title: Effects of curcumin and tannic acid on the aluminum- and lead-induced oxidative neurotoxicity and alterations in NMDA receptors.
abstract: Exposure to aluminum (Al) and lead (Pb) can cause brain damage. Also, Pb and Al exposure alters N-methyl-d-aspartate receptor (NMDAR) subunit expression. Polyphenols such as tannic acid and curcumin are very efficient chelator for metals. The effects of curcumin and tannic acid (polyphenols) on Al(3+)- and Pb(2+)-induced oxidative stress were examined by investigating lipid peroxidation (LPO) levels, antioxidant enzyme activities, acetyl cholinesterase (AChE) activity and also NMDA receptor subunits 2A and 2B concentrations in the brain tissue of rats sub-chronically. Rats were divided into seven groups as control, Al, Pb, aluminum-tannic acid treatment (AlT), aluminum-curcumin treatment (AlC), lead-tannic acid treatment (PbT) and lead-curcumin treatment (PbC). After 16 weeks of treatment, LPO levels in the brain and hippocampus were higher in Al(3+)-exposed rats than that of Pb(2+)-exposed group. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in brain tissue of Al- and Pb-exposed rats increased significantly compared with control, while catalase (CAT) and AChE activities decreased. It was observed that metal exposure affected NR2A concentrations more than NR2B concentrations and also that polyphenol treatments increased these receptor protein concentrations.
authors.affiliation: Faculty of Science, Department of Chemistry, Dokuz Eylul University , Izmir , Turkey and.
authors.forename: Münire Nalan
authors.initials: MN
authors.lastname: Tüzmen
authors.forename: Nilgün Candan
authors.initials: NC
authors.lastname: Yücel
authors.forename: Tülden
authors.initials: T
authors.lastname: Kalburcu
authors.forename: Nazan
authors.initials: N
authors.lastname: Demiryas
mesh_terms: D000085:Acetates; D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D002374:Catalase / Q000378:metabolism; D003474:Curcumin / Q000494:pharmacology*; D004195:Disease Models, Animal; D058851:GPI-Linked Proteins / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D020263:Lead Poisoning, Nervous System / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D020258:Neurotoxicity Syndromes / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D009942:Organometallic Compounds; D018384:Oxidative Stress / Q000187:drug effects*; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects* / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D013634:Tannins / Q000494:pharmacology*; D015854:Up-Regulation
chemical_list: D000085:Acetates; D000110:Acetylcholinesterase; D000975:Antioxidants; D002374:Catalase; D003474:Curcumin; D058851:GPI-Linked Proteins; D005978:Glutathione; D005979:Glutathione Peroxidase; D018696:Neuroprotective Agents; D009942:Organometallic Compounds; D016194:Receptors, N-Methyl-D-Aspartate; D013482:Superoxide Dismutase; D013634:Tannins; C121001:NR2B NMDA receptor; C013396:aluminum acetate; C548246:Ache protein, rat; C008261:lead acetate
keywords: Metals; NMDAR; oxidative stress; polyphenols