Antioxidant activity of Aulosira fertilisima on CCl4 induced hepatotoxicity in rats.

Free radicals cause cell injury, when they are generated in excess or when the antioxidant defense is impaired. Carbon tetrachloride (CCl4) is used as a model for liver injury. In this study antioxidant activity of ethanol extract of A. fertilisima (EEA) was investigated using CCl4 intoxicated rat liver as the experimental model. Oral administration of EEA at a dose of 100 mg/kg body weight, for 14 consecutive days, the rate of the production of antioxidant enzymes like super oxide dismutase, catalase, glutathione peroxidase and glutathione transferase in rats compared to the CCl4 treated group without any supporting treatment. Liver damage is detected by the measurement of the activities of serum enzymes like aspartate aminotransferase, alanine aminotransferase, gamma glutamyl transpeptidase and alkaline phosphatase which were released in to the blood from damaged cells. The normalization of these enzymes levels was observed in rats treated with EEA (100 mg/kg body weight) by reducing the leakage of the above enzymes in to the blood. The findings provide a rationale for further studies on isolation of active principles and its pharmacological evaluation. Protection offered by silymarin (standard reference drug) seemed relatively greater.

Metabolism of glycosaminoglycans in rats during methionine deficiency and administration of excess methionine.

Methionine deficiency in rats caused significant decrease in the concentration of many sulphated glycosaminoglycans in the aorta and other tissues, while administration of excess methionine caused an increase in these constituents. The activity of some important biosynthetic enzymes decreased in methionine deficiency and increased on administration of excess methionine. No uniform pattern was observed in the changes in the activity of enzymes concerned with degradation of glycosaminoglycans. The concentration of 3'-phosphoadenosine 5'-phosphosulphate and the activities of the sulphate activating system and sulphotransferase were decreased in methionine deficiency, while feeding excess methionine did not affect these parameters as compared to controls.