Wednesday, July 31, 2019

Journals on Cancer Medicine - BJSTR Journal

Abstract

Iron is an essential element, which is abundant in the red blood cells and plays a key role during oxidative phosphorylation in the mitochondria of all cells. The excess of iron has been indicated in several diseases as it induces oxidative stress. The present study was undertaken to understand the modulation of iron induce oxidative stress in mice by hesperidin. The mice were administered with 250 mg/kg body weight of hesperidin for five days before feeding with 5000, 10,000 and 20000 ppm FeCl3 for 30 days. The #glutathione, glutathione-s-transferase, catalase, superoxide dismutase, lipid peroxidation, lactate dehydrogenase, aspartic acid transaminase, and alanine aminotransaminase levels were estimated in the liver of iron treated mice after 30 days post-iron treatment. The feeding of different concentrations of iron for 30 days led to an increase in the oxidative stress as indicated by a decline in the #glutathione concentration, and glutathione-s-transferase, catalase, and superoxide dismutase activities accompanied by the rise in the lactate dehydrogenase, aspartic acid transaminase, and alanine aminotransaminase levels. Treatment of hesperidin for 5 days before iron overload elevated the activities of glutathione-s-transferase, catalase, and #superoxide dismutase and glutathione concentration, whereas the activities of lactate dehydrogenase, aspartic acid transaminase, and alanine aminotransaminase and lipid peroxidation declined significantly. Our study demonstrates that pre-treatment of hesperidin for five days reduced the iron induced oxidative stress indicated by the reduction in lipid peroxidation, #lactate dehydrogenase, aspartic acid transaminase, and alanine #aminotransaminase activities and a rise in the glutathione-s-transferase, catalase, and superoxide dismutase and glutathione contents in the mice liver.

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