VanUffelen B E, de Koster B M, VanSteveninck J, Elferink J G
Department of Medical Biochemistry, Sylvius Laboratories, Leiden University, The Netherlands.
Biochem Biophys Res Commun. 1996 Sep 4;226(1):21-6. doi: 10.1006/bbrc.1996.1305.
Carbon monoxide (CO) enhanced random migration of human neutrophils. An optimally stimulatory effect was observed with 10 microM CO. CO caused a rapid and transient increase in intracellular level of guanosine-3',5'-cyclic monophosphate (cGMP). The enhancing effect of CO on random migration was reversed to a large extent by inhibitors of cGMP accumulation, and by antagonists of cGMP-dependent protein kinase (G-kinase). These results strongly suggest that the enhancement of random migration by CO is mediated by cGMP and G-kinase. Using hemoglobin, a scavenger of CO, we could show that stimulation of soluble guanylate cyclase over an extended period of time, rather than the observed fast and transient increase in intracellular cGMP levels, is responsible for CO-activated migration. We postulate that CO, like nitric oxide (NO), acts as a biological signal in the immune system.
一氧化碳（CO）增强了人类中性粒细胞的随机迁移。在10微摩尔CO的作用下观察到了最佳刺激效果。CO导致细胞内鸟苷-3',5'-环磷酸（cGMP）水平迅速且短暂地升高。cGMP积累抑制剂以及cGMP依赖性蛋白激酶（G激酶）拮抗剂在很大程度上逆转了CO对随机迁移的增强作用。这些结果强烈表明，CO对随机迁移的增强作用是由cGMP和G激酶介导的。使用血红蛋白（一种CO清除剂），我们可以证明，长时间刺激可溶性鸟苷酸环化酶，而非观察到的细胞内cGMP水平的快速短暂升高，是CO激活迁移的原因。我们推测，CO与一氧化氮（NO）一样，在免疫系统中充当生物信号。
