S Subash1, P Subramanian. 1. Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar 608002, Tamil Nadu, India.
Abstract
INTRODUCTION: Hyperammonaemia is a major contributing factor to neurological abnormalities observed in hepatic encephalopathy and in congenital defects of ammonia detoxication. Ammonia toxicity results in free radical generation that leads to oxidative stress and tissue damage. Morin is a bioflavonoid, a constituent of many herbs and fruits that are used as herbal medicines and also several biological activities. Our aim was to investigate the effect of morin on circulatory liver markers, lipid peroxidation and antioxidant status in ammonium chloride (AC)-induced hyperammonaemic rats. METHODS: Male albino Wistar rats weighing 180-200 g were used for the study. The hyperammonaemia was induced by interaperitonial injection of AC (100 mg/kg body weight). Rats were treated with morin (30 mg/kg body weight) via oral administration. Administration of morin in hyperammonaemic rats reduced the levels of ammonia and urea. The antioxidant property of morin was studied by assessing the activities of thiobarbituric acid reactive substances (TBARS), hydroperoxides (HP) and liver markers (alanine transaminase, aspartate transaminase and alkaline phosphatase) and the levels of glutathione peroxidase, superoxide dismutase, catalase, reduced glutathione, vitamins A, C and E in AC-treated rats. RESULTS: Oxidative stress was effectively modulated by morin administration. Morin significantly improved the status of antioxidants and decreased the levels of ammonia, urea, TBARS, HP and liver markers enzymes, as compared to the AC-treated group. CONCLUSION: The study offers evidence for the antihyperammonaemic, hepatoprotective and antioxidant effects of morin against oxidative stress induced by AC.
INTRODUCTION: Hyperammonaemia is a major contributing factor to neurological abnormalities observed in hepatic encephalopathy and in congenital defects of ammonia detoxication. Ammoniatoxicity results in free radical generation that leads to oxidative stress and tissue damage. Morin is a bioflavonoid, a constituent of many herbs and fruits that are used as herbal medicines and also several biological activities. Our aim was to investigate the effect of morin on circulatory liver markers, lipid peroxidation and antioxidant status in ammonium chloride (AC)-induced hyperammonaemic rats. METHODS: Male albino Wistar rats weighing 180-200 g were used for the study. The hyperammonaemia was induced by interaperitonial injection of AC (100 mg/kg body weight). Rats were treated with morin (30 mg/kg body weight) via oral administration. Administration of morin in hyperammonaemic rats reduced the levels of ammonia and urea. The antioxidant property of morin was studied by assessing the activities of thiobarbituric acid reactive substances (TBARS), hydroperoxides (HP) and liver markers (alanine transaminase, aspartate transaminase and alkaline phosphatase) and the levels of glutathione peroxidase, superoxide dismutase, catalase, reduced glutathione, vitamins A, C and E in AC-treated rats. RESULTS: Oxidative stress was effectively modulated by morin administration. Morin significantly improved the status of antioxidants and decreased the levels of ammonia, urea, TBARS, HP and liver markers enzymes, as compared to the AC-treated group. CONCLUSION: The study offers evidence for the antihyperammonaemic, hepatoprotective and antioxidant effects of morin against oxidative stress induced by AC.
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