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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Hesperidin, A Citrus Bioflavonoid Attnuates Iron- Induced Biochemical Oxidative Stress in Mouse Liver by Ganesh Chandra Jagetia in BJSTR
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