体外脑脂质过氧化：一氧化氮与羟自由基

Peroxidation of brain lipids in vitro: nitric oxide versus hydroxyl radicals.

作者信息

Rauhala P, Sziraki I, Chiueh C C

机构信息

Unit on Neurotoxicology and Neuroprotection, Laboratory of Clinical Science, National Institute of Mental Health, NIH Clinical Center, Bethesda, MD 20892-1264, USA.

出版信息

Free Radic Biol Med. 1996;21(3):391-4. doi: 10.1016/0891-5849(96)00043-3.

DOI:10.1016/0891-5849(96)00043-3

PMID:8855451

Abstract

The pro-oxidant effects of hydroxyl radical (.OH, ferrous ammonium sulfate/Fe2+) or nitric oxide (NO., S-nitroso-N-acetylpenicillamine/SNAP) generating compounds were studied in rat brain homogenate preparations. Submicromolar concentrations of Fe2+, but not SNAP (up to 100 microM), increased the formation of fluorescent products of malondialdehyde in cortical homogenates. In fact, iron-catalyzed brain lipid peroxidation was inhibited by SNAP (100 microM), but not by light-exposed SNAP or its degradation product penicillamine (100 microM). This study provides relevant evidence to suggest that submicromolar concentrations of Fe2+ can potentiate lipid peroxidation in disrupted brain tissue. NO. released from SNAP did not stimulate, but rather inhibited brain lipid peroxidation. These results support the hypothesis that NO., as opposed to .OH radicals, is not a pro-oxidant but rather an antioxidant.

摘要

在大鼠脑匀浆制剂中研究了产生羟自由基（·OH，硫酸亚铁铵/Fe²⁺）或一氧化氮（·NO，S-亚硝基-N-乙酰青霉胺/SNAP）的化合物的促氧化作用。亚微摩尔浓度的Fe²⁺可增加皮质匀浆中丙二醛荧光产物的形成，但高达100微摩尔的SNAP却无此作用。事实上，SNAP（100微摩尔）可抑制铁催化的脑脂质过氧化，但光照后的SNAP或其降解产物青霉胺（100微摩尔）则无此作用。本研究提供了相关证据表明，亚微摩尔浓度的Fe²⁺可增强受损脑组织中的脂质过氧化。SNAP释放的·NO并未刺激反而抑制了脑脂质过氧化。这些结果支持了以下假设：与·OH自由基相反，·NO不是促氧化剂而是抗氧化剂。