<i>N</i>-Acetyl cysteine and erdosteine treatment in acetaminophen-induced liver damage

Sarıtaş, Ayhan; Kandiş, Hayati; Baltaci, Davut; Yıldırım, Ümran; Kaya, Halil; Karakuş, Ali; Çolakoğlu, Serdar; Memişoğulları, Ramazan; Kara, İsmail Hamdi

doi:10.1177/0748233712463780

Cited by 14 publications

(20 citation statements)

References 34 publications

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“…We were therefore unable to compare our results with those of previous studies. However, in an experimental rat study of paracetamolinduced hepatotoxicity, rats treated with paracetamol were reported to have higher TOS levels and lower TAS levels than the controls (14). Additionally, TOS levels have been shown to increase in rats treated with methotrexate, while TAS levels remained unchanged (13).…”

Section: Histopathological Assessmentmentioning

confidence: 99%

“…It has been reported that oxidative stress is the common pathophysiological pathway of most types of intoxications. The role of increased oxidative stress has been demonstrated in experimental organophosphate, paracetamol, and methotrexate models (12)(13)(14). Recent in vitro and in vivo studies have suggested that oxidative stress is probably responsible for α-amanitininduced hepatotoxicity in studies (7,(15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 99%

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The role of oxidative stress in α-amanitin-induced hepatotoxicityin an experimental mouse model

et al. 2017

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Background/aim: This study aimed to evaluate oxidative stress markers of liver tissue in a mouse α-amanitin poisoning model with three different toxin levels. Materials and methods:The mice were randomly divided into Group 1 (control), Group 2 (0.2 mg/kg), Group 3 (0.6 mg/kg), and Group 4 (1.0 mg/kg). The toxin was injected intraperitoneally and 48 h of follow-up was performed before sacrifice.Results: Median superoxide dismutase activities of liver tissue in Groups 3 and 4 were significantly higher than in Group 1 (for both, P = 0.001). The catalase activity in Group 2 was significantly higher, but in Groups 3 and 4 it was significantly lower than in Group 1

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Section: Histopathological Assessmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The role of oxidative stress in α-amanitin-induced hepatotoxicityin an experimental mouse model

et al. 2017

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“…Erdosteine also has an antiinflammatory effect which is mediated through the inhibition of LPS-induced NF-kB activation 4 . The hepatoprotective effects of erdosteine against acetaminophen-induced liver damage, cyclosporine-A-induced hepatotoxicity, experimental biliary obstruction, cisplatininduced hepatic oxidant injury, doxorubicininduced hepatotoxicity, and vancomycininduced oxidative stress in the rat liver have been shown in previous studies [5][6][7][8][9][10][11] . Erdosteine has beneficial effects on ischemia-reperfusion injury in various organs including lung, brain, kidney, intestines, ovaries, and spinal cord [12][13][14][15][16][17] .…”

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confidence: 69%

Erdosteine ameliorates the harmful effects of ischemia-reperfusion injury on the liver of rats

et al. 2017

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1 AbstractPurpose: To investigate the potential protective effects of erdosteine against the harmful effects of ischemia-reperfusion injury on the liver in an experimental rat model. Methods: Forty rats were divided into 4 groups. In the sham group, only the hepatic pedicle was mobilized. No other manipulation or treatment was performed. In the other groups, ischemia was achieved by clamping the hepatic pedicle for 60 min. After that, 90 min reperfusion was provided. In the control group, no treatment was given. In the perioperative treatment group, 100 mg/kg erdosteine was administered 2 hours before ischemia induction. In the preoperative treatment group, 100 mg/kg/day erdosteine was administered daily for ten days before the operation. At the end of the procedures, blood and liver samples were obtained for biochemical and histopathological assessment. Results: Treatment with erdosteine ameliorated the histopathological abnormalities when compared with the control group. Furthermore, this treatment significantly decreased the serum liver function test values. It was also found that erdosteine ameliorated the oxidative stress parameters in both the perioperative and preoperative treatment groups. Conclusion: The current study is the first to have shown the favorable effects of erdosteine on the harmful effects of experimental hepatic ischemia-reperfusion injury.

