Enhanced synthesis of prostaglandins and hydroxyeicosatetraenoic acids in retina from a canine model of Batten's disease.
Enhanced synthesis of prostaglandins and hydroxyeicosatetraenoic acids in retina from a canine model of Batten's disease.
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巴顿病犬模型视网膜中前列腺素和羟基二十碳四烯酸的合成增强。
DOI：
10.1007/bf03160187
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Bazan,NG
中科院分区：
文献类型：
--
作者：
Birkle,DL;Reddy,TS;Armstrong,D;Bazan,NG
研究了正常英国塞特犬和患有遗传性犬蜡样脂褐质沉积症的英国塞特犬的完整视网膜和视网膜色素上皮细胞中[1- 14 C]花生四烯酸（20∶4，n-6）的代谢。花生四烯酸酰化成膜甘油脂和氧化脂氧合酶和环氧合酶的类花生酸的放射色谱技术进行了测量。此外，还对视网膜神经节细胞和色素上皮细胞中积聚的蜡样颗粒进行了电镜组织病理学研究。在犬蜡样脂褐质沉积症视网膜中，矢车菊素和羟基二十碳四烯酸的合成增加，但在视网膜色素上皮中不增加。前列腺素D2，假定的神经元类花生酸，增加了近8倍，而其他类花生酸增加了2至3倍。超微结构研究显示，积累的蜡样物质和神经元和色素上皮细胞结构的恶化。这些实验表明，虽然脂色素在两种组织中积累，但类花生酸合成的改变对视网膜（神经元组织）是特异性的。前列腺素D2的特异性增加和视网膜变化的特异性表明，类花生酸合成增强可能是神经元中花生四烯酸氧合控制受损的结果。
The metabolism of [1-14C]arachidonic acid (20∶4,n−6) was studied in intact retina and retinal pigment epithelial cells from normal English setters and English setters affected with hereditary canine ceroid lipofuscinosis. Acylation of arachidonic acid into membrane glycerolipids and oxygenation by lipoxygenase and cyclooxygenase to eicosanoids were measured by radiochromatographic techniques. In addition, the histopathology of accumulated ceroid particles in retinal ganglion cells and pigment epithelial cells was studied by electron microscopy. Synthesis of prostaglandins and hydroxyeicosatetraenoic acids was increased in canine ceroid lipofuscinosis retina, but not in retinal pigment epithelium. Prostaglandin D2, the putative neuronal eicosanoid, was increased nearly eightfold, whereas other eicosanoids increased two- to threefold. Ultrastructural studies revealed accumulation of ceroid and deterioration of neuronal and pigment epithelial cell architecture. These experiments demonstrate that, although lipopigment accumulates in both tissues, alterations of eicosanoid synthesis are specific for the retina, a neuronal tissue. The specific increase in prostaglandin D2and the specificity of changes for the retina indicate that enhanced eicosanoid synthesis may be a result of an impairment of the control of oxygenation of arachidonic acid in neurons.