Antioxidant enzyme status in biliary obstructed rats: effects of N-acetylcysteine

Pastor, Ana; Collado, Pilar S.; Almar, Mar; González‐Gallego, Javier

doi:10.1016/s0168-8278(97)80183-3

Cited by 139 publications

(130 citation statements)

References 39 publications

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“…In the group treated with NAC, a lesser expression of iNOS was observed, possibly due to a reduction of the inflammatory process triggered by carbon tetrachloride. This decrease is due, as remarked by PASTOR et al (26) , to the direct and indirect antioxidant actions of NAC, inhibiting the expression/liberation of cytokines and the expression of adhesion molecules and of NF B (4) In conclusion, NAC seams to offer protection against hepatic fibrosis in the liver of cirrhotic rats, decreasing lipoperoxidation and iNOS expression and regenerating glutathione levels.…”

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confidence: 65%

“…It presents potent ability to interact directly with oxidant agents, acting as a scavenger of free radicals, and it exerts an indirect effect on the antioxidant mechanism, since it contributes to restore glutathione. This drug is defined as a precursor for the synthesis of this antioxidant enzyme (26) . Glutathione peroxidase is a key enzyme in the antioxidant defense system, and it acts by catalyzing the transformation of hydrogen peroxide into water, being dependent on selenium and reduced glutathione (18) .…”

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confidence: 99%

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

Pereira-Filho

Ferreira

Schwengber

et al. 2008

Arq. Gastroenterol.

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-Background -Hepatic cirrhosis is the final stage of liver dysfunction, characterized by diffuse fibrosis which is the main response to the liver injury. The inhalatory carbon tetrachloride is an effective experimental model that triggers cirrhosis and allows to obtain histological and physiological modifications similar to the one seen in humans. Aim -To investigate the effects of N-acetylcysteine (NAC) on the fibrosis and oxidative stress in the liver of cirrhotic rats, analyzing liver function tests, lipoperoxidation, activity of glutathione peroxidase enzyme, collagen quantification, histopathology, as well as the nitric oxide role. Methods -The animals were randomly in three experimentals groups: control (CO); cirrhotic (CCl4) and CCl4 + NAC. Evaluate the lipid peroxidation, the glutathione peroxidase enzyme, the collagen and the expression of inducible nitric oxide synthase (iNOS). Results -The cirrhotic group treated with N-acetylcysteine showed trough the histological analysis and collagen quantification lower degrees of fibrosis. This group has also shown less damage to the cellular membranes, less decrease on the glutathione peroxidase levels and less expression of inducible nitric oxide synthase when matched with the cirrhotic group without treatment. Conclusion -N-acetylcysteine seams to offer protection against hepatic fibrosis and oxidative stress in cirrhotic rat livers.

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confidence: 65%

mentioning

confidence: 99%

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

Pereira-Filho

Ferreira

Schwengber

et al. 2008

Arq. Gastroenterol.

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“…The BDL model is used as an animal model for secondary biliary cirrhosis and cirrhosis caused by progressive and fatal damage to the liver. This model simulates the effects of the disease present in humans, causing changes in the inflammatory reaction by leaking bile and the subsequent disorganization of parenchymal inflammation, collagen deposition and formation of fibrosis (7,13,20) . Studies by Kontouras et al (14) showed that 15 days after bile duct ligation (BDL), the metabolic and biochemical changes were not fully established.…”

Section: Discussionmentioning

confidence: 99%

Lung and Liver Changes Due to the Induction of Cirrhosis in Two Experimental Models

Ferrari

Tieppo

Rosa

et al. 2013

Arq. Gastroenterol.

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-Context -To evaluate lung and liver changes in two experimental models using intraperitoneal carbon tetrachloride (CCl 4 ) and bile duct ligation (BDL). Methods -Twenty-four male Wistar rats were divided into a control group (CO) and an experimental group (EX). We evaluated the liver transaminases (AST, ALT, AP), arterial blood gases (PaO 2 , PCO 2 and SpO 2 ) and lipid peroxidation by TBARS (substances that react to thiobarbituric acid) and chemiluminescence. We also evaluated the antioxidant enzyme superoxide dismutase (SOD) and histology of lung tissue and liver. Results -There were significant differences in AST, ALT, ALP and PaO 2 between CO group and EX group (P<0.05). The levels of TBARS, chemiluminescence and activity of enzyme superoxide dismutase were increased to different degrees in the CCl 4 groups: CO and in the BDL -EX (P<0.05, respectively). In the lung histology, an increase in the wall thickness of the pulmonary artery and a diameter reduction in the CCl 4 animal model were observed: comparing CO group with EX group, we observed a reduction in thickness and an increase in the diameter of the artery wall lung. Conclusion -Both experimental models have caused liver damage and alterations in the artery wall that are associated with major changes in pulmonary gas exchange.