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“…Based on these concepts, we found that apoptotic hepatocytes were significantly increased in the liver of rats after acetaminophen treatment and the hepatocyte apoptosis was significantly reduced by both curcumin and N-acetylcysteine treatment as detected by quantitative analysis of the immunohistochemical study of p53 antigen. A recent study showed that curcumin exerts a potent anti-apoptotic effect by decreasing the expression of pro-apoptotic genes (Bax, caspase-3) and increasing the expression of anti-apoptotic genes (Bcl-XL) [42]. NAC attenuates lipopolysaccharide induced apoptotic liver injury via its strong ROS scavenging and anti-apoptotic effects [46].…”

Section: Discussionmentioning

confidence: 99%

“…In this study the oxidative damage caused by acetaminophen overdose was significantly attenuated by administrating curcumin and N-acetylcysteine. The most accepted explanation for the protective actions of N-acetylcysteine is that it serves as a source of L-cysteine for GSH synthesis and, hence, it can help the detoxification of NAPQI before this reactive metabolite can initiate hepatic injury [41,42] and acts as a scavenger of ROS that it supports mitochondrial energy metabolism [43]. Likewise to N-acetylcysteine, curcumin could save against free radical mediated oxidative stress by scavenging for free radicals that restricts lipid peroxidation incorporated in membrane damage.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Curcumin versus N-acetylcystein on Acetaminophen Induced Hepatotoxicity in Adult Albino Rats

AB¹,

HE²

2015

J Cytol Histol

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Curcumin exerted hepatoprotective influences on various animal models of liver injury such as carbon tetrachloride, endotoxin and thioacetamide. This Study aimed to investigate the protective effects of curcumin as compared to N-acetylcysteine in the rat model of acetaminophen induced hepatotoxicity. 55 albino rats were divided into four groups: group (control group). Group II received acetaminophen. Group III received both acetaminophen and N-acetylcysteine and Group IV received both acetaminophen and curcumin. At the end of the experiment, liver specimens were processed for histological study by light microscope and stained immunohistochemically for detection of apoptosis in hepatic cells by using anti p53 and the oxidative damage by anti-inducible nitric oxide synthase (anti iNOS). Serum levels of liver injury markers were assessed as well as the levels of malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) activity were determined in all dissected tissues. Histological examination of liver sections of acetaminophen treated group revealed degeneration, cytoplasmic vacuolation and hydropic necrosis of hepatocytes. The central and the portal veins were dilated and congested and invading infiltrative inflammatory cells were appeared in association with significant increase in p53 and iNOS positive cells. Significant rise in serum levels of liver injury markers and MDA in liver tissues were recorded. However, levels of GSH and SOD were significantly decreased. Both curcumin and N-acetylcysteine resolved most of these morphological, immunohistochemical and biochemical alterations. Curcumin has protective effect similar to N-acetylcysteine against liver damage induced by acetaminophen in rats by reducing oxidative stress and apoptosis.

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N-Acetyl cysteine and erdosteine treatment in acetaminophen-induced liver damage

Abstract: The present study demonstrated that, in the prevention of liver damage induced by acetaminophen intoxication, an early treatment with a single dose of erdosteine was beneficial instead of NAC administration.

Cited by 14 publications

References 34 publications

The role of oxidative stress in α-amanitin-induced hepatotoxicityin an experimental mouse model

The role of oxidative stress in α-amanitin-induced hepatotoxicityin an experimental mouse model

Erdosteine ameliorates the harmful effects of ischemia-reperfusion injury on the liver of rats

Protective Effect of Curcumin versus N-acetylcystein on Acetaminophen Induced Hepatotoxicity in Adult Albino Rats

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