Asaad M M, Barry H, Clarke D E, Dixit B N
Br J Pharmacol. 1974 Feb;50(2):277-82. doi: 10.1111/j.1476-5381.1974.tb08573.x.
1 The effect of a wide range of ethanol concentrations (v/v) on indoleacetic acid (IAA) formation from the oxidative deamination of tryptamine was studied in vitro, in rat whole liver homogenate.2 IAA production was inhibited progressively by ethanol in concentrations between 0.01% to 0.2%, but the inhibition declined when the ethanol concentration was increased further to 6%.3 Ethanol-induced inhibition of IAA formation was only partially reversed by excess aldehyde dehydrogenase, whereas reductions in IAA formation were completely prevented by pyrazole or ethanol (6% and 10%) itself.4 Excess nicotinamide adenine dinucleotide failed to alter the inhibitory effect of ethanol and no evidence was obtained for inhibition of monoamine oxidase by ethanol or its metabolite, acetaldehyde.5 We conclude that ethanol indirectly inhibits IAA production as a result of oxidation of ethanol by alcohol dehydrogenase, during which the oxidative metabolism of tryptamine is shifted towards the reductive pathway, thus favouring the formation of tryptophol in place of IAA.
在大鼠全肝匀浆中进行体外研究，考察了多种乙醇浓度（体积/体积）对色胺氧化脱氨生成吲哚乙酸（IAA）的影响。
乙醇浓度在0.01%至0.2%之间时，IAA生成逐渐受到抑制，但当乙醇浓度进一步增至6%时，抑制作用减弱。
过量的醛脱氢酶仅部分逆转了乙醇对IAA生成的抑制作用，而吡唑或乙醇（6%和10%）本身则完全阻止了IAA生成的减少。
过量的烟酰胺腺嘌呤二核苷酸未能改变乙醇的抑制作用，且未获得乙醇或其代谢产物乙醛抑制单胺氧化酶的证据。
我们得出结论，乙醇通过乙醇脱氢酶氧化乙醇，间接抑制IAA生成，在此过程中色胺的氧化代谢转向还原途径，从而有利于生成色醇而非IAA。
