title: Protective effect of quercetin on experimental chronic cadmium nephrotoxicity in rats is based on its antioxidant properties.
abstract: Oxidative stress can play a key role in Cd-induced dysfunctions. Quercetin is a potent oxygen free radicals scavenger and a metal chelator. Our aim was to study the effect of quercetin on Cd-induced kidney damage and oxidative stress as well as its mechanism of action. Wistar rats were distributed in four experimental groups: control rats; Cd; quercetin and Cd+quercetin. Renal toxicity was evaluated by measuring urinary excretion of proteins, albumin, glucose and enzymes markers of tubular necrosis, as well as plasma concentration of creatinine. Plasma TBARS concentration and activity of antioxidant enzymes in kidney were also measured. Renal cell damage was assessed by electron microscopy. Animals that received both Cd and quercetin showed a better renal function than those receiving Cd alone. Cd-induced tubular lesions were markedly reduced in rats that also received quercetin. Cd-induced increase in plasma TBARS was prevented by the administration of quercetin. Total plasma antioxidants and renal superoxide dismutase and glutathione-reductase activities were higher in the group that received Cd and quercetin than in rats that received Cd alone. Quercetin administration does not modify the renal content or the urinary excretion of Cd. In conclusion, quercetin treatment prevents renal tubular damage and increased oxidative stress induced by chronic Cd administration, most probably throughout its antioxidant properties.
authors.affiliation: Instituto Reina Sofía de Investigación Nefrológica, Departamento de Fisiología y Farmacología, Edificio Departamental, Campus Miguel de Unamuno, Universidad de Salamanca, 37007 Salamanca, Spain.
authors.forename: A I
authors.initials: AI
authors.lastname: Morales
authors.forename: C
authors.initials: C
authors.lastname: Vicente-Sánchez
authors.forename: J M Santiago
authors.initials: JM
authors.lastname: Sandoval
authors.forename: J
authors.initials: J
authors.lastname: Egido
authors.forename: P
authors.initials: P
authors.lastname: Mayoral
authors.forename: M A
authors.initials: MA
authors.lastname: Arévalo
authors.forename: M
authors.initials: M
authors.lastname: Fernández-Tagarro
authors.forename: J M
authors.initials: JM
authors.lastname: López-Novoa
authors.forename: F
authors.initials: F
authors.lastname: Pérez-Barriocanal
mesh_terms: D000818:Animals; D002104:Cadmium / Q000633:toxicity*; D002105:Cadmium Poisoning / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D002908:Chronic Disease; D004195:Disease Models, Animal; D004336:Drug Antagonism; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D005980:Glutathione Reductase / Q000378:metabolism; D007674:Kidney Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D007677:Kidney Function Tests; D007687:Kidney Tubules, Proximal / Q000187:drug effects* / Q000648:ultrastructure; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D011794:Quercetin / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D016166:Free Radical Scavengers; D002104:Cadmium; D011794:Quercetin; D013482:Superoxide Dismutase; D005980:Glutathione Reductase