Micromolar HgCl2 concentrations transitorily duplicate the ATP level in Saccharomyces cerevisiae cells

Eduardo Silles1, Hugo Osorio, Rita Maia

  • 1Departamento de Bioquímica, Instituto de Investigaciones Biomédicas Alberto Sols UAM/CSIC, Facultad de Medicina, 28029 Madrid, Spain.

FEBS Letters
|July 19, 2005
PubMed

Insights

Mercury(II) chloride (HgCl2) initially boosts then depletes ATP in yeast. This mercury toxicity affects energy metabolism and inhibits key enzymes like plasma membrane proton ATPase.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Environmental Toxicology

Background:

  • Mercury(II) chloride (HgCl2) is a toxic heavy metal compound.
  • Understanding its effects on cellular energy metabolism is crucial.
  • Saccharomyces cerevisiae serves as a model organism for studying cellular responses to toxins.

Purpose of the Study:

  • To investigate the impact of low HgCl2 concentrations on ATP levels in Saccharomyces cerevisiae.
  • To elucidate the effects of HgCl2 on key metabolic intermediates and enzymes.
  • To determine the mechanism of HgCl2 toxicity in yeast energy production.

Main Methods:

  • Treatment of Saccharomyces cerevisiae with varying concentrations of HgCl2 (1 microM and 10 microM).
  • Measurement of intracellular ATP levels over time.
  • Analysis of hexose phosphates and inosine levels.
  • Assay of plasma membrane proton ATPase, hexokinase, and 6-phosphofructokinase activities.

Main Results:

  • Low HgCl2 concentrations caused a transient increase in ATP, followed by a significant decrease.
  • The duration of the initial ATP increase was dose-dependent (30 min at 1 microM, 5 min at 10 microM).
  • HgCl2 altered hexose phosphate and inosine levels, and inhibited plasma membrane proton ATPase activity, but not hexokinase or 6-phosphofructokinase.

Conclusions:

  • HgCl2 disrupts cellular energy homeostasis in yeast by affecting ATP production and utilization.
  • The inhibition of plasma membrane proton ATPase is a key mechanism in HgCl2 toxicity.
  • Yeast metabolism shows complex adaptive and detrimental responses to mercury exposure.

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