Rice D C, Gilbert S G
Toxicology Research Division, Department of Health, Ottawa, Ontario, Canada.
Toxicol Appl Pharmacol. 1995 Sep;134(1):161-9. doi: 10.1006/taap.1995.1180.
Paresthesias are a frequently reported symptom of methylmercury exposure in adults, while peripheral neuropathy has long been known to result from high-level lead exposure. Despite this, no objective determination of somatosensory function has been performed in either humans or animals for either toxicant. Somatosensory function was assessed following developmental methylmercury exposure or lifetime lead exposure in monkeys (Macaca fascicularis) by determination of sensitivity to vibration applied to the fingertip. Vibration thresholds were determined over a number of frequencies, from 25 to 250 Hz, by means of a behavioral procedure. The underside of the tip of the monkey's middle finger was precisely positioned over a blunt probe attached to a vibrator. The monkey signaled detection of the vibration by breaking contact with a stainless steel bar with the free hand. At each of the five frequencies tested, the amplitude of the vibration was manipulated systematically to determine the monkey's threshold of detection. Four of five monkeys dosed with methylmercury from birth to 7 years of age, with blood mercury levels during dosing of 0.8-1.1 micrograms/g, exhibited elevated thresholds when tested at 18 years of age. Two monkeys dosed in utero through 4 years of age, with blood mercury levels of 0.35 micrograms/g during dosing, were impaired when tested at 15 years of age, while two monkeys with histories of blood mercury levels of 0.70 were relatively unimpaired. Lifetime exposure to lead resulting in stable blood lead levels of 20-25 micrograms/dl resulted in elevated vibration sensitivity only at the highest frequency in all four individuals tested. However, only two of six individuals with high lead levels (60-130 micrograms/dl) exhibited impairment. These results represent severe impairment in methylmercury-exposed monkeys 11 years after cessation of dosing and extend previous research documenting visual and auditory impairment in these monkeys. While effects of lifetime lead exposure on vibration sensitivity observed in the present study are suggestive, there is clearly a need for further research.
感觉异常是成人甲基汞暴露后经常报告的症状，而长期以来已知高水平铅暴露会导致周围神经病变。尽管如此，尚未对人类或动物进行过针对这两种毒物的体感功能客观测定。通过测定对施加于指尖的振动的敏感性，对猕猴（食蟹猴）进行发育性甲基汞暴露或终生铅暴露后评估体感功能。通过行为程序在25至250赫兹的多个频率上测定振动阈值。将猕猴中指指尖的下侧精确放置在连接到振动器的钝探针上。猕猴通过用空手断开与不锈钢棒的接触来发出振动检测信号。在测试的五个频率中的每个频率上，系统地操纵振动幅度以确定猕猴的检测阈值。五只从出生到7岁服用甲基汞的猴子中，有四只在给药期间血汞水平为0.8 - 1.1微克/克，在18岁时测试时表现出阈值升高。两只在子宫内至4岁给药的猴子，给药期间血汞水平为0.35微克/克，在15岁时测试时受损，而两只血汞水平为0.70的猴子相对未受损。终生暴露于铅导致血铅水平稳定在20 - 25微克/分升，仅在所有测试的四个个体中的最高频率下导致振动敏感性升高。然而，六名高铅水平（60 - 130微克/分升）的个体中只有两名表现出受损。这些结果表明，在停止给药11年后，甲基汞暴露的猴子出现了严重损伤，并扩展了先前记录这些猴子视觉和听觉损伤的研究。虽然本研究中观察到的终生铅暴露对振动敏感性的影响具有提示性，但显然需要进一步研究。
