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Isoniazid genetic susceptibility factors

Human CYP2E1 is one of the most efficient P450s to catalyze the oxidation of acetaminophen to NAPQI (157-159). Ethanol and isoniazid cause a time-dependent inhibition and induction of acetaminophen oxidation to NAPQI in humans (160,161) that can decrease risk for hepatotoxicity over the interval of concurrent administration and increase risk for hepatotoxicity a few hours after removal of ethanol or isoniazid. The latter induction phase of CYP2E1 may, in part, be responsible for cases of acetaminophen hepatotoxicity associated with the use of ethanol (162-165) or isoniazid (166-168). However, the induction is modest (2- to 3-fold) therefore, other susceptibility factors, genetic and others such as decreased glutathione stores and nutritional status, are likely to play an important role in some individuals (169-174). [Pg.698]

Susceptibility factors Genetic Hepatic metabolism of isoniazid involves acetylation to acetylisoniazid by 7V-acetyltransferase... [Pg.483]


See other pages where Isoniazid genetic susceptibility factors is mentioned: [Pg.559]    [Pg.346]    [Pg.428]    [Pg.432]    [Pg.1018]    [Pg.688]    [Pg.9]    [Pg.10]    [Pg.168]   
See also in sourсe #XX -- [ Pg.12 , Pg.257 ]




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