Abstract
The protective effect of cold-pressed coriander (Coriandrum sativum) oil (CO) against the toxicity caused by carbon tetrachloride (CCl4) in rats was studied. CO is characterized by its high levels of monounsaturated fatty acids and polyunsaturated fatty acids, tocopherols and phenolic compounds. Male Wistar rats were orally treated with two doses of CO (100 and 200mg/kg) with administration of CCl4 (1mL/kg, CCl4 in olive oil) for 8 weeks. Liver biochemical parameters were determined in animals treated with CO. The results clearly demonstrated that CO augments the antioxidants' defense mechanism against CCl4-induced toxicity and provides evidence that CO may have a therapeutic role in free radical-mediated diseases. Treatment with CO significantly reduced the impact of CCl4 toxicity on aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase, kidney function indicators, protein profile, lipid profile and antioxidant markers of CCl4-induced liver injury rats. The overall potential of the antioxidant system was significantly enhanced by the CO supplements as the hepatic malondialdehyde levels were lowered, whereas reduced glutathione levels were elevated. The hepatoprotective impact of CO was also supported by histopathological studies of liver tissue. Histopathological examination showed that CO reduced fatty degeneration, cytoplasmic vacuolization and necrosis in CCl4-treated rats. The results indicate the potentiality of CO to act as natural antioxidant by preventing the peroxidative damage caused by CCl4.
Practical ApplicationsBiologically active natural compounds are of interest for pharmaceutical industry in the prevention of different diseases caused by lipid peroxidative damage (i.e., ischemia, coronary atherosclerosis, Alzheimer's disease and carcinogenesis). In the present study, the capability of cold-pressed Coriandrum sativum oil (CO) to protect against CCl4-induced hepatotoxicity was investigated. The study suggested that CO has potent hepatoprotective activity in CCl4-induced liver injury in rats. CO possesses antioxidant potential and inhibits the deleterious effect of free radicals generated by CCl4. CO is rich in tocols, phenolic compounds and other bioactive constituents, which might be responsible for the protective effects. These observations provide biochemical data supporting the potential clinical use of CO in the treatment of some hepatic disorders. The results suggest that the ability of CO to ameliorate CCl4-induced liver injury is associated with its antioxidant and radical-scavenging characteristics.