Mercurial toxicity in yeast: evidence for catabolic pathway inhibition.

AUTOR(ES)

Brunker, R L

RESUMO

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.

Documentos Relacionados

• Cystathionine Synthesis in Yeast: an Alternative Pathway for Homocysteine Biosynthesis
• Centromere position in budding yeast: evidence for anaphase A.
• Genetic analysis of iron citrate toxicity in yeast: Implications for mammalian iron homeostasis
• Evidence for a Protein Mutator in Yeast: Role of the Hsp70-Related Chaperone Ssb in Formation, Stability, and Toxicity of the [PSI] Prion
• Replicating Instabilities in Yeast: Evidence from Single Cell Isolation