Alterations of arachidonate metabolism in cardiovascular system by cigarette smoking

H. H. Tai, W. C. Chang, Y. Liu, S. Fukuda

研究成果: 書貢獻/報告類型會議貢獻

7 引文 斯高帕斯(Scopus)


Male rats were exposed to freshly generated cigarette smoke once daily for various lengths of time. Inhalation of smoke was verified by elevated levels of carboxyhemoglobin. Metabolism of arachidonate in the cardiovascular system to thromboxane and prostacyclin through the cyclooxygenase pathway and their further metabolism to 15-keto-derivates, and to 12-hydroxyeicosatetraenoic acid (12-HETE) through lipoxygenase pathway was investigated. Synthesis of thromboxane and prostacyclin in platelets and aortas respectively was not changed within 8 weeks of smoke exposure. However, formation of 12-HETE in platelets was significantly increased after 4 weeks of smoke exposure. Catabolism of thromboxane and prostacyclin as determined by NAD+-dependent 15-hydroxyprostaglandin dehydrogenase activity was greatly decreased in lung but not in kidney and stomach following 4 weeks of smoke exposure. Increased 12-lipoxygenase activity in platelets may lead to stimulation of migration and proliferation of smooth muscle cells and to increased synthesis of leukotrienes in neutrophils. Decreased pulmonary prostaglandin catabolic activity may result in increase in circulating thromboxane/prostacyclin ratio and subsequently alteration of vascular homeostasis. The consequence of these biochemical changes may contribute to the development of atherosclerosis, thromboembolism and emphysema commonly found in smokers.

主出版物標題Advances in Experimental Medicine and Biology
出版狀態已發佈 - 1990


名字Advances in Experimental Medicine and Biology

ASJC Scopus subject areas

  • 一般生物化學,遺傳學和分子生物學


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