Liu Y, Tai H H
Biochem Pharmacol. 1985 Dec 15;34(24):4275-8. doi: 10.1016/0006-2952(85)90284-9.
Acrolein, a highly reactive aldehyde found in cigarette smoke, was shown to induce time-dependent inactivation of NAD+-linked 15-hydroxyprostaglandin dehydrogenase from porcine lung. The inactivation process followed pseudo-first-order kinetics and was irreversible. Inactivation by acrolein can be prevented by prior incubation of the enzyme with GSH but not by subsequent addition of GSH during assay. Inactivation can be also protected fully by prior incubation of the enzyme with NAD+, but only partially with prostaglandin E1. The results suggest that acrolein alkylates the enzyme at the coenzyme binding site and inactivates the enzyme. Inactivation of pulmonary NAD+-linked 15-hydroxyprostaglandin dehydrogenase by acrolein may alter cellular and circulating thromboxane/prostacyclin ratios and subsequently disturb vascular homeostasis and augment inflammatory and anaphylactic responses in smokers.
丙烯醛是香烟烟雾中发现的一种高反应性醛，已证明它能诱导猪肺中与NAD+相关的15-羟基前列腺素脱氢酶随时间失活。失活过程遵循假一级动力学且是不可逆的。丙烯醛导致的失活可通过酶与谷胱甘肽（GSH）预先孵育来防止，但在测定过程中随后添加GSH则不能防止。酶与NAD+预先孵育也能完全保护其不被失活，但与前列腺素E1预先孵育只能部分保护。结果表明丙烯醛在辅酶结合位点使酶烷基化并使其失活。丙烯醛使肺中与NAD+相关的15-羟基前列腺素脱氢酶失活可能会改变细胞和循环中的血栓素/前列环素比例，进而扰乱血管稳态，并增强吸烟者的炎症和过敏反应。
