OBJECTIVES: Carotenoids are a class of natural fat-soluble pigments that are found in many fruits and vegetables. Consumption of a diet rich in carotenoids has been epidemiologically correlated with a lower risk for several diseases. In the present study the carotenoid lutein (3,3'-dihydroxy-beta,epsilon-carotene) was evaluated for its hepatoprotective activity in rats. METHODS: Paracetamol, 20% ethanol and carbon tetrachloride were used to induce liver toxicity. KEY FINDINGS: Levels of serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase and alkaline phosphatases, which were increased in the serum, were found to be significantly reduced by the treatment of lutein in a dose-dependent manner, indicating that lutein may reduce the hepatotoxicity induced by these agents(. )Serum bilirubin was also significantly lower in lutein-treated groups compared with control. Increased lipid peroxidation, conjugated diene and hydroperoxides in the liver tissue produced by the administration of paracetamol were found to be reduced in the lutein-treated groups. Levels of antioxidant enzymes, like superoxide dismutase, catalase, glutathione peroxidase and glutathione, were found to be increased in lutein-treated groups compared with control group during alcohol- and CCl(4)-induced liver toxicity. Hydroxyproline, which is an indicator of fibrosis in liver tissue, was high in the ethanol-treated control group. Hydroxyproline levels were decreased by simultaneous lutein administration. CONCLUSIONS: Histopathological evidence confirmed the protection offered by lutein from the tissue damage caused by hepatotoxins. The hepatoprotective action may be due to lutein's ability to scavenge reactive oxygen radicals.
OBJECTIVES:Carotenoids are a class of natural fat-soluble pigments that are found in many fruits and vegetables. Consumption of a diet rich in carotenoids has been epidemiologically correlated with a lower risk for several diseases. In the present study the carotenoid lutein (3,3'-dihydroxy-beta,epsilon-carotene) was evaluated for its hepatoprotective activity in rats. METHODS:Paracetamol, 20% ethanol and carbon tetrachloride were used to induce liver toxicity. KEY FINDINGS: Levels of serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase and alkaline phosphatases, which were increased in the serum, were found to be significantly reduced by the treatment of lutein in a dose-dependent manner, indicating that lutein may reduce the hepatotoxicity induced by these agents(. )Serum bilirubin was also significantly lower in lutein-treated groups compared with control. Increased lipid peroxidation, conjugated diene and hydroperoxides in the liver tissue produced by the administration of paracetamol were found to be reduced in the lutein-treated groups. Levels of antioxidant enzymes, like superoxide dismutase, catalase, glutathione peroxidase and glutathione, were found to be increased in lutein-treated groups compared with control group during alcohol- and CCl(4)-induced liver toxicity. Hydroxyproline, which is an indicator of fibrosis in liver tissue, was high in the ethanol-treated control group. Hydroxyproline levels were decreased by simultaneous lutein administration. CONCLUSIONS: Histopathological evidence confirmed the protection offered by lutein from the tissue damage caused by hepatotoxins. The hepatoprotective action may be due to lutein's ability to scavenge reactive oxygen radicals.
Authors: G Smilin Bell Aseervatham; T Sivasudha; J M Sasikumar; P Hephzibah Christabel; R Jeyadevi; D Arul Ananth Journal: J Physiol Biochem Date: 2013-07-20 Impact factor: 4.158