Bernstein P S, Lloyd M B, O'Day W T, Bok D
Jules Stein Eye Institute, Department of Ophthalmology, UCLA School of Medicine 90024-7008.
Exp Eye Res. 1992 Dec;55(6):869-78. doi: 10.1016/0014-4835(92)90013-i.
Refsum's disease (heredopathia atactica polyneuritiformis) is an autosomal recessive retinitis pigmentosa syndrome caused by the excessive deposition of phytanic acid in ocular tissues. It is thought that phytanic acid causes retinal degeneration either by interfering with vitamin A metabolism in the retinal pigment epithelium or by altering photoreceptor cell membrane structure. Efforts to elucidate the molecular mechanism of phytanic acid's retinal toxicity have been hampered by the rarity of human pathological specimens and by the inability to reproduce the disease in living animal models. In this study, an in vitro model for Refsum's disease was established by exposing cultured human and bovine retinal pigment epithelial cells to phytanic acid bound to bovine serum albumin at concentrations comparable to levels found in affected humans. Ultrastructural studies show that these cells exhibit morphological changes consistent with those observed in pathological specimens from patients with Refsum's disease. Biochemical assays of retinoid metabolism by cell membranes from control cells and from cells exposed to 200 microM phytanic acid demonstrate that the ability to esterify retinol and to isomerize all-trans retinoids to 11-cis retinoids remains intact despite the deposition of large amounts of phytanic acid. The work described here is strong evidence against the hypothesis that phytanic acid inhibits vitamin A metabolism in the retinal pigment epithelium, and it demonstrates the potential use of cultured retinal pigment epithelial cells in modeling this and other degenerative diseases of the retina.
雷夫叙姆病(遗传性共济失调性多神经炎)是一种常染色体隐性遗传性色素性视网膜炎综合征,由植烷酸在眼组织中过度沉积所致。据认为,植烷酸导致视网膜变性的机制,要么是干扰视网膜色素上皮细胞中的维生素A代谢,要么是改变光感受器细胞膜结构。由于人类病理标本稀少,且无法在活体动物模型中再现该病,因此对植烷酸视网膜毒性分子机制的研究工作受到了阻碍。在本研究中,通过将培养的人及牛视网膜色素上皮细胞暴露于与患病人类体内浓度相当的、与牛血清白蛋白结合的植烷酸中,建立了雷夫叙姆病的体外模型。超微结构研究表明,这些细胞呈现出的形态变化与雷夫叙姆病患者病理标本中观察到的一致。对对照细胞及暴露于200微摩尔植烷酸的细胞的细胞膜进行类视黄醇代谢的生化分析表明,尽管有大量植烷酸沉积,但酯化视黄醇以及将全反式类视黄醇异构化为11-顺式类视黄醇的能力仍保持完好。本文所述工作有力地反驳了植烷酸抑制视网膜色素上皮细胞中维生素A代谢这一假说,并证明了培养的视网膜色素上皮细胞在模拟该病及其他视网膜退行性疾病方面的潜在用途。