Acetaminophen Toxicity

Bartlett, Dana

doi:10.1016/j.jen.2004.01.023

Cited by 26 publications

(19 citation statements)

References 7 publications

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“…APAP hepatotoxicity is the result of a cascade of interrelated biochemical events (Bartlett 2004). In the course of acute liver failure, oxidative stress expressed by oxidant-antioxidant imbalance is profound in liver tissue.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of Indian honey on acetaminophen induced oxidative stress and liver toxicity in rat

et al. 2009

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The present study was undertaken to investigate the protective effect of Indian honey on acetaminophen induced oxidative stress and liver damage in rat. Honey serves as a source of natural medicine, which is effective to reducing the risk of heart disease, liver toxicity and inflammatory processes. The hepatoprotective activity of the Indian honey was determined by assessing levels of Serum transaminases, ALP and total bilirubin. Finally, the effects of the test substances on the antioxidant enzymes of the liver were also studied by assessing changes in the level of reduced glutathione, glutathione peroxidase, catalase and superoxide dismutase. Serum transaminase, ALP and total bilirubin level were significantly elevated and the antioxidant status in liver such as activities of SOD, CAT, GPx and the levels of GSH were declined significantly in APAP alone treated animals. Pretreatment with honey and silymarin prior to the administration of APAP significantly prevented the increase in the serum levels of hepatic enzyme markers and reduced oxidative stress. The histopathological evaluation of the livers also revealed that honey reduced the incidence of liver lesions induced by APAP. Results suggest that the Indian honey protects liver against oxidative damage and it could be used as an effective hepatoprotector against APAP induced liver damage.

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Section: Discussionmentioning

confidence: 99%

Protective effect of Indian honey on acetaminophen induced oxidative stress and liver toxicity in rat

et al. 2009

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“…APAP hepatotoxicity is the result of a cascade of interrelated biochemical events [31,32]. Each of the eventualities, protein oxidation, covalent modification and inhibition of enzyme activity, lipid peroxidation, transnuclear transport of "acetaminophen-binding proteins" and inhibition of protein phosphatase activity, although not of equal importance, probably have a role in the mechanism causing liver damage after APAP intoxication [33,34].…”

Section: Discussionmentioning

confidence: 99%

Recombinant Platelet-Activating Factor–Acetylhydrolase Attenuates Paracetamol-Induced Liver Oxidative Stress, Injury, and Regeneration

et al. 2006

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The aim of this study was to investigate the effects of platelet-activating factor (PAF) inactivator, recombinant PAF-acetylhydrolase (rPAF-AH), on post-paracetamol treatment functional outcome of the liver in the rat. Fifty male Wistar rats were divided into two groups: the control group received a toxic dose of paracetamol (3.5 g/kg body weight [BW]) by gastric tube and the rPAF-AH-treated group received the same dose of paracetamol followed by a dose of rPAF-AH (10 mg/kg BW) intraperitoneally. The animals were sacrificed at time points of 56, 66, 72, 84, and 96 hr after paracetamol treatment. Hepatic injury was evaluated by determination of AST, ALT, and ALP activities and degree of necrosis and apoptosis. Liver regeneration was estimated by [3H]thymidine incorporation into hepatic DNA, liver thymidine kinase activity, and hepatocyte mitotic index. Hepatic levels of malondialdehyde (MDA) and serum cholesterol/high-density lipoprotein cholesterol fraction were also measured as parameters of oxidant-antioxidant balance. The positive effects of rPAF-AH were expressed by (1) reduction of oxidative stress, (2) large decrease in hepatic injury, and (3) diminution of regenerating activity. These results indicate that the use of PAF inactivator enhances the liver's recovery from paracetamol intoxication and attenuates the severity of experimental liver injury, providing important means of improving liver function following paracetamol intoxication.

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“…25 N-acetyl-p-benzoquinone imine (NAPQI) has a direct toxic effect on the liver and on erythrocytes. Low MW toxins such as ethylene glycol (EG), with a MW of 62 Da, There are two main pathways for acetaminophen metabolism: conjugation with sulfate and glucuronide (accounting for 90% of the ingested dose) and metabolism by the cytochrome P-450 oxidase enzyme system (accounting for 5% of ingested dose).…”

Section: Toxin Overviewmentioning

confidence: 99%