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 endoplasmic reticulum and mitochondria. CCl4's liver cytotoxicity depends on its metabolism by ferric cytochrome P450. 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 liver delving into its role in oxidative stress, lipid peroxidation, inflammation and models of liver toxicity such as fibrosis and cirrhosis.