Oxidative stress, impaired calcium homeostasis and mitochondrial dysfunction are the key elements of carbon tetrachloride-induced liver damage. Activation of lipid peroxidation is accompanied by changes in the activity of antioxidant enzymes, the concentration of reduced glutathione, catabolic preference of metabolic processes and amino acid imbalance. Taurine, a nonproteinogenic β-amino acid, is one of the key regulators of metabolism, antioxidant and amino acid balance corrector. The hepatoprotective properties of taurine are mainly associated with its zonal distribution within the liver lobes, significant differences in the concentrations of taurine between periportal and pericentral regions; the latter is manifested in different protective properties that depend on compartmentalization of detoxification processes in the liver lobule. Administration of taurine under conditions of carbon tetrachloride-induced liver injury prevents the increase of plasma transaminases and bilirubin, reduces the histological changes in the liver by decreasing the degree of necrosis of hepatocytes, inflammatory and fatty infiltration.
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Haretskaya et al. (2014) studied this question.
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