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Time course and mechanism of brain oxidative stress and damage for redox active and inactive transition metals overload

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BIOCELL 2016年第1期40卷 19-21页

作者： NIDIA FERRAROTTI ROSARIO MUSACCO-SEBIO christian saporito-magrina JUAN MANUEL ACOSTA MARISA REPETTO Clinical Biochemistry Department Faculty of Pharmacy and BiochemistryInstitute of Biochemistry and Molecular Medicine(IBIMOL)University of Buenos Aires-CONICETBuenos AiresArgentina General and Inorganic Chemistry Faculty of Pharmacy and BiochemistryInstitute of Biochemistry and Molecular Medicine(IBIMOL)University of Buenos Aires-CONICETBuenos AiresArgentina.

The objective of this work was to study the in vivo time course of biochemical processes of oxidative damage in the brain of Sprague-Dawley rats that received an acute overload of the redox active metals iron(Fe)and copper(Cu),and the redox inactive cobalt(Co)and nickel(Ni).Oxidative stress indicators(phospholipid and protein oxidation),glutathione(GSH),antioxidant enzymes and NADPH oxidase activities,and the plasma inflam-matory cytokine(IL-6)were *** results showed that in brain oxidative mechanisms for both sets of metal are different,however in both cases are *** mechanism for Fe and Cu oxidative damage is mediated by the generation of the free radical hydroxyl(Fenton reaction and homolytic cleavage of hydroperoxides).Two events of antioxidant protection prior to oxidation of phospholipids and proteins by Fe and Cu are *** first process is the use of GSH and the second is the increased activity of the Cu,Zn-SOD and catalase *** oxidative mechanism for metal redox inactive is the consumption of GSH,NADPH oxidase activation and inflammatory response mediated by *** increased protein oxidation as a result of the inflammatory *** produced increments of phospholipid oxidation and SOD activity.

关键词： metals oxidative damage oxidative stress brain lipid peroxidation

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