Miyama T, Minowa K, Seki H, Tamura Y, Mizoguchi I, Ohi G, Suzuki T
Arch Toxicol. 1983 Mar;52(3):173-81. doi: 10.1007/BF00333897.
In order to see chronological relationship between electrophysiological changes and "early" neurological sign (tail rotation) elicited in rats poisoned with methylmercury, we made serial measurements of amplitude of compound action potential and sensory nerve conduction velocity of the tail nerve in rats with five dose schedules [methylmercury vs selenium, (1)20 ppm:0.1 ppm, (2)20: 0.3, (3)20: 0.6, (4)10: 0.1, (5)10: 0.6]. We observed the following sequence in the onset of neuro-electro-physiolo-somatic signs: fall in compound action potential greater than decrease in sensory nerve conduction velocity greater than tail rotation greater than weight loss. Protective potency of dietary selenium against neurotoxicity of methylmercury was observed with regard to both electrophysiological changes and neurological signs.
为了观察甲基汞中毒大鼠电生理变化与“早期”神经体征(尾部旋转)之间的时间关系,我们采用五种剂量方案[甲基汞与硒,(1)20 ppm:0.1 ppm,(2)20:0.3,(3)20:0.6,(4)10:0.1,(5)10:0.6]对大鼠尾神经复合动作电位幅度和感觉神经传导速度进行了系列测量。我们观察到神经-电-生理体征出现的顺序如下:复合动作电位下降大于感觉神经传导速度下降大于尾部旋转大于体重减轻。在电生理变化和神经体征方面均观察到膳食硒对甲基汞神经毒性的保护作用。