title: Mitigating role of quercetin against sodium fluoride-induced oxidative stress in the rat brain.
abstract: BACKGROUND
  Quercetin is a well known aglycone flavonoid that is widely found in different food sources.
  
  
  OBJECTIVE
  In this study, the in vivo neuroprotective potential of quercetin against sodium fluoride-induced oxidative stress was evaluated.
  
  
  METHODS
  Wistar rats were divided into five treatment groups and then subjected to daily intraperitoneally treatment with quercetin (at 10 and 20 mg/kg body weight), vitamin C (at 10 mg/kg), or vehicle. After a 1 week treatment period, all groups except saline treated (normal group), were intoxicated with sodium fluoride (NaF) for 1 week. Rat brains were then removed and homogenized for measurement of antioxidant markers including superoxide dismutase (SOD), reduced glutathione, catalase, and lipid peroxidation final products.
  
  
  RESULTS
  The thiobarbituric acid reactive substances (TBARS) levels in the heart homogenate of sodium fluoride treated rats (42.04 ± 2.14 nmol MDA eq/g tissue) increased compared to the normal rats (35.99 ± 1.08 nmol MDA eq/g tissue). Animals which were pretreated with quercetin at 20 mg/kg for 1 week prior to sodium fluoride intoxication showed significant reduction in the TBARS level (36.13 ± 1.12 nmol MDA eq/g tissue). Also, pretreatment with quercetin (20 mg/kg) restored the SOD and catalase activities and modified the level of reduced glutathione compared with the control group (p > 0.05).
  
  
  CONCLUSIONS
  The present study revealed a potent neuroprotective potential of quercetin against NaF-induced toxicity.
authors.affiliation: Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, 19945-546, Tehran, Iran. Nabavi208@gmail.com
authors.forename: Seyed Fazel
authors.initials: SF
authors.lastname: Nabavi
authors.forename: Seyed Mohammad
authors.initials: SM
authors.lastname: Nabavi
authors.forename: Ali Mohammad
authors.initials: AM
authors.lastname: Latifi
authors.forename: Morteza
authors.initials: M
authors.lastname: Mirzaei
authors.forename: Solomon
authors.initials: S
authors.lastname: Habtemariam
authors.forename: Akbar Hajizadeh
authors.initials: AH
authors.lastname: Moghaddam
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology; D001921:Brain / Q000187:drug effects* / Q000473:pathology; D002374:Catalase / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000378:metabolism; D007274:Injections, Intraperitoneal; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects*; D011794:Quercetin / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D012969:Sodium Fluoride / Q000633:toxicity; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D018696:Neuroprotective Agents; D017392:Thiobarbituric Acid Reactive Substances; D012969:Sodium Fluoride; D011794:Quercetin; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione