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The galactose-induced decrease in phosphate levels leads to toxicity in yeast models of galactosemia.

Caio M Machado1, Evandro A De-Souza1, Ana Luiza F V De-Queiroz1

  • 1Instituto de Bioquímica Médica Leopoldo de Meis, Programa de Biologia Molecular e Biotecnologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-902, Brazil.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|February 19, 2017
PubMed
