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Hesperidin, an antioxidant flavonoid, prevents acrylonitrile‐induced oxidative stress in rat brain
Author(s) -
ElSayed ElSayed M.,
AboSalem Osama M.,
AbdEllah Mohamed F.,
AbdAlla Gamil M.
Publication year - 2008
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.20237
Subject(s) - chemistry , hesperidin , lipid peroxidation , glutathione , oxidative stress , antioxidant , pharmacology , malondialdehyde , superoxide dismutase , glutathione peroxidase , biochemistry , flavonoid , glutathione reductase , catalase , enzyme , medicine , pathology , alternative medicine
Acrylonitrile (ACN) is a volatile, toxic liquid used as a monomer in the manufacture of synthetic rubber, styrene plastics, acrylic fiber, and adhesives. ACN is a potent neurotoxin. A role for free radical mediated lipid peroxidation in the toxicity of ACN has been suggested. We examined the ability of hesperidin, an antioxidant flavonoid, to attenuate ACN‐induced alterations in lipid peroxidation in rat brains. The daily oral administration of ACN to male albino rats in a dose of 50 mg/kg bwt for a period of 28 days produced a significant elevation in brain lipid peroxides measured as malondialdehyde (MDA) amounting to 107%, accompanied by a marked decrease in brain‐reduced glutathione (GSH) content reaching 63%. In addition, ACN administration resulted in significant reductions in the enzymatic antioxidant parameters of brain; superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH‐Px), and glutathione‐ S ‐transferase (GST) recording 43%, 64%, 52%, and 43%, respectively. On the other hand, pretreatment with hesperidin and its coadministration with ACN once daily in a dose of 200 mg/kg bwt i.p. for 28 days ameliorated ACN‐induced alterations in brain lipid peroxidation. These results suggest that hesperidin may have a beneficial role against ACN‐induced oxidative stress in the brain; an effect that is mainly attributed to the antioxidant property of hesperidin. © 2008 Wiley Periodicals, Inc. J Biochem Mol Toxicol 22:268–273, 2008; Published online in Wiley InterScience ( www.interscience.wiley.com ). DOI 10.1002/jbt.20237