Protective effect of N-acetylcysteine and deferoxamine on carbon tetrachloride-induced acute hepatic failure in rats

Ritter, Cristiane; Reinke, Adalisa; Andrades, Michael Éverton; Martins, Márcio Rodrigo; Rocha, José Antonio; Menna-Barreto, Sérgio Saldanha; Quevedo, Joao L De; Moreira, José Cláudio Fonseca; Dal‐Pizzol, Felipe

doi:10.1097/01.ccm.0000142699.54266.d9

Cited by 74 publications

(53 citation statements)

References 31 publications

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“…In fact, a number of papers reported the preventive effects of various antioxidants on the accumulation of lipid peroxidation products and on the increase in plasma transaminase activities induced by CCl 4 treatment. [10][11][12]14) In the present study, by assessing the effects of chitobiose and chitotriose on the amounts of lipid peroxidation products and the activities of plasma transaminases in CCl 4 -treated rats, we examined whether the 2 compounds could exert antioxidant activity when given orally.…”

Section: Resultsmentioning

confidence: 99%

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Effect of Chitobiose and Chitotriose on Carbon Tetrachloride-Induced Acute Hepatotoxicity in Rats

Chen

Taguchi

Sakai

et al. 2005

Biological & Pharmaceutical Bulletin

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The purpose of the present study was to examine whether chitobiose and chitotriose can protect rats from CCl 4 -induced hepatic toxicity when given orally. We studied the effects of the 2 chitooligosaccharides given orally to rats on the acute hepatotoxicity induced by CCl 4 -dependent lipid peroxidation. The increase in the sum of malondialdehyde and 4-hydroxy-2-alkenals, a marker of lipid peroxidation, in both plasma and liver of CCl 4 -treated rats was suppressed by oral administration of chitobiose or chitotriose. The elevation in the levels of plasma aspartate transaminase and alanine transaminase activities, markers of hepatic injury, induced by CCl 4 intoxication was also counteracted by oral administration of either chitooligosaccharide. The results indicate that chitobiose and chitotriose have the ability to exert a protective action against CCl 4 -induced acute hepatoxicity, probably by their antioxidant activity.

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Section: Resultsmentioning

confidence: 99%

“…[10][11][12][13] It is rational, therefore, to expect that antioxidative compounds can prevent CCl 4 hepatotoxicity. In fact, a number of papers reported the preventive effects of various antioxidants on the accumulation of lipid peroxidation products and on the increase in plasma transaminase activities induced by CCl 4 treatment.…”

Section: Resultsmentioning

confidence: 99%

Effect of Chitobiose and Chitotriose on Carbon Tetrachloride-Induced Acute Hepatotoxicity in Rats

Chen

Taguchi

Sakai

et al. 2005

Biological & Pharmaceutical Bulletin

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“…Treatment of animals with CCl 4 causes severe hepatic injury, and CCl 4 is used to prepare an experimental model of ALF [Ritter et al, 2004;Terblanche and Hickman, 1991]. It is generally thought that CCl 4 toxicity is caused by the generation of a reactive intermediate, due to its reductive metabolism by hepatic CYP.…”

Section: Both Ho-1 Pre-induction and Biliverdin Ixa Treatment Can Prementioning

confidence: 99%

Heme oxygenase‐1: a new drug target in oxidative tissue injuries in critically ill conditions

Takahashi

Shimizu

Akagi

et al. 2006

Drug Development Research

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Oxidative stresses associated with ischemia/reperfusion, neutrophil activation, and anesthesia with certain volatile agents, etc., are thought to play an important role in the development of acute organ failure in critical illnesses, such as acute lung injury, acute coronary artery insufficiency, acute liver failure, acute renal failure, and multiple organ dysfunction syndrome. Such oxidative stressors provoke a set of cellular responses, particularly those that participate in the defense against tissue injuries. Free heme, which can be rapidly released from hemeproteins, may constitute a major threat in the oxidant stress because it catalyzes the formation of reactive oxygen species. To counteract such insults, cells respond by inducing the 33-kDa heat shock protein, heme oxygenase (HO)-1, the rate-limiting enzyme in heme degradation. Induced HO-1 as such removes free heme by an enzymatic process. In addition, HO-1 induction itself confers protection to tissues from further oxidative injuries. In contrast, the abrogation of HO-1 induction, or chemical ablation of HO activity abolishes the beneficial effect of HO-1, and results in the aggravation of tissue injuries. In this article, we review recent advances in the essential role of HO-1 in tissue protection in various models of experimental oxidative tissue injuries as well as in human disorders, which is related to critically ill conditions, with special emphasis on the role of its induction in tissue defense and its potential therapeutic implications. Drug Dev. Res. 67:130-153, 2006.

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“…Among the antioxidant therapeutic interventions we find N-acetylcysteine (NAC) [9,11,12,14,15], deferoxamine (DFX) [13] and taurine [16]. In this regard, we have recently demonstrated that the combination of NAC and DFX is an effective treatment of severe sepsis in a rodent animal model [16], and in other models of inflammatory disease [15,[17][18][19]. Taurine is a naturally occurring free amino acid that has been shown to have neurotrophic and neuroprotective properties [20,21].…”

Section: Introductionmentioning

confidence: 98%

Effects of N-Acetylcysteine/Deferoxamine, Taurine and RC-3095 on Respiratory Chain Complexes and Creatine Kinase Activities in Rat Brain After Sepsis

et al. 2009

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The pathogenesis of sepsis is characterized by an overwhelming systemic inflammatory response that can lead to multiple organ failure. Considering that we have recently demonstrated that mitochondrial respiratory chain and creatine kinase (CK) are altered in the brain of rats after cecal ligation and perforation (CLP) and that a combination of N-acetylcysteine/deferoxamine (NAC/DFX), taurine and RC-3095 were shown to be an effective treatment of sepsis, we investigated whether the alterations of these enzymes may be reversed by these drugs. The results demonstrated that CLP inhibited complexes I and II, and that all the treatments were able to reverse this inhibition in all brain areas studied in the present work. On the other hand, complexes III and IV were not affected by sepsis neither by any of the treatments. An increase in CK activity in brain of rats 12 h after CLP was also verified; the administration of NAC/DFX and taurine reversed the increase in CK activity in hippocampus, cerebral cortex, cerebellum and striatum. On the other hand, RC-3095 significantly decreased CK activity, when compared to sham group in all brain areas studied. This is a preliminary study which showed beneficial effects of the treatments we proposed.

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Protective effect of N-acetylcysteine and deferoxamine on carbon tetrachloride-induced acute hepatic failure in rats

Abstract: Our data provide the first experimental demonstration that N-acetylcysteine plus deferoxamine reduces mortality rate, decreases oxidative stress, and limits inflammatory infiltration and hepatocyte necrosis induced by CCl4 in the rat.

Cited by 74 publications

References 31 publications

Effect of Chitobiose and Chitotriose on Carbon Tetrachloride-Induced Acute Hepatotoxicity in Rats

Effect of Chitobiose and Chitotriose on Carbon Tetrachloride-Induced Acute Hepatotoxicity in Rats

Heme oxygenase‐1: a new drug target in oxidative tissue injuries in critically ill conditions

Effects of N-Acetylcysteine/Deferoxamine, Taurine and RC-3095 on Respiratory Chain Complexes and Creatine Kinase Activities in Rat Brain After Sepsis

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