甲醇
格式化
甲酸
毒性
甲醇中毒
化学
新陈代谢
代谢性酸中毒
甲醛
甲酸甲酯
生物化学
环境化学
医学
有机化学
内科学
催化作用
作者
Robert Kavet,Kathleen M. Nauss
标识
DOI:10.3109/10408449009089872
摘要
Methanol could become a major automotive fuel in the U.S., and its use may result in increased exposure of the public to methanol vapor. Nearly all of the available information on methanol toxicity in humans relates to the consequences of acute, rather than chronic, exposures. Acute methanol toxicity evolves in a well-understood pattern and consists of an uncompensated metabolic acidosis with superimposed toxicity to the visual system. The toxic properties of methanol are rooted in the factors that govern both the conversion of methanol to formic acid and the subsequent metabolism of formate to carbon dioxide in the folate pathway. In short, the toxic syndrome sets in if formate generation continues at a rate that exceeds its rate of metabolism. Current evidence indicates that formate accumulation will not challenge the metabolic capacity of the folate pathway at the anticipated levels of exposure to automotive methanol vapor.
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