Mercurial toxicity in yeast: evidence for catabolic pathway inhibition.
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.
D000255:Adenosine Triphosphate / Q000378:metabolism; D004352:Drug Resistance, Microbial; D005636:Fructosephosphates / Q000096:biosynthesis; D005958:Glucosephosphates / Q000096:biosynthesis; D008628:Mercury / Q000494:pharmacology*; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium / Q000378:metabolism; D012441:Saccharomyces cerevisiae / Q000187:drug effects / Q000378:metabolism*
D005636:Fructosephosphates; D005958:Glucosephosphates; D000255:Adenosine Triphosphate; D008628:Mercury; D011188:Potassium