Acetaminophen Hepatotoxicity and Cytokines.
نویسندگان
چکیده
منابع مشابه
Acetaminophen-related hepatotoxicity.
Acetaminophen (APAP) is the leading worldwide cause of drug overdose and acute liver failure (ALF). Single overdose ingestion and therapeutic misadventure may cause hepatotoxicity. Several factors, such as concomitant alcohol use or abuse, concurrent medications, genetic factors, and nutritional status, can influence the susceptibility and severity of APAP hepatotoxicity. Early manifestations o...
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In this issue of Blood, Miyakawa et al show that platelets and protease-activated receptor (PAR)-4 contribute to acetaminophen (APAP)-induced liver damage. Using various strategies in a mouse model of APAP overdose, the authors demonstrate that platelets participate in the progression of liver damage, and that the direct thrombin inhibitor lepirudin and PAR-4 deficiency attenuate hepatotoxicity...
متن کاملAcetaminophen-induced hepatotoxicity.
The analgesic acetaminophen causes a potentially fatal, hepatic centrilobular necrosis when taken in overdose. The initial phases of toxicity were described in Dr. Gillette's laboratory in the 1970s. These findings indicated that acetaminophen was metabolically activated by cytochrome P450 enzymes to a reactive metabolite that depleted glutathione (GSH) and covalently bound to protein. It was s...
متن کاملSevere hepatotoxicity after therapeutic doses of acetaminophen.
BACKGROUND Acetaminophen overdose is a frequent cause of acute liver failure. Controversy exists over the rare association of severe hepatotoxicity or acute liver failure with therapeutic doses of acetaminophen. CASE SUMMARY A 45-year-old white man weighing 85 kg with asymptomatic HIV, hepatitis B virus, and hepatitis C virus (HCV) infection presented with signs of severe hepatotoxicity: aspa...
متن کاملSIRT3-dependent deacetylation exacerbates acetaminophen hepatotoxicity.
Acetaminophen/paracetamol-induced liver failure--which is induced by the binding of reactive metabolites to mitochondrial proteins and their disruption--is exacerbated by fasting. As fasting promotes SIRT3-mediated mitochondrial-protein deacetylation and acetaminophen metabolites bind to lysine residues, we investigated whether deacetylation predisposes mice to toxic metabolite-mediated disrupt...
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ژورنال
عنوان ژورنال: Drug Metabolism and Pharmacokinetics
سال: 2001
ISSN: 0916-1139
DOI: 10.2133/dmpk.16.151