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大鼠视网膜中的脂质介质:光照和创伤在体外引发白三烯B4释放。

Lipid mediators in the rat retina: light exposure and trauma elicit leukotriene B4 release in vitro.

作者信息

Reinboth J J, Gautschi K, Clausen M, Remé C E

机构信息

Department of Ophthalmology, University Hospital Zürich, Switzerland.

出版信息

Curr Eye Res. 1995 Nov;14(11):1001-8. doi: 10.3109/02713689508998521.

Abstract

Light exposure not only elicits a visual response but may also alter functional and structural characteristics of the retina. Furthermore, light exposure can lead to reversible or irreversible lesions of photoreceptors and pigment epithelium. Previous studies in our laboratory have shown that light liberates arachidonic acid from retinal membrane phospholipids mainly by activating the phospholipase A2. In this study we show that light and trauma elicit the synthesis of leukotriene B4 in the isolated rat retina in vitro. Male albino rats were dark adapted for 36 h, isolated retinae were taken, incubated and exposed a) either to darkness or to 5,000 lux of cool white fluorescent light for 5, 10 or 15 min at 37 degrees C, b) either to darkness or to 5,000 lux of cool white fluorescent light for 15 min at 0 degrees C or c) either to darkness or to 5,000 lux of cool white fluorescent light for 15 min at 37 degrees C with a 5-lipoxygenase inhibitor (zileuton). Eicosanoids were extracted and leukotriene B4 levels were determined by radioimmunoassay. Removal of retinae and incubation in darkness caused a significant rise in leukotriene B4 levels with increasing incubation time. This rise was further augmented significantly after light exposure. The leukotriene B4 levels obtained when incubating the retinae either at 0 degree C or with the lipoxygenase inhibitor zileuton as well as the high specificity of the radioimmunoassay indicate that the light- and trauma-elicited synthesis of leukotriene B4 is mediated by activating the 5-lipoxygenase. Leukotriene B4 may be involved, at least in part, in the pathogenesis of retinal diseases including light damage. Curr. Eye Res. 14: 1001-1008, 1995.

摘要

光照不仅会引发视觉反应,还可能改变视网膜的功能和结构特征。此外,光照可导致光感受器和色素上皮的可逆或不可逆损伤。我们实验室之前的研究表明,光照主要通过激活磷脂酶A2从视网膜膜磷脂中释放花生四烯酸。在本研究中,我们发现光照和外伤在体外可诱导分离的大鼠视网膜合成白三烯B4。雄性白化大鼠暗适应36小时后,取出分离的视网膜,进行孵育,并分别进行以下处理:a)在37℃下,置于黑暗中或暴露于5000勒克斯冷白色荧光灯下5、10或15分钟;b)在0℃下,置于黑暗中或暴露于5000勒克斯冷白色荧光灯下15分钟;c)在37℃下,置于黑暗中或暴露于5000勒克斯冷白色荧光灯下15分钟,同时加入5-脂氧合酶抑制剂(齐留通)。提取类花生酸,通过放射免疫测定法测定白三烯B4水平。取出视网膜并在黑暗中孵育会导致白三烯B4水平随孵育时间增加而显著升高。光照后,这种升高进一步显著增强。在0℃下孵育视网膜或使用脂氧合酶抑制剂齐留通时获得的白三烯B4水平以及放射免疫测定法的高特异性表明,光照和外伤诱导的白三烯B4合成是通过激活5-脂氧合酶介导的。白三烯B4可能至少部分参与包括光损伤在内的视网膜疾病的发病机制。《当代眼科研究》1995年第14卷:1001 - 1

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