Role of N-acetylcysteine on fibrosis and oxidative stress in cirrhotic rats

Pereira-Filho, Gustavo de Azambuja; Ferreira, Clarissa Santos; Schwengber, Alex; Marroni, Cláudio Augusto; Zettler, Claudio Galleano; Marroni, Norma Possa

doi:10.1590/s0004-28032008000200013

Cited by 55 publications

(21 citation statements)

References 37 publications

(21 reference statements)

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“…When the liver lesion parameters (AST and ALT) were analyzed, only the NAC-treated group presented a reduction in the AST plasma levels compared to the septic group, demonstrating its hepatoprotective role. This protective ability has been previously described in the literature, using carbon tetrachloride (CCl 4 )-induced cirrhotic animals, suggesting a protective effect related to the glutathione peroxidase, an endogenous antioxidant enzyme key in combating the ROS [49]. To verify that NAC would increase the cellular antioxidant defenses, we have also measured hepatic reduced glutathione levels.…”

Section: Discussionsupporting

confidence: 56%

Effect of N-Acetylcysteine and Fructose-1,6-Bisphosphate in the Treatment of Experimental Sepsis

et al. 2010

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Sepsis is a syndrome caused by uncontrolled systemic inflammatory response of the individual, which represents a serious epidemiological problem worldwide. The aim of this study was to investigate the effect of N-acetylcysteine (NAC) and fructose-1,6-bisphosphate (FBP) in the treatment of experimental sepsis. We used rats that were divided into five experimental groups: normal control (not induced), septic control (induced using a capsule with non sterile fecal content and Escherichia coli), treated with FBP (500 mg/kg i.p.), treated with NAC (150 mg/kg i.p.), and treated with the combination of FBP with NAC. In the group treated with NAC, 16.68% of the mice survived, the FBP reduced the mortality of mice during the acute stage of the disease and increased the animals' survival time in 33.34%, and the combination of drugs had no effect. Our results show that NAC prevented the mortality of animals after septic induction. These data confirm the validity of the use of NAC in the treatment of sepsis. Our data also show that the synergistic action with FBP does not improve the picture.

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“…Oxidative stress plays an important role in the activation of hepatic stellate cells. Antioxidants such as albumin, can prevent this activation and their subsequent role in liver fibrogenesis 7 . Studies show that there is a decrease in plasma levels of albumin in rats with common bile duct ligation, although they have conflicting results 8,9 , with two weeks of the beginning of the experiments, probably due to increased capillary permeability and a lack of compensation by increasing its hepatic synthesis, to a decrease of the same, and also by an increase in plasma volume after four weeks of the beginning of the experiment 10 .…”

Section: Introductionmentioning

confidence: 99%

Effects of albumin administration in serum liver enzymes of rats in the presence of extrahepatic biliary obstruction

Lessa¹,

Rangel²,

Junior³

et al. 2011

Acta Cir. Bras.

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PURPOSE:To study the influence of albumin on changes of liver function in the extrahepatic biliary obstruction through an experimental model in rats. METHODS: Sixty rats were divided into four groups: Group C (Control): 6 animals. Group M (Fictitious Operation): 18 rats underwent laparotomy and handling of the bile ducts; Groups O (extrahepatic biliary obstruction) and A (Treated with 2% albumin): 18 animals in each group underwent ligation of the ductus liver; The animals in groups M, O and A were divided into three subgroups of 6 animals each to be killed in the 7, 14 and 21 days postoperative (POD). Blood was drawn for determination of total bilirubin (TB), indirect bilirubin (IB), direct bilirubin (DB), alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT). RESULTS: On POD 7, BI levels were 4.5 mg / dl in group O and 2.1 mg / dl in group A (p = 0.025). On the 14th POD, the levels of PA were 1185.2 U / l in the group and O 458.3 U / l in group A (p = 0.004). ALT levels were 101.7 U / l in the group O and 75.7 U / l in group A (= 0.037). On POD 21, the levels of ALP were 1069.5 U / l in the group O and 468.3 U / l in group A (p = 0, 004). CONCLUSION: The administration of albumin reduced the serum levels of bilirubin in the 7th day of supplementation

