the experimental groups were decreased when compared to the control group. Activities of ALT, AST and GGT of the liver tissue in all experimental groups were found significantly higher than that of the control group. GSH levels of the liver tissue of the experimental groups were lower than the control group especially in group IV. When we compared MDA levels among study groups, MDA levels of experimental groups were found significantly higher than the control group. Exposure to BAP resulted in hepatocellular changes in the periportal area and inflammatory cell infiltration . On the other hand, liver tissue in group III and IV, which was treated with BAP plus EtOH and EtOH alone respectively, showed seldom inflammatory cell infiltrations. BAP and EtOH administration alone or together discretely determined changes in the GSH, MDA levels and SOD ALT,AST and GGT enzyme activities in the liver tissues. Additionally, we noted BAP induced hepatocellular changes in the periportal area.

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