Brunker R L
Appl Environ Microbiol. 1976 Oct;32(4):498-504. doi: 10.1128/aem.32.4.498-504.1976.
Evidence that the mechanism of mercurial toxicity is a blockage of catabolic metabolism is presented. Yeast cells (Saccharomyces cerevisiae) were found to cease respiratory activities within 1.5 min of contrast time with culture mercurials (as HgCl2). This cessation was followed by the rapid depletion of endogenous adenosine 5'-triphosphate (ATP) and a concomitant increase in phosphorylated hexoses. Levels of ATP in the culture medium remained essentially unchanged during this interval suggesting that the structural integrity of the membrane was not affected. Medium potassium concentrations did not increase until after endogenous ATP levels had begun to fall, suggesting that the loss of cellular potassium was the result of the inability of membrane ATPases to function because of the unavailability of sufficient substrate ATP to maintain this gradient.
有证据表明汞毒性的机制是分解代谢的阻断。发现酵母细胞(酿酒酵母)在与培养汞剂(如氯化汞)接触1.5分钟内停止呼吸活动。随后内源性腺苷5'-三磷酸(ATP)迅速耗尽,同时磷酸化己糖增加。在此期间,培养基中ATP水平基本保持不变,表明膜的结构完整性未受影响。直到内源性ATP水平开始下降后,培养基中钾浓度才升高,这表明细胞内钾的流失是由于膜ATP酶因缺乏足够的底物ATP来维持该梯度而无法发挥作用的结果。