Parson S H, Price J F, Ribchester R R
Department of Anatomy, University Medical School, Edinburgh.
Neurodegeneration. 1995 Mar;4(1):99-106. doi: 10.1006/neur.1995.0012.
We have measured the effects of cytosine-beta-D-arabinofuranoside (AraC) on cell survival and neurite outgrowth in cultures of dissociated 4-6 day embryonic chick neural tube cells. High concentrations of AraC (greater than 100 microM) reduced neuronal cell survival and neurite outgrowth from viable cells. Concentrations normally used to inhibit mitotic cell division (1-10 microM) were toxic to the neurones cultured in serum free medium on a poly-DL-ornithine/laminin substrate. AraC does not appear to have a neurite promoting effect on dissociated neurones that are cultured in the presence of low numbers of non-neuronal cells. This suggests that the neurite promoting effects of AraC reported by others is likely to be through the non-neuronal cells that were an inherent feature of the culturing systems in these studies. AraC cytotoxicity was completely blocked by the addition of the competitive antagonist: 2'deoxycytidine (2'DC) but not by its metabolic precursor cytosine (cyt). We suggest that the acute effects of AraC on neurones which are actively growing neurites are the result of interference with lipid metabolism.
我们已经检测了胞嘧啶-β-D-阿拉伯呋喃糖苷（AraC）对解离的4-6日龄鸡胚神经管细胞培养物中细胞存活和神经突生长的影响。高浓度的AraC（大于100 microM）会降低神经元细胞的存活率以及存活细胞的神经突生长。通常用于抑制有丝分裂细胞分裂的浓度（1-10 microM）对在聚-DL-鸟氨酸/层粘连蛋白底物上的无血清培养基中培养的神经元有毒性。AraC似乎对在少量非神经元细胞存在下培养的解离神经元没有神经突促进作用。这表明其他人报道的AraC的神经突促进作用可能是通过这些研究中培养系统固有的非神经元细胞实现的。添加竞争性拮抗剂2'-脱氧胞苷（2'DC）可完全阻断AraC的细胞毒性，但添加其代谢前体胞嘧啶（cyt）则不能。我们认为，AraC对正在积极生长神经突的神经元的急性作用是干扰脂质代谢的结果。
