Biochemical, Histological, and Immunohistochemical Changes Associated with Alcl3- Induced Hepatic Injury in Rats: Protective Effects of L-carnitine

Abstract

Background: There has been a great interest in the toxicity of Aluminum (Al) due to its environmental wide distribution and every day usage. The key mechanisms of Al -induced toxicity in the liver are recognized as reactive oxygen species (ROS), development of free radicals, oxidative stress, and lipid peroxidation. L-carnitine is a conditionally important amino-acid (4-N-trimethylammonium-3-hydroxybutyric acid). By L-carnitine, long-chain fatty acids are taken into the mitochondria contributing to the metabolism of cellular energy. Also, it can enhance the antioxidant status by accelerating the free radicals removal from cells.Objective: The purpose of this report was to determine the possible detrimental impact of AlCl3 and to evaluate for the first time the possible potential hepato-protective effect of exogenous L-carnitine supplementation in ameliorating these possible deteriorations. Materials and methods: Thirty two rats were subdivided into equal four groups, Group I: Control rats, Group II: Rats treated with L-carnitine at a dose of 200 mg/kg. b.wt., Group III: Rats treated with Alcl3 at a dose of 100 mg/kg. b.wt., and Group IV: Rats treated with L-carnitine and Alcl3 (200 and 100 mg/kg. b.wt., respectively). All procedures of given materials to animals were orally once daily for one month. Results: The current investigation showed that Alcl3 ingestion caused an obvious hepatic deterioration evidenced by increased liver enzymes level and imbalance in oxidant/antioxidant status. This was accompanied by histological changes and increased Ki-67 and caspase-3 immunoreactivity. These effects were significantly improved by L-carnitine supplementation.Conclusion: These findings suggested that L-carnitine may have a protective effect against hepatic damage sustained by Alcl3 through its antioxidative property and its inhibitory effect on prolife ration and apoptosis.