Abstract Background Drug-induced hepatotoxicity is one of the most important causes liver dysfunction. Acetaminophen (paracetamol) an analgesic-antipyretic drug generally considered safe but its overdose may cause toxicity. Marine macro-algae (seaweeds) especially brown seaweeds possess unique biological activities including hepatoprotective potential. The current study focused on effect differ...

background: using human skin-fibroblast cell line hf2ff, the efficacy of some drugs was evaluated against sulfur mustard (sm) cytotoxicity. the drugs were the sulfhydryl containing molecule including n-acetylcysteine (nac), 2-oxo-thiazolidine-4-carboxylate (otc) and acetaminophen as glutathione (gsh) stimulator pathway. methods: the protective effects of nac (0.1 mm), otc (1.8 mm), and acetamin...

The mechanism by which acetaminophen (APAP) causes liver damage evokes many aspects drug metabolism, oxidative chemistry, and genetic-predisposition. In this study, we leverage the relative resistance of female C57BL/6 mice to APAP-induced liver damage (AILD) compared to male C57BL/6 mice in order to identify the cause(s) of sensitivity. Furthermore, we use mice that are either heterozygous (HZ...

Despite pathophysiological similarities to alcoholic liver disease, susceptibility to acetaminophen hepatotoxicity in metabolic syndrome-related nonalcoholic steatohepatitis (NASH) has not been well elucidated. In this study, therefore, we investigated acetaminophen-induced liver injury in KK-A(y) mice, an animal model of metabolic syndrome. Twelve-week-old male KK-A(y) and C57Bl/6 mice were in...

The hepatotoxicity of the analgesic acetaminophen is believed to be mediated by covalent binding to critical proteins. Radiolabeled 3'-hydroxyacetanilide, a regioisomer of acetaminophen, covalently binds to proteins at levels similar to those of acetaminophen, but without toxicity. Covalent binding has recently been detected by Western blot to a 50-kDa microsomal protein that comigrated with CY...