Gordon J A, Heller S K, Rhead W J, Watkins P A, Spector A A
Department of Internal Medicine, College of Medicine, University of Iowa, Iowa City 52242, USA.
Prostaglandins Leukot Essent Fatty Acids. 1995 Feb-Mar;52(2-3):77-81. doi: 10.1016/0952-3278(95)90001-2.
A new radiolabeled metabolite was released into the extracellular fluid by normal human skin fibroblasts that were labeled with [5,6,8,9,11,12,14,15-3H] arachidonic acid. This product continued to accumulate during a 24 h incubation, and its formation was not saturated at arachidonic acid concentrations up to 15 mumol/L. The compound, identified as hexadecatrienoic acid, was not produced by Zellweger fibroblasts which are deficient in peroxisomal fatty acid beta-oxidation. By contrast, radiolabeled hexadecatrienoic acid was produced by mutant fibroblasts having other peroxisomal defects, including X-linked adrenoleukodystrophy, adult Refsum's disease, and rhizomelic chondrodysplasia punctata. This radiolabeled metabolite also was produced by mutant fibroblasts that cannot oxidize long-chain fatty acids in the mitochondria. These results indicate that hexadecatrienoic acid is synthesized from arachidonic acid by peroxisomal beta-oxidation. The absence of this pathway may account for some of the biochemical and functional abnormalities that occur in Zellweger's syndrome.
用[5,6,8,9,11,12,14,15-3H]花生四烯酸标记的正常人皮肤成纤维细胞将一种新的放射性标记代谢产物释放到细胞外液中。在24小时的孵育过程中,该产物持续积累,在花生四烯酸浓度高达15μmol/L时其形成未达到饱和。该化合物被鉴定为十六碳三烯酸,缺乏过氧化物酶体脂肪酸β氧化的泽尔韦格成纤维细胞不产生这种化合物。相比之下,具有其他过氧化物酶体缺陷的突变成纤维细胞会产生放射性标记的十六碳三烯酸,这些缺陷包括X连锁肾上腺脑白质营养不良、成人Refsum病和点状软骨发育不良。这种放射性标记的代谢产物也由不能在线粒体中氧化长链脂肪酸的突变成纤维细胞产生。这些结果表明,十六碳三烯酸是通过过氧化物酶体β氧化由花生四烯酸合成的。该途径的缺失可能是泽尔韦格综合征中出现的一些生化和功能异常的原因。