Effects of Benzo(a)pyrene and Ethanol on Morphology and Antioxidant Status and Transaminases in Rat Liver

Abstract

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. First group (control group). Second group treated with benzo(a)pyrene [B(a)P], third group treated with benzo(a)pyrene[B(a)P] plus ethanol (EtOH) and fourth group was given ethanol(EtOH). 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 [B(a)P] and (EtOH) separately and together. SOD activities of the liver tissue in the experimental groups were decreased when compared to the first group. Activities of ALT, AST and GGT of the liver tissue in all experimental groups were found significantly higher than that of the first group. GSH levels of the liver tissue of the experimental groups were lower than the first group especially in fourth group. When we compared MDA levels among study groups, MDA levels of experimental groups were found significantly higher than the first group. Exposure [B(a)P] to resulted in hepatocellular changes in the periportal area and inflammatory cell infiltration . On the other hand, liver tissue in third group and fourth group, which was treated with [B(a)P] plus EtOH and EtOH alone respectively, showed seldom inflammatory cell infiltrations. [B(a)P] 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 [B(a)P] induced hepatocellular changes in the periportal area.