Carbon tetrachloride: A classic model for liver toxicity.

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1 Biochemistry Department, Faculty of Science, Zagazig University, Egypt.

2 Physical Chemistry Department, Surface and Catalysis Lab., National Research Center, El Bohouth St. 33, Dokki, Giza, Egypt

3 Biochemistry Department, Faculty of Science, Zagazig University, Egypt

Abstract

Carbon tetrachloride (CCl₄), an efficient hepatotoxin, is employed to trigger liver damage in experimental animals. CCl₄ disrupts liver cell membranes and impairs the activity of the endoplasmic reticulum and mitochondria. CCl₄'s liver cytotoxicity depends on its metabolism by ferric cytochrome P450. The trichloromethyl free radical is responsible for lipid peroxidation. Carbon tetrachloride (CCl₄) interacts with triacylglycerols and phospholipids within subcellular compartments, initiating lipid peroxidation in hepatic parenchymal cells. Long-term use of CCl₄ can result in fatty deposits in the liver, fibrotic cells, as well as hepatic cancer. Reactive free radicals stimulate a range of biological processes, such as programmed cell death, necrosis, ferroptosis, and autophagy. A proper ratio of free radicals and antioxidants is essential for optimal physiological function. If the equilibrium favors free radicals, many pathological diseases can arise. In this review, we demonstrated the efficacy of carbon tetrachloride on the liver, delving into its role in oxidative stress, lipid peroxidation, inflammation, and models of liver toxicity such as fibrosis and cirrhosis.

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