Chang W C, Fukuda S, Tai H H
Life Sci. 1984 Mar 26;34(13):1261-8. doi: 10.1016/0024-3205(84)90549-6.
Male rats were exposed to freshly generated cigarette smoke once daily for 4 to 13 weeks. Inhalation of smoke was verified by elevated level of carboxyhemoglobin. NAD+-dependent 15-hydroxyprostaglandin dehydrogenase activity, the key enzyme responsible for biological inactivation of prostaglandins, was found to decrease in lung but not in kidney or stomach following cigarette smoke exposure. The consequence of impaired pulmonary metabolism of prostaglandins and thromboxane may result in alteration of vascular homeostasis and subsequently lead to cardiovascular disorders commonly found in smokers.
雄性大鼠每天暴露于新产生的香烟烟雾中，持续4至13周。通过羧基血红蛋白水平升高来证实烟雾吸入情况。NAD⁺依赖性15-羟基前列腺素脱氢酶活性是负责前列腺素生物失活的关键酶，发现香烟烟雾暴露后，肺中的该酶活性降低，而肾或胃中的酶活性未降低。前列腺素和血栓素肺代谢受损的后果可能导致血管稳态改变，进而导致吸烟者常见的心血管疾病。
