The effect of lead exposure and serum deprivation on mesencephalic primary cultures.
The effect of lead exposure and serum deprivation on mesencephalic primary cultures.
复制标题
铅暴露和血清剥夺对中脑原代培养物的影响。
作者：
M. Scortegagna;I. Hanbauer
研究了Pb2+在含有神经元和胶质细胞的胚胎中脑原代培养物中的作用。在无血清的情况下，Pb2+暴露比有血清的情况下更有效地破坏培养细胞。在无血清培养基中，Pb2+诱导的细胞主要是坏死和凋亡，最多13%。在含Pb2+的血清培养基中，胶质原纤维酸性蛋白（GFAP）含量降低。血清剥夺也降低了GFAP的丰度，在无血清培养基中添加12.5微米Pb2+使GFAP的丰度增强。在无血清培养基中暴露于6微米Pb2+ 6h也降低了低亲和力3h - d -天冬氨酸的摄取。在无血清培养基中，将中脑细胞暴露于3-25微米Pb2+中6小时，不能改变酪氨酸羟化酶和calretinin免疫反应细胞的数量，而50微米Pb2+可使这两种细胞消失。细胞在无血清培养基中暴露于3微米Pb2+ 6h后，3h -多巴胺摄取减少50%，12.5微米Pb2+使其完全消失。在无血清培养基中加入白蛋白不能阻止Pb2+引起的对[3H]-多巴胺摄取的抑制，这表明血清提供的细胞死亡延迟可能不是由于蛋白/螯合物形成去除活性Pb2+，而是由于胶质细胞的Pb2+清除功能。血清剥夺可能通过损害星形胶质细胞的金属清除功能而加重Pb2+诱导的神经毒性。
The effect of Pb2+ was studied in embryonic mesencephalic primary cultures that contain neurons and glia. Pb2+ exposure in absence of serum, damaged more efficaciously the cultured cells than Pb2+ exposure in presence of serum. In serum-free medium, Pb2+ elicited mainly necrosis and apoptosis in maximally 13% of the cells in culture. The glial fibrillary acidic protein (GFAP) content was decreased by Pb2+ exposure in serum-containing medium. The abundance of GFAP was also decreased by serum deprivation that was augmented by the addition of 12.5 microM Pb2+ in serum-free medium. A 6h exposure to 6 microM Pb2+ in serum-free medium also lowered the low affinity 3H-D-aspartate uptake. A 6h exposure of mesencephalic cells to 3-25 microM Pb2+ in serum-free medium failed to alter the number of tyrosine hydroxylase- and calretinin-immunoreactive cells, whereas, 50 microM Pb2+ obliterated both cell types. A 6h exposure of cells to 3 microM Pb2+ in serum-free medium decreased 3H-dopamine uptake by 50 % and 12.5 microM Pb2+ obliterated it. Addition of albumin to serum-free medium failed to prevent the Pb2+ -elicited inhibition of [3H]-dopamine uptake suggesting that the serum-afforded delay of cell death may not be due to a removal of reactive Pb2+ by protein/chelate formation but rather to the Pb2+ -scavenging function of glial cells. Serum deprivation may exacerbate the Pb2+ -induced neurotoxicity presumably by impairing the metal scavenging function of astrocytes.