一氧化氮可保护一氧化氮合酶功能免受羟自由基诱导的抑制。

Nitric oxide protects nitric oxide synthase function from hydroxyl radical-induced inhibition.

作者信息

Xu K Y

机构信息

Department of Medicine, Division of Cardiology, The Johns Hopkins Medical Institutions, Johns Hopkins Asthma and Allergy Center, Room 1A2, 5501 Hopkins Bayview Circle, Baltimore, MD 21224, USA.

出版信息

Biochim Biophys Acta. 2000 Aug 31;1481(1):156-66. doi: 10.1016/s0167-4838(00)00113-8.

DOI:10.1016/s0167-4838(00)00113-8

PMID:10962103

Abstract

The interdependent relationships among nitric oxide synthase (NOS), its coenzyme, cofactors and nitric oxide (NO(free radical) were studied using electron paramagnetic resonance spectroscopy. It was found that superoxide-dependent hydroxyl free radical (OH(free radical), derived from NOS coenzyme and cofactors, inhibits NOS activity, and that endogenous NO(free radical) generated by NOS scavenges OH(free radical) and protects NOS function. These results reveal a new role for NO(free radical) that may be important in NOS function and cellular free radical homeostasis.

摘要

利用电子顺磁共振波谱研究了一氧化氮合酶（NOS）、其辅酶、辅因子与一氧化氮（NO自由基）之间的相互依存关系。研究发现，源自NOS辅酶和辅因子的超氧化物依赖性羟基自由基（OH自由基）会抑制NOS活性，而NOS产生的内源性NO自由基会清除OH自由基并保护NOS功能。这些结果揭示了NO自由基的一种新作用，这可能在NOS功能和细胞自由基稳态中具有重要意义。