A simple analogue of well known natural antioxidant glutathione (GSH) called S-allyl-glutathione (SAG) was evaluated against carbon tetrachloride (CCl4)-induced oxidative stress liver injury in rat. Pretreatment of SAG attenuated the CCl4-toxicity induced elevation of liver injury markers such as enzymes (AST, ALT, GGT, ALP and LDH) and bilirubin in the blood circulation. Such protective effect of SAG resulted in preservation of liver function observed as normal level of total protein and albumin in plasma as well as inhibition of dyslipidemia in liver. In addition, in silico analysis has proved that SAG has strong affinity with the amino acids present in active site of the human cytochrome P450 2E1 and 3A4. Three important mechanisms provided by SAG such as scavenging of reactive oxidants, replenishing of endogenous antioxidants (SOD, catalase, GPx, GSH and vitamin C) and protection of mitochondrial function (oxidative phosphorylation complex activities) are involved in the optimal function of liver against CCl4-toxicity.
Keywords: Allyl sulfur compounds; Glutathione; Hepatoprotection; Oxidative stress; Peptide analogue.
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