Alcohol withdrawal syndrome: assessment and treatment with the use of the Clinical Institute Withdrawal Assessment for Alcohol-revised.

Alcoholism is a chronic, complex disease and addictive disorder. Sudden cessation of alcohol consumption can lead to alcohol withdrawal, an acute process with devastating and potentially life-threatening consequences. Assessment of alcohol withdrawal is key to a successful outcome.

Enhancement of rat liver microsomal metabolism of azoxymethane to methylazoxymethanol by chronic ethanol administration: similarity to the microsomal metabolism of N-nitrosodimethylamine.

We compared the metabolism of azoxymethane (AOM) and of N-nitrosodimethylamine (NDMA) by liver microsomes obtained from male F344 rats pair-fed for 3 weeks either a control liquid diet or an isocaloric liquid diet containing ethanol at a concentration of 6.6% by volume. High-performance liquid chromatographic analysis of the products of the microsomal metabolism of AOM showed that methylazoxymethanol was the only primary metabolite.

Differential effects of 4-iodopyrazole and 3-methylpyrazole on the metabolic activation of methylazoxymethanol to a DNA methylating species by rat liver and rat colon mucosa in vivo.

Using a hybrid ion-exchange reverse phase HPLC system, we found that F344 rat liver microsomes, in the presence of an NADPH-generating system, can metabolize methylazoxymethanol (MAM), a colon and liver carcinogen, to methanol and formic acid. This is in contrast to the spontaneous decomposition of MAM which yields methanol and formaldehyde. The metabolism of MAM by rat liver microsomes is sensitive to inhibition by carbon monoxide as well as to inhibition by 3-methylpyrazole (3-MeP) and 4-iodopyrazole (4-IP), with 4-IP being more potent in this respect than 3-MeP.

Differential susceptibility of rat and guinea pig colon mucosa DNA to methylation by methylazoxymethyl acetate in vivo.

Methylazoxymethanol (MAM) and methylazoxymethyl acetate (MAMOAc) are powerful colon carcinogens in rats, mice and hamsters. In contrast, these agents are not carcinogenic to the colon of the guinea pig. To probe the mechanism responsible for this species difference, we determined the levels of DNA methylation in the livers and colon mucosae of F344 rats and strain-2 guinea pigs after the s.