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Liver is the largest gland of body that plays a pivotal role in regulating various physiological processes in the body such as metabolism, secretion and storage. Hepatotoxicity is a term that indicates damage to the cells, tissues, and structure or liver functions. Currently, millions of people are suffering from hepatic damage known to be induced by alcohol, chemicals, and drugs, infections, and immune response (Al-Harbi et al., 2014). Genetic condition modifies susceptibility to various types of causative factors (Bose et al., 2011).Chemicals, in the form of some drugs such as paracetamol, and antitubercular drugs (isoniazid, rifampicin), toxic compounds like carbontetrachloride (CCl4), thioacetamide, dimethylnitrosamine, D-galactosamine/ lipopolysaccharide, gamma radiations, cadmium and arsenic heavy metals, mycotoxin (aflatoxin) are unquestionably various risk factors for hepatic injury (Deepa et al., 2013; Domenicali et al., 2009; Larson et al., 2005). Carbontetrachloride (CCl4) is a clear, colorless, volatile, heavy and noninflammable liquid. (Deepa et al., 2013; Domenicali et al., 2009; Larson et al., 2005; Alkreathy et al., 2014) CCl4is a lipophillic molecule metabolized in liver and spread easily in the lipid compartments of the body. CCl4is a well-known hepatotoxin or classic model used extensively to investigate the hepatotoxicity in animals by initiating lipid peroxidation (Harbi et al., 2014; Weber et al., 2013; Recknagel et al., 1989). Lipid peroxidation induce membrane disintegration of liver hepatocytes, which in turn increases the release of cytosolic enzymes such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) (Suzek et al., 2015; Mohamed et al., 2014). CCl4 also causes the activation of immune system through the infiltration of inflammatory cells to the site of injury, responsible for the release of pro-inflammatory cytokines such as tumor necrosis factorα (TNF-α), interleukin-6 (IL-6) and c-reactive protein (CRP), which further enhance hepatotoxicity through repeated cycle of inflammation (Mohamed et al., 2001a). Administration of CCl4 increased triglycerides (TG), total cholesterol (TC), low density lipoprotein (LDL), whereas lowered the high density lipoprotein (HDL) (Boll et al., 2001a; Andritoiu et al., 2014). CCl4 induced hepatotoxicity lead toaccumulation of Ca 2+ in mitochondria, activate many membrane damaging enzymes, causes disruption of mitochondrial metabolism, decreased ATP synthesis and damage micro-filaments that support cell structure(Deepa et al., 2013; Nicotera et al., 1990). Free radicals of CCl4 induced an increase in the number of Agyrophillic nucleolar organizer region (AgNORs) and enhance activity of telomerase enzyme hepatic architecture (Khanna et al., 2003). CCl4 caused various histological Evaluation of Ginger Oleoresin in Carbon Tetrachloride Induced Hepatotoxicity in Rats