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 c...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 measured.The results showed that in brain oxidative mechanisms for both sets of metal are different,however in both cases are irreversible.The 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 considered.The first process is the use of GSH and the second is the increased activity of the Cu,Zn-SOD and catalase enzymes.The oxidative mechanism for metal redox inactive is the consumption of GSH,NADPH oxidase activation and inflammatory response mediated by IL-6.Co increased protein oxidation as a result of the inflammatory process.Ni produced increments of phospholipid oxidation and SOD activity.展开更多
Several authors have addressed the importance of mitochondrial function in inflammatory syn-dromes,as it may play a role in the genesis of tissue injury.Sepsis and exposition to environmental particles are examples of...Several authors have addressed the importance of mitochondrial function in inflammatory syn-dromes,as it may play a role in the genesis of tissue injury.Sepsis and exposition to environmental particles are examples of inflammatory conditions.Sepsis occurs with an exacerbated inflammatory response that damages tissue mitochondria and impairs bioenergetic processes.One of the current hypotheses for the molecular mech-anisms underlying the complex condition of sepsis is that enhanced NO production and oxidative stress lead to mitochondrial dysfunction,bioenergetic derangement and organ failure.The mechanism of particulate mat-terhealth effects are believed to involve inflammation and oxidative stress.Components in particles that elicit inflammation have been poorly investigated,although recent research points out to the contribution of composi-tional elements and particle size.Oxygen metabolism and mitochondrial function appear to be important areas of study in inflammatory conditions for clarifying molecular mechanisms involved.展开更多
基金supported by grants from Agencia Nacional de Promoción Científica y Tecnológica(PICT 2012-00964)Universidad de Buenos Aires(UBACYT 0380,2014-2017).
文摘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 measured.The results showed that in brain oxidative mechanisms for both sets of metal are different,however in both cases are irreversible.The 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 considered.The first process is the use of GSH and the second is the increased activity of the Cu,Zn-SOD and catalase enzymes.The oxidative mechanism for metal redox inactive is the consumption of GSH,NADPH oxidase activation and inflammatory response mediated by IL-6.Co increased protein oxidation as a result of the inflammatory process.Ni produced increments of phospholipid oxidation and SOD activity.
文摘Several authors have addressed the importance of mitochondrial function in inflammatory syn-dromes,as it may play a role in the genesis of tissue injury.Sepsis and exposition to environmental particles are examples of inflammatory conditions.Sepsis occurs with an exacerbated inflammatory response that damages tissue mitochondria and impairs bioenergetic processes.One of the current hypotheses for the molecular mech-anisms underlying the complex condition of sepsis is that enhanced NO production and oxidative stress lead to mitochondrial dysfunction,bioenergetic derangement and organ failure.The mechanism of particulate mat-terhealth effects are believed to involve inflammation and oxidative stress.Components in particles that elicit inflammation have been poorly investigated,although recent research points out to the contribution of composi-tional elements and particle size.Oxygen metabolism and mitochondrial function appear to be important areas of study in inflammatory conditions for clarifying molecular mechanisms involved.