Gallagher P J, Lee R L
Toxicology. 1980;15(2):129-34. doi: 10.1016/0300-483x(80)90006-2.
Although the clinical patterns of organic and inorganic mercury poisoning are very different, systemic toxicity experiments have shown that the histological changes in the kidneys and dorsal root ganglia neurones are identical with the 2 classes of compounds. It has been further suggested that the toxicity of organic mercurials is the result of biotransformation to inorganic mercury. To test this hypothesis, between 10(-7) and 10(-10) mol of mercuric chloride and methyl mercuric acetate were injected directly into the cerebrum of rats. The comparative size of lesions was estimated anatomically and by reference to blood brain barrier dysfunction. Inorganic lesions were only slightly larger than those produced by equimolar amounts of organic mercury. Consequently both organic and inorganic mercury must be regarded as neurotoxic in their own right. Conversion of organic mercury certainly occurs but is not the only mechanism by which organic mercury exerts its toxicological effect.
尽管有机汞中毒和无机汞中毒的临床症状差异很大,但全身毒性实验表明,这两类化合物在肾脏和背根神经节神经元中的组织学变化是相同的。进一步有人提出,有机汞的毒性是生物转化为无机汞的结果。为了验证这一假设,将10(-7)至10(-10)摩尔的氯化汞和甲基汞醋酸盐直接注射到大鼠大脑中。通过解剖学方法并参考血脑屏障功能障碍来估计损伤的相对大小。无机汞造成的损伤仅比等摩尔量有机汞造成的损伤略大。因此,有机汞和无机汞本身都必须被视为具有神经毒性。有机汞的转化肯定会发生,但这不是有机汞发挥其毒理学作用的唯一机制。