Substances in the aqueous fraction of cigarette smoke inhibit lipid peroxidation in synaptosomes of rat cerebral cortex
Substances in the aqueous fraction of cigarette smoke inhibit lipid peroxidation in synaptosomes of rat cerebral cortex
复制标题
香烟烟雾水相中的物质抑制大鼠大脑皮层突触体的脂质过氧化
DOI：
10.1080/15216549700202371
复制
发表时间：
1997
期刊：
影响因子：
4.6
通讯作者：
T. Itoh
中科院分区：
文献类型：
--
作者：
Y. Kamisaki;K. Wada;K. Nakamoto;Y. Kishimoto;K. Ashida;T. Itoh
以大鼠大脑皮层神经末梢为材料，研究了香烟烟雾中的水溶性物质对脂质过氧化的影响。制备的烟雾剂显著降低突触体内硫代巴比妥酸反应物质的自发增加，且呈稀释因子依赖性。此外，水提物还能抑制过氧化自由基生成物2，2‘-偶氮(2-氨基丙烷)二盐酸盐引起的脂质过氧化作用。烟物质清除从刺激的人类白细胞和黄嘌呤/黄嘌呤氧化酶系统产生的超氧阴离子自由基。尼古丁不能模仿这些效果。烟物质的抗氧化作用在5℃或-80℃保存数天。结果表明，烟物质具有较长的半衰期，可清除引起突触体膜脂质过氧化的自由基。
The effects of water‐soluble substances in cigarette smoke on lipid peroxidation were investigated using nerve terminals prepared from the rat cerebral cortex. The prepared smoke‐substances significantly reduced the spontaneous increase in thiobarbituric acid‐reactive substances in synaptosomes in a dilution factor‐dependent manner. Furthermore, the aqueous extract also inhibited the elevation of lipid peroxidation induced by 2,2′‐azobis (2‐amidinopropane) dihydrochloride, a peroxyl radical generator. Smoke‐substances scavenged superoxide radicals generated from stimulated human leukocytes and from the xanthine/xanthine oxidase system. These effects were not mimicked by nicotine. The antioxidant effects of smoke‐substances were preserved for several days at 5 ° or ‐80 °C. The results suggest that the smoke‐substances may possess long half‐lives and scavenge the radicals which cause lipid‐peroxidation in synaptosome membranes.
影响因子：
10.4
作者：
Pryor WA;Prier DG;Church DF
通讯作者：
Church DF