Alcohol and Aldehyde Dehydrogenase Activity.

Endogenous ADH and ALDH activity in naive Rxfp3 KO (n = 7) and WT (n = 5) liver samples and liver preparations from Rxfp3 KO (n = 6) and WT (n = 6) mice that chronically consumed alcohol (5%-20% v/v) for 10 weeks, as measured by substrate-dependent increase in NADH absorbance. Nicotinamide adenine dinucleotide (β-NADH) was produced from the reduction of β-NAD+. (a) Increase in β-NADH as a result of ADH activity in the cytosolic fraction over various assay ethanol (Eth) concentrations. (b) Impact of pyrazole (Pyr; 10 mM), a specific ADH inhibitor, on the increase in β-NADH produced by the addition of 10 mM ethanol, the assay ethanol concentration that elicited maximal ADH activity. (c) Increase in β-NADH as a result of ALDH activity in the mitochondrial fraction over various assay acetaldehyde (Ace) concentrations. (d) Impact of disulfiram (Dis; 0.1 mM), a specific ALDH inhibitor, on the increase in β-NADH produced by the addition of 10 mM acetaldehyde, the assay acetaldehyde concentration that elicited maximal ALDH activity. Data are presented as mean ± S.E.M.