Howland R D, Alli P
Brain Res. 1986 Jan 22;363(2):333-9. doi: 10.1016/0006-8993(86)91019-x.
The activity of protein kinase has been assayed in neurofilament preparations from spinal cords of rats treated with acrylamide. Animals received 50 mg/kg, i.p., of acrylamide per day for a total of 5 or 10 days; these doses produce mild and marked symptoms of neurological damage, respectively. Incorporation of phosphate into proteins was determined using [gamma-32P]ATP followed by SDS-PAGE. Total phosphorylation of neurofilament preparations was significantly increased only in the animals treated with the 500 mg/kg cumulative dose of acrylamide. Phosphorylation of the 200 and 155 kdalton subunits of the neurofilaments was increased by 20-40% in the acrylamide treated groups. The phosphorylation of the 70 kdalton neurofilament subunit was unchanged in the 250 mg/kg group and was significantly decreased in the 500 mg/kg group. Phosphorylation of other protein bands was not altered. These results suggest a mechanism by which acrylamide might produce axonal neurofilamentous accumulations.
已对用丙烯酰胺处理的大鼠脊髓神经丝制剂中的蛋白激酶活性进行了测定。动物每天腹腔注射50毫克/千克丙烯酰胺，共注射5天或10天；这些剂量分别产生轻度和明显的神经损伤症状。使用[γ-32P]ATP，随后进行SDS-PAGE，测定蛋白质中磷酸盐的掺入情况。仅在接受500毫克/千克累积剂量丙烯酰胺处理的动物中，神经丝制剂的总磷酸化显著增加。在丙烯酰胺处理组中，神经丝200和155千道尔顿亚基的磷酸化增加了20%-40%。70千道尔顿神经丝亚基的磷酸化在250毫克/千克组中未改变，而在500毫克/千克组中显著降低。其他蛋白条带的磷酸化未改变。这些结果提示了一种丙烯酰胺可能产生轴突神经丝积聚的机制。