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“…Ko et al, 1995 reported that certain natural extracts containing antioxidants protect against the CCl4-induced increased lipid peroxide levels and impairment in hepatic GSH status.Hepatic malondialdehyde (MDA) levels were also highly significantly increased in CCl4 treated group, showing an increased oxidative stress compared to control group. The increased MDA level suggests enhanced lipid peroxidation leading to tissue damage and failure of antioxidant defense mechanisms to prevent formation of excessive free radicals as described by (Pereira- Filho et al, 2008) and confirmed by (Kim et al, 2010).…”

Section: Discussionmentioning

confidence: 55%

Hepatotoxicity Implies Chemical-Driven Liver Damage Induced By Certain Medicinal and Other Chemical Agents

2015

American Research Journal of Pharmacy

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Abstract:There are increasing evidences that free radicals and reactive oxygen species play a crucial role in the various steps that initiate and regulate the progression of liver diseases. Oxidative stress in hepato-toxicity resulting from increased generation of reactive oxygen species (ROS) and other reactive intermediates as well as by decreased efficiency of antioxidant defenses actively contributes to excessive tissue remodeling. Drug-induced nephropathy is reported to be the third most common cause of acute renal failure in hospitalized patients. Excess ROS production and depressed antioxidant defence mechanism are responsible for nephrotoxicity.So, pharmacological studies in this work were done to evaluate: presence of protective effects of an antioxidant Hesperedine on carbon tetrachlorideinduced hepatic toxicity and nephro-toxicity, to evaluate its effects on oxidants and antioxidants parameters and to evaluate its effect on kidney and liver functions and histo-pathological changes.Liver enzymes level AST and ALT : was increased significantly in rats treated with CCl4 but decreased significantly in rats treated with antioxidant HDN (100 mg/ kg/ day) and in rats treated with antioxidant HDN (200 mg/ kg/ day) . in comparison between antioxidant treated rats groups liver enzymes level was decreased significantly in rats treated with antioxidant HDN (200 mg/ kg/ day) than in rats treated with antioxidant HDN (100 mg/ kg/ day) .Serum creatinine level: was increased insignificantly in rats treated with CCl4 but decreased insignificantly in rats treated with antioxidant HDN (100 mg/ kg/ day) and in rats treated with antioxidant HDN (200 mg/ kg/ day). in comparison between antioxidant treated rats groups liver enzymes level was decreased insignificantly in rats treated with antioxidant HDN (200 mg/ kg/ day) than in rats treated with antioxidant HDN (100 mg/ kg/ day) . So, we recommend uses of antioxidant Hesperedine as it has a valuable role in improvement of liver functions and as a prophylactic of hepatic and renal tissues against toxicity achieved by free radicals.

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“…Many experimental studies are also available using NAC on ROS-mediated hepatotoxicity induced by CCl 4 [10,11,24] , as it is the case in the present study. Experimental evidence indicates NAC is able to enhance the intracellular biosynthesis of GSH [9][10][11][12]24] , and therefore NAC increases GSH levels and replenish GSH store [8] .…”

Section: Discussionmentioning

confidence: 91%

The Effect of N-acetylcysteine on Pyrrolized Protein, Lipid Hydroperoxide and Thiol Levels in the Carbon Tetrachloride Hepatotoxicity

