Mohamed, B., Fares, N., Ashaat, N., Abozeid, F. (2022). Biochemical, Histological, and Immunohistochemical Changes Associated with Alcl3- Induced Hepatic Injury in Rats: Protective Effects of L-carnitine. Egyptian Journal of Histology, 45(1), 90-100. doi: 10.21608/ejh.2021.52300.1395
Basant Mohamed; Nagui Hassan Fares; Neveen Aseem Ashaat; Faten Abozeid. "Biochemical, Histological, and Immunohistochemical Changes Associated with Alcl3- Induced Hepatic Injury in Rats: Protective Effects of L-carnitine". Egyptian Journal of Histology, 45, 1, 2022, 90-100. doi: 10.21608/ejh.2021.52300.1395
Mohamed, B., Fares, N., Ashaat, N., Abozeid, F. (2022). 'Biochemical, Histological, and Immunohistochemical Changes Associated with Alcl3- Induced Hepatic Injury in Rats: Protective Effects of L-carnitine', Egyptian Journal of Histology, 45(1), pp. 90-100. doi: 10.21608/ejh.2021.52300.1395
Mohamed, B., Fares, N., Ashaat, N., Abozeid, F. Biochemical, Histological, and Immunohistochemical Changes Associated with Alcl3- Induced Hepatic Injury in Rats: Protective Effects of L-carnitine. Egyptian Journal of Histology, 2022; 45(1): 90-100. doi: 10.21608/ejh.2021.52300.1395
Biochemical, Histological, and Immunohistochemical Changes Associated with Alcl3- Induced Hepatic Injury in Rats: Protective Effects of L-carnitine
2Zoology department, Faculty of Science, Ain Shams University, Cairo, Egypt
3Faculty of Women for Arts, Science and Education, Ain Shams University
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 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 apoptosis.
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