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“…Following bile duct ligation, there is cholestatic liver injury, with depletion of endogenous antioxidants 1,2 and increased levels of markers of oxidant injury. 1,3 This is followed by the development of ductular proliferation and fibrosis, and is associated with the development of portal hypertension and a hyperdynamic circulation, characterized by a high cardiac output and low systemic vascular resistance. Previous studies have shown protective effects of antioxidants on liver damage in this model as assessed by biochemical and histological parameters, 1,4,5 and also a moderate reduction in portal pressure (PP).…”

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confidence: 99%

“…cal and histological parameters, 1,4,5 and also a moderate reduction in portal pressure (PP). 6 The hyperdynamic circulation that occurs in this model following the development of biliary cirrhosis is central to the development of many of the complications that occur in advanced liver disease, including ascites and renal dysfunction, portal hypertension, and the hepatopulmonary syndrome.…”

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confidence: 99%

Lipoic Acid Prevents Development of the Hyperdynamic Circulation in Anesthetized Rats With Biliary Cirrhosis

et al. 1999

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Chronic bile duct ligation is associated with the development of oxidant injury, biliary cirrhosis, portal hypertension, and a hyperdynamic circulation. We have previously demonstrated that the hyperdynamic circulation in the partial portal vein-ligated rat can be prevented by the administration of N-acetylcysteine. To extend these findings, we have examined the effect of lipoic acid, a thiolcontaining antioxidant, on hemodynamics, oxidative stress, and nitric oxide (NO) production in bile duct-ligated (BDL) cirrhotic rats. Lipoic acid was given continuously in drinking water to normal and BDL rats; control rats received ordinary drinking water, and animals were studied at 24 days following surgery. Lipoic acid prevented the development of the hyperdynamic circulation (cardiac index [CI]: 15.7 ؎ 2.0 vs. 29.5 ؎ 2.1 mL и min ؊1 и 100 g ؊1 ; P F .05) and significantly attenuated the rise in portal pressure (PP) (12.7 ؎ 0.8 vs. 15.2 ؎ 0.5 mm Hg; P F .05). Hepatic nitric oxide synthase (NOS) activity and plasma nitrite/nitrate concentration increased significantly following bile duct ligation, and both of these were prevented by lipoic acid. Lipoic acid had no effect on the biochemical or histological parameters of liver function in the cirrhotic group. We conclude that lipoic acid prevents the development of the hyperdynamic circulation in the rat model of biliary cirrhosis, and that this is associated with decreased synthesis of NO. (HEPATOLOGY 1999;29:1358-1363.)Chronic bile duct ligation leads to biliary cirrhosis within 3 to 4 weeks in the rat. Following bile duct ligation, there is cholestatic liver injury, with depletion of endogenous antioxidants 1,2 and increased levels of markers of oxidant injury. 1,3 This is followed by the development of ductular proliferation and fibrosis, and is associated with the development of portal hypertension and a hyperdynamic circulation, characterized by a high cardiac output and low systemic vascular resistance. Previous studies have shown protective effects of antioxidants on liver damage in this model as assessed by biochemical and histological parameters, 1,4,5 and also a moderate reduction in portal pressure (PP). 6 The hyperdynamic circulation that occurs in this model following the development of biliary cirrhosis is central to the development of many of the complications that occur in advanced liver disease, including ascites and renal dysfunction, portal hypertension, and the hepatopulmonary syndrome. We previously demonstrated that chronic administration of N-acetylcysteine prevents development of the hyperdynamic circulation following partial portal vein ligation 7 and is accompanied by decreased plasma concentrations of the metabolic products of nitric oxide (NO), nitrite and nitrate. However, in the above study, N-acetylcysteine was given twice daily by intraperitoneal injection, because it has a limited oral bioavailability. Therefore, to extend these studies to a cirrhotic model, we have used the sodium salt of lipoic acid, a thiol-containing antioxidant with g...

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Antioxidant enzyme status in biliary obstructed rats: effects of N-acetylcysteine

Cited by 139 publications

References 39 publications

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

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

Lung and Liver Changes Due to the Induction of Cirrhosis in Two Experimental Models

Lipoic Acid Prevents Development of the Hyperdynamic Circulation in Anesthetized Rats With Biliary Cirrhosis

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