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首页> 外文期刊>The Biochemical Journal >POLYENOIC VERY-LONG-CHAIN FATTY ACIDS MOBILIZE INTRACELLULAR CALCIUM FROM A THAPSIGARGIN-INSENSITIVE POOL IN HUMAN NEUTROPHILS - THE RELATIONSHIP BETWEEN CA2+ MOBILIZATION AND SUPEROXIDE PRODUCTION INDUCED BY LONG- AND VERY-LONG-CHAIN FATTY ACIDS
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POLYENOIC VERY-LONG-CHAIN FATTY ACIDS MOBILIZE INTRACELLULAR CALCIUM FROM A THAPSIGARGIN-INSENSITIVE POOL IN HUMAN NEUTROPHILS - THE RELATIONSHIP BETWEEN CA2+ MOBILIZATION AND SUPEROXIDE PRODUCTION INDUCED BY LONG- AND VERY-LONG-CHAIN FATTY ACIDS

机译：聚丙烯酰胺长链脂肪酸从人中性粒细胞中的糖蛋白敏感性池中移动细胞内钙-长链和超长链引起的CA2 +移动性与超氧化物生产之间的关系

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Fatty acids with more than 22 carbon atoms (very-long-chain fatty acids; VLCFAs) are normal cellular components that have been implicated in the pathophysiology of a number of peroxisomal disorders. To date, however, essentially nothing is known regarding their biological activities. Ca2+ mobilization is an important intracellular signalling system for a variety of agonists and cell types. Given that several polyunsaturated long-chain fatty acids mobilize intracellular Ca2+ and that we have postulated that the VLCFAs may be involved in signal transduction, we examined whether the tetraenoic VLCFA induced Ca2+ mobilization in; human neutrophils. We report that fatty acid-induced intracellular Ca2+ mobilization declined for fatty acid species of more than 20 carbon atoms, but increased again as the carbon chain length approached 30. This Ca2+ mobilization occurred independently of inositol 1,4,5-trisphosphate production and protein kinase C translocation and involved both the release of Ca2+ from the intracellular stores and changes to the influx or efflux of the ion. We further observed that triacontatetraenoic acid [30:4 (n-6)] mobilized Ca2+ from a thapsigargin-insensitive intracellular pool distinct from the thapsigargin-sensitive pools affected by arachidonic acid [20:4 (n-6)] or N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP). 20:4 (n-6) induced strong superoxide production (chemiluminescence) which was inhibited by thapsigargin pretreatment. In contrast, fatty acid-induced superoxide production progressively declined as the carbon chain length increased beyond 20-22 carbon atoms. Further studies suggested that the thapsigargin-insensitive Ca2+ mobilization elicited by 30:4 (n-6) was not related to oxy radical formation, while the-thapsigargin-sensitive Ca2+ mobilization induced by 20:4 (n-6) may be involved in the initiation but not necessarily the maintenance of superoxide production. In conclusion, this is the first report to demonstrate a biological activity for the VLCFA and indicates that 30:4 (n-6) influences second messenger systems in intact cells that differ from those affected by long-chain fatty acids such as 20:4 (n-6).
机译：碳原子数超过22的脂肪酸（超长链脂肪酸; VLCFA）是正常的细胞成分，已与许多过氧化物酶体异常的病理生理有关。然而，迄今为止，关于它们的生物学活性基本上还一无所知。 Ca2 +动员是多种激动剂和细胞类型的重要细胞内信号传导系统。鉴于几种多不饱和长链脂肪酸可动员细胞内Ca2 +，并且我们假设VLCFA可能参与信号转导，我们研究了四烯酸VLCFA是否诱导了Ca2 +的动员。人类中性粒细胞。我们报告说，脂肪酸诱导的细胞内Ca2 +动员对于超过20个碳原子的脂肪酸种类下降，但随着碳链长度接近30而再次增加。这种Ca2 +动员独立于肌醇1,4,5-三磷酸生产和蛋白质而发生激酶C易位并涉及细胞内存储中Ca2 +的释放以及离子流入或流出的变化。我们进一步观察到，triacontatetraenoic acid [30：4（n-6）]从毒胡萝卜素不敏感的细胞内池中调动了Ca2 +，这与受花生四烯酸[20：4（n-6）]或N-甲酰基影响的thapsigargin敏感池不同。 -L-甲硫酰基-L-亮氨酰-L-苯丙氨酸（fMLP）。 20：4（n-6）诱导了强烈的超氧化物生成（化学发光），而毒胡萝卜素预处理则抑制了该生成。相反，随着碳链长度增加超过20-22个碳原子，脂肪酸诱导的超氧化物的产生逐渐下降。进一步的研究表明，由30：4（n-6）引起的毒胡萝卜素不敏感的Ca2 +动员与氧自由基的形成无关，而由20：4（n-6）引起的对毒胡萝卜素敏感的Ca2 +的动员可能与引发但不一定维持超氧化物的产生。总之，这是第一份证明VLCFA具有生物学活性的报告，并表明30：4（n-6）影响完整细胞中的第二信使系统，该细胞不同于受长链脂肪酸（例如20：4）影响的细胞（n-6）。

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