This can be summarized as follows: Acetaldehyde + NAD+ + Coenzyme A ↔ Acetyl-CoA + NADH + H+ In humans, there are three known genes which encode this enzymatic activity, ALDH1A1, ALDH2, and the more recently discovered ALDH1B1 (also known as ALDH5).

Furthermore, the preceding sequence Gln-Gly-Gln-Cys is conserved in both isozymes for both human and horse, which is consistent with Cys-302 being crucial to catalytic function.

[2] As discovered by site-directed mutagenesis, glutamate-268 is a key component of liver acetaldehyde dehydrogenase and is also critical to catalytic activity.

[7] Other symptoms can include severe abdominal and urinary tract cramping, hot and cold flashes, profuse sweating, and profound malaise.

A single point mutation (G → A) at exon 12 of the ALDH2 gene causes a replacement of glutamate with lysine at residue 487, resulting in the ALDH2K enzyme.

[11] The drug disulfiram (Antabuse) prevents the oxidation of acetaldehyde to acetic acid and is used in the treatment of alcoholism.

[13] Metronidazole (Flagyl), which is used to treat certain parasitic infections as well as pseudomembranous colitis, causes similar effects to disulfiram.

Coprine (which is an amino acid found in certain coprinoid mushrooms) metabolizes in vivo to 1-aminocyclopropanol which causes similar effects as well.