Lu X, Badiani K, Arthur G
Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Metabolism. 1993 Dec;42(12):1506-8. doi: 10.1016/0026-0495(93)90143-c.
The effect of 3-deazaadenosine (DZA) and the hypolipidemic drug MDL29350 (2-[3,5-di(t-butyl-4-hydroxyphenyl)thio]hexanoic acid) on the synthesis and methylation of phosphatidylethanolamine (PE) originating from the cytidine diphosphate (CDP) ethanolamine pathway and PE originating from decarboxylation of phosphatidylserine (PS) was investigated. DZA and MDL29350 did not affect the synthesis of PE by either pathway; however, methylation of ethanolamine-derived PE was inhibited by 80% and methylation of serine-derived PE was inhibited by 36% by 20 mumol/LDZA or MDL29350. The differential inhibition of the methylation of PE synthesized via serine or ethanolamine suggests that in Hep G2 cells PE-N-methyltransferase (PENMT) may be segregated into distinct compartments that are differentially accessible to the drugs.
研究了3-脱氮腺苷（DZA）和降血脂药物MDL29350（2-[3,5-二（叔丁基-4-羟苯基）硫代]己酸）对源自胞苷二磷酸（CDP）乙醇胺途径的磷脂酰乙醇胺（PE）以及源自磷脂酰丝氨酸（PS）脱羧的PE的合成和甲基化的影响。DZA和MDL29350均不影响任一途径的PE合成；然而，20μmol/L DZA或MDL29350使源自乙醇胺的PE甲基化受到80%的抑制，使源自丝氨酸的PE甲基化受到36%的抑制。通过丝氨酸或乙醇胺合成的PE甲基化受到的差异性抑制表明，在Hep G2细胞中，PE-N-甲基转移酶（PENMT）可能被分隔到不同的区室中，而这些区室对药物的可及性存在差异。
