Ohwada A, Kira S, Yamashita T
Department of Respiratory Medicine, School of Medicine, Juntendo University, Tokyo, Japan.
Prostaglandins Leukot Essent Fatty Acids. 1990 Jan;39(1):69-73. doi: 10.1016/0952-3278(90)90176-l.
The effect of hypoxia was studied on the ionophore A23187-induced leukotriene production by rat alveolar macrophages. The production of LTB4 and LTC4 decreased with reducing oxygenation without change of cell viability. The synthesis of 5-HETE increased during hypoxia and the total production of LTB4, LTC4 and 5-HETE, the major metabolites of the 5-lipoxygenase pathway in rat alveolar macrophages, was equal during normoxia and hypoxia. Arachidonate release and LTA4-converting into LTB4 and LTC4 was unaffected by hypoxia. LTB4- and LTC4-degradating activities were not affected by hypoxia. These results suggest that LTA4 synthase reaction of leukotrienes biosynthesis might be suppressed by hypoxia.
研究了缺氧对离子载体A23187诱导的大鼠肺泡巨噬细胞白三烯生成的影响。随着氧合降低，LTB4和LTC4的生成减少，而细胞活力无变化。缺氧期间5-HETE的合成增加，并且在常氧和缺氧状态下，大鼠肺泡巨噬细胞中5-脂氧合酶途径的主要代谢产物LTB4、LTC4和5-HETE的总生成量相等。花生四烯酸释放以及LTA4转化为LTB4和LTC4不受缺氧影响。LTB4和LTC4的降解活性也不受缺氧影响。这些结果表明，缺氧可能会抑制白三烯生物合成中的LTA4合酶反应。
