Add time:10/01/2019         Source:infona.pl

Acetaminophen (APAP) hepatotoxity is due to metabolic activation to a toxic reactive metabolite via the hepatic mixed function oxidases. Potassium ethylxanthate (cas 140-89-6) (PEX) has been shown to be a potent inhibitor of cytochrome P-450-mediated drug matabolism in experimental animals, both in vivo and in vitro. The effect of PEX on the APA toxity was studied in male albino mice and in fresh isolated mouse hepatocytes. The hepatotoxicity of APAP (737 mg/kg, orally) was evaluated by the changes in serum AST and ALT, liver histology, GSH content, TBA-reactive substances, cytochrome P-450 content and some drug metabolising enzyme activities. The administration of PEX (80 mg/kg, orally) one hour before or simultaneously with APAP, significantly reduced the hepatic injury to nearly the control level. Hepatocytes exposed to APAP (0.5, 1.0 and 5.0 mM) exhibited concentration and time dependent GSH depletion followed by increased LDH leakage. These effects were reduced by PEX (0.1 mM). PEX has no effect by itself on the GSH level in vivo and in vitro. PEX decreases APAP hepatotoxity probably by reducing the amount of APA toxic metabolite(s) formed.

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