Hepatoprotective Effect of Alpha Lipoic Acid Against Bromobenzene-Induced Liver Damage in Rats

The hepatic lesion produced as a result of oxidative stress is of wide occurrence. In this study, the effect of the antioxidant alpha lipoic acid (ALA) on liver necrosis induced by bromobenzene (BB), which is known to produce oxidative stress, in rats had been studied. Treatment of animals with ALA for one week before the induction of chemical liver injury with BB had been carried out. Various biochemical changes associated with liver damage and oxidative stress were measured. The activities of isocitrate dehydrogenase (ICDH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) as indices of liver function were measured. Hepatic reduced glutathione (GSH) content, malondialdehyde (MDA), and nitric oxide (NO) were measured as oxidative stress markers as well as hepatic total protein (TP). Histopathological studies had been carried out to ascertain the cause of hepatic cell death and to provide further evidence to support the hepatoprotective effect of ALA and correlate it with any biochemical changes. Administration of BB produced a significant rise in the serum activities of ICDH and ALT together with a marked reduction in hepatic GSH content and a significant elevation of liver MDA and NO. Histopathological examination revealed loss of cell boundaries, marked centrilobular necrosis and disappearance of nuclei. Congestion and inflammatory cells around central vein were also observed. Pretreatment with ALA significantly reduced serum ALT activity and normalizes that of lCD H. Hepatic GSH content was significantly increased, while MDA and NO were normalized together with preservation of the hepatocyte architecture suggesting a clear hepatoprotective role of ALA against BE-induced liver damage