Role of L-carnitine in the prevention of acute liver damage induced by carbon tetrachloride in rats

Abstract

Background and aim: Lipid peroxidation is the most important mechanism in the pathogenesis of acute liver damage with carbon tetrachloride (CCl4). L-carnitine may prevent lipid peroxidation and thus may protect against liver damage. In the present study we investigated the protective effect of L-carnitine in experimental acute liver damage induced by CCl4.

Methods: Fifty rats were allocated to five equal groups. The first group was the control (group 1), the second group received an intraperitoneal CCl4 injection for 3 days (group 2), and the third group received a 50 mg/kg subcutaneous L-carnitine injection for 4 days, beginning a day before CCl4 injection. The CCl4 injection was continued for 3 days in the concerned group (group 3). Group 4 was given a CCl4 injection for 7 days and group 5 received a 50 mg/kg subcutaneous L-carnitine injection for 8 days, beginning a day before CCl4 injection. This group continued to receive a CCl4 injection for 7 days. Rats in groups 2 and 3 were killed on the fifth day. Rats in groups 1, 4 and 5 were killed on the ninth day. Plasma and liver tissue malondialdehyde (MDA) levels, glutathione peroxidase (GSH-Px) activity and liver enzyme levels were studied. Histopathological investigations were conducted.

Results: Liver tissue MDA levels decreased significantly in group 3 compared to group 2 (P<0.001). Liver tissue MDA levels in group 5 decreased significantly in comparison to those of group 4 (P<0.001). Liver tissue GSH-Px activity in group 5 was significantly lower than that in group 4 (P<0.05). There were no significant differences between groups 3 and 4 regarding GSH-Px activity (P>0.05). Steatosis, inflammation and necrosis in group 3 were significantly reduced when compared to group 2 (P<0.01). Fibrosis development was not identified in groups 2 and 3. Steatosis in group 5 was significantly lower than that in group 4 (P<0.05) and there were no significant differences between groups 4 and 5 with regards to inflammation and necrosis (P>0.05). Mild fibrosis development was identified in groups 4 and 5 but the difference between the groups was not significant.

Conclusion: It appears that L-carnitine has a protective effect in the early stage of experimental acute liver damage induced by CCl4. As the toxic effect or damage continues, its effect lessens.