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Peak blood alcohol concentrations may be estimated by dividing the amount of ethanol ingested by the body weight of the individual and correcting for water dilution. [4] For time-dependent calculations, Swedish professor Erik Widmark developed a model of alcohol pharmacokinetics in the 1920s. [ 120 ]
The last steps of alcoholic fermentation in bacteria, plants, and yeast involve the conversion of pyruvate into acetaldehyde and carbon dioxide by the enzyme pyruvate decarboxylase, followed by the conversion of acetaldehyde into ethanol. The latter reaction is again catalyzed by an alcohol dehydrogenase, now operating in the opposite direction.
The microsomal ethanol oxidizing system (MEOS) is an alternate pathway of ethanol metabolism that occurs in the smooth endoplasmic reticulum in the oxidation of ethanol to acetaldehyde. While playing only a minor role in ethanol metabolism in average individuals, MEOS activity increases after chronic alcohol consumption.
Individuals with two copies of the ALDH2*2 allele are known to have high blood acetaldehyde levels and experience “hangover” symptoms such as heart palpitations for longer durations, even with low alcohol consumption. [15] [16] [2] Individuals who work with DMF have shown a dose-related increase in alcohol intolerance complaints. [26]
The best-known consequence of ALDH2 dysfunction is in relation to the consumption of ethanol. People heterozygous or homozygous for the ALDH2*2 metabolize ethanol to acetaldehyde normally but metabolize acetaldehyde poorly. As a result, they accumulate increased levels of acetaldehyde after consumption of alcoholic beverages.
In the liver, ethanol is converted into acetyl CoA by a two step process. In the first step, ethanol is converted to acetaldehyde by alcohol dehydrogenase. In the second step, the acetaldehyde is converted to acetyl CoA by acetaldehyde dehydrogenase. Acetaldehyde is more toxic than alcohol and is responsible for many hangover symptoms. [5]
After alcohol intake under the influence of disulfiram, the concentration of acetaldehyde in the blood may be five to 10 times higher than that found during metabolism of the same amount of alcohol alone. As acetaldehyde is one of the major causes of the symptoms of a hangover, this produces immediate and severe negative reaction to alcohol ...
The idea that acetaldehyde is the cause of the flush is also shown by the clinical use of disulfiram (Antabuse), which blocks the removal of acetaldehyde from the body via ALDH inhibition. The high acetaldehyde concentrations described share similarity to symptoms of the flush (flushing of the skin, accelerated heart rate, shortness of breath ...