Yazici¹,

Kose²,

Delibas³

et al. 2016

ijps

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Yazici, et al.: N-acetylcysteine Effect on Oxidative Stress in RatsThis study was performed, on the rat model, to form oxidative stress by carbon tetrachloride and to reveal the relationship between toxicity and oxidative/thiol stresses through lipid/protein oxidation and to investigate the effects of N-acetylcysteine on the hepatotoxicity induced oxidative stress. Wistar albino male rats were divided into four groups as carbon tetrachloride, N-acetylcysteine, carbon tetrachloride-N-acetylcysteine and control, each of ten rats. Carbon tetrachloride (1.0 ml, 800 mg/kg; single dose) and N-acetylcysteine (200 mg; three doses) were intraperitoneally applied to corresponding groups as per kg of rat weight. Hepatotoxicity was identified with histopathological methods. Besides the thiol levels in plasma/tissue samples, pyrrolized protein and total lipid hydroperoxide levels in serum samples were measured. Carbon tetrachloride-induced hepatotoxic lesions remarkably improved in the presence of N-acetylcysteine. There was no significant difference between control and N-acetylcysteine groups, in terms of parameters measured in serum/plasma and tissue samples. When compared to these groups, pyrrolized protein and total lipid hydroperoxide levels were found to be higher; whereas plasma/tissue thiol levels lower in the carbon tetrachloride group. N-acetylcysteine in combination with carbon tetrachloride significantly lowered pyrrolized protein and total lipid hydroperoxide levels, and increased thiol levels, so that the values were reached to those of control and N-acetylcysteine groups. As reflected by higher pyrrolized protein and total lipid hydroperoxide, and lower thiol levels, enhanced free radical production in the carbon tetrachloride hepatotoxicity may lead to oxidative and thiol stresses mediated lipid/protein oxidation. In addition, N-acetylcysteine, a powerful antioxidant, may be added as a thiol source to the treatment protocols of several diseases whose pathogenesis is of oxidative and thiol stress.

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“…NAC exerts its antioxidant action by facilitating reduced glutathione biosynthesis and scavenging the reactive oxygen species formed during oxidative stress [18]. Many are the reports of beneficial effects of NAC such as renoprotective [19], antiangiogenic [20], anticancer [21], hepatoprotective [22], antifibrotic [23], as chelating agent in metal poisoning treatment [24], and as neuroprotective [25]. However, few are the reports about NAC direct effects on cerebral AChE activity.…”

Section: Introductionmentioning

confidence: 99%

N-Acetyl Cysteine Decreases Mice Brain Acetyl Cholinesterase Activity: An In Vitro Kinetic Study

M¹,

J²,

L³

et al. 2016

Enz Eng

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Here a kinetic in vitro study of n-acetylcysteine (NAC) on mouse brain acetylcholinesterase (AChE) activity was performed, as well, few studies with the aim to improve Ellman's methodology based on SH contain compounds. The ideal 5,5´-dithio-bis-2-nitrobenzoic acid (DTNB) concentration was of 0.3 mM and ideal medium pH=7.4. AChE demonstrated linear activity for all acetylthiocholine iodide (ATCh) tested concentrations (0.025-0.450 mM). To avoid any DTNB-NAC interaction interference, 30 sec were applied to the assay method, so-called stabilization time. No differences in Km (mM) for all NAC tested concentrations were observed. At the NAC concentrations started from 75 µM significant differences in Vmax were achieved, characterizing a non-competitive type of AChE activity inhibition induced by NAC. In conclusion, NAC decreased AChE activity in vitro and the Ellman method was reliable for the analysis of AChE activity when inhibited by compounds that contain SH groups.

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Role of N-acetylcysteine on fibrosis and oxidative stress in cirrhotic rats

Cited by 55 publications

References 37 publications

Effect of N-Acetylcysteine and Fructose-1,6-Bisphosphate in the Treatment of Experimental Sepsis

Effects of albumin administration in serum liver enzymes of rats in the presence of extrahepatic biliary obstruction

Hepatotoxicity Implies Chemical-Driven Liver Damage Induced By Certain Medicinal and Other Chemical Agents

The Effect of N-acetylcysteine on Pyrrolized Protein, Lipid Hydroperoxide and Thiol Levels in the Carbon Tetrachloride Hepatotoxicity

N-Acetyl Cysteine Decreases Mice Brain Acetyl Cholinesterase Activity: An In Vitro Kinetic Study

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