title: Locomotor damage and brain oxidative stress induced by lead exposure are attenuated by gallic acid treatment.
abstract: We investigated the antioxidant potential of gallic acid (GA), a natural compound found in vegetal sources, on the motor and oxidative damages induced by lead. Rats exposed to lead (50 mg/kg, i.p., once a day, 5 days) were treated with GA (13.5mg/kg, p.o.) or EDTA (110 mg/kg, i.p.) daily, for 3 days. Lead exposure decreased the locomotor and exploratory activities, reduced blood ALA-D activity, and increased brain catalase (CAT) activity without altering other antioxidant defenses. Brain oxidative stress (OS) estimated by lipid peroxidation (TBARS) and protein carbonyl were increased by lead. GA reversed the motor behavior parameters, the ALA-D activity, as well as the markers of OS changed by lead exposure. CAT activity remained high, possibly as a compensatory mechanism to eliminate hydroperoxides during lead poisoning. EDTA, a conventional chelating agent, was not beneficial on the lead-induced motor behavior and oxidative damages. Both GA (less) and EDTA (more) reduced the lead accumulation in brain tissue. Negative correlations were observed between the behavioral parameters and lipid peroxidation and the lead levels in brain tissue. In conclusion, GA may be an adjuvant in lead exposure, mainly by its antioxidant properties against the motor and oxidative damages resulting from such poisoning.
authors.affiliation: Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria (UFSM), RS, Brazil.
authors.forename: Patrícia
authors.initials: P
authors.lastname: Reckziegel
authors.forename: Verônica Tironi
authors.initials: VT
authors.lastname: Dias
authors.forename: Dalila
authors.initials: D
authors.lastname: Benvegnú
authors.forename: Nardeli
authors.initials: N
authors.lastname: Boufleur
authors.forename: Raquel Cristine
authors.initials: RC
authors.lastname: Silva Barcelos
authors.forename: Hecson Jesser
authors.initials: HJ
authors.lastname: Segat
authors.forename: Camila Simonetti
authors.initials: CS
authors.lastname: Pase
authors.forename: Clarissa Marques Moreira
authors.initials: CM
authors.lastname: Dos Santos
authors.forename: Erico Marlon Moraes
authors.initials: EM
authors.lastname: Flores
authors.forename: Marilise Escobar
authors.initials: ME
authors.lastname: Bürger
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001522:Behavior, Animal / Q000187:drug effects*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002614:Chelating Agents / Q000494:pharmacology; D004195:Disease Models, Animal; D004492:Edetic Acid / Q000494:pharmacology; D005106:Exploratory Behavior / Q000187:drug effects; D005707:Gallic Acid / Q000494:pharmacology*; D007854:Lead; D020263:Lead Poisoning, Nervous System / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control* / Q000523:psychology; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009043:Motor Activity / Q000187:drug effects*; D009566:Nitrates; D018384:Oxidative Stress / Q000187:drug effects*; D000623:Porphobilinogen Synthase / Q000378:metabolism; D050050:Protein Carbonylation / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000975:Antioxidants; D002614:Chelating Agents; D009566:Nitrates; D007854:Lead; D005707:Gallic Acid; C017461:lead nitrate; D004492:Edetic Acid; D002374:Catalase; D000623:Porphobilinogen Synthase