美国哈佛大学与匹兹堡大学的科学家，首度的揭露出由细胞里粒腺体所调控，利用微量的一氧化碳 (Carbon Monoxide)，进行身体抗发炎反应的机制，就这个新的发现来说，科学家有可能在未来，利用这个原本会造成身体中毒的分子，发展出新一代的抗发炎治疗方法。
发炎身体所拥有的自然反应，也是抵抗外来感染的一道防线，当身体有感染物入侵的时候，发炎反应会立刻启动，快速的活化相关的免疫细胞，而就进行器官移殖的病人来说，发炎反应的发生，反而会危及殖入器官的正常功能，因此不当的发炎反应，不管是急性的发炎或者是慢性的发炎，都有可能造成身体组织的伤害，而就现阶段来说，临床上控制发炎反应的作法并非全然成功，这样的结果使得探究发炎反应的真正过程，成为临床研究一个很重要的目标。
据了解这次由研究团队共同发表在 FASEB期刊上的论文指出，具有细胞内分子引擎 (molecular engines)的粒线体 (mitochondria)，会和非常微量的一氧化碳反应，因而释放出适量的化学讯号分子来降低或者是关闭身体的不当发炎反应，目前就动物模型的研究数据看来，这个新发现有极大的可能，成为新一代调控发炎反应的药物发展方向。
(资料来源 : Bio.com)
原始出处: http://www.bio.com/newsfeatures/newsfeatures_research.jhtml?cid=27600005
部分英文原文：
The FASEB Journal. 2007;21:1099-1106
Carbon monoxide signals via inhibition of cytochrome c oxidase and generation of mitochondrial reactive oxygen species
Brian S. Zuckerbraun*,1, Beek Yoke Chin, Martin Bilban, Joana de Costa d’Avila, Jayashree Rao*, Timothy R. Billiar* and Leo E. Otterbein
Departments of Surgery,
* University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA; and
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
1Correspondence: University of Pittsburgh School of Medicine, NW653 MUH, 3459 Fifth Ave., Pittsburgh, PA 15213, USA. E-mail: zuckerbraunbs@upmc.edu
Carbon monoxide (CO), which is produced endogenously in the breakdown of heme, has been recognized as an important physiological second messenger similar to NO. Additionally, pharmacological delivery of CO is protective in numerous models of injury, including ischemia/reperfusion, transplantation, hemorrhagic shock, and endotoxemia. However, the mechanism of action of CO is only partially elucidated focused primarily on how it modulates the cellular response to stress. The purpose of these investigations is to test the hypothesis that CO acts via inhibition of cytochrome c oxidase leading to the generation of low levels of reactive oxygen species (ROS) that in turn mediate subsequent adaptive signaling. We show here that CO increases ROS generation in RAW 264.7 cells, which is inhibited by antimycin A and is absent in respiration-deficient 0 cells. CO inhibits cytochrome c oxidase, while maintaining cellular ATP levels and increasing mitochondrial membrane potential. The addition of antioxidants or inhibition of complex III of the electron transport chain by antimycin A attenuates the inhibitory effects of CO on lipopolysaccharide (LPS)-induced TNF- and blocked CO-induced p38 MAPK phosphorylation, which we previously have shown to be important in the anti-inflammatory effects of CO.—Zuckerbraun, B. S., Chin, B. Y., Bilban, M., de Costa d’Avila, J., Rao, J., Billiar, T. R., Otterbein, L. E. Carbon monoxide signals via inhibition of cytochrome c oxidase and generation of mitochondrial reactive oxygen species.
Key Words: macrophage • p38 MAPK • tumor necrosis factor-alpha
