Paredes S R, Kozicki P A, Fukuda H, Rossetti M V, Batlle A M
Alcohol. 1987 Mar-Apr;4(2):81-5. doi: 10.1016/0741-8329(87)90003-6.
The effect of disulfiram and S-adenosyl-L-methionine (SAM) administration to acute ethanol intoxicated mice on the hepatic glutathione (GSH) concentration and aminolevulinic and dehydratase (ALA-D) activity was investigated. It was found that both GSH levels and ALA-D activity were decreased, and evidence suggested that the toxic action of ethanol was due to its conversion into acetaldehyde. Administration of SAM reverses the effects of acute alcohol abuse by increasing liver GSH availability. In vitro, hepatic ALA-D activity was not modified by ethanol; instead it was non-competitively inhibited by acetaldehyde. This inhibition was efficiently reversed by GSH and cysteine (CySH). Therefore, a mechanism for the action of ethanol on ALA-D, based on the inhibitory effect of acetaldehyde, is proposed.
研究了给予双硫仑和S-腺苷-L-蛋氨酸（SAM）对急性乙醇中毒小鼠肝脏谷胱甘肽（GSH）浓度及δ-氨基-γ-酮戊酸脱水酶（ALA-D）活性的影响。结果发现，GSH水平和ALA-D活性均降低，且有证据表明乙醇的毒性作用是由于其转化为乙醛所致。给予SAM可通过增加肝脏GSH的可利用性来逆转急性酒精滥用的影响。在体外，乙醇不会改变肝脏ALA-D活性；相反，它受到乙醛的非竞争性抑制。这种抑制作用可被GSH和半胱氨酸（CySH）有效逆转。因此，提出了一种基于乙醛抑制作用的乙醇对ALA-D的作用机制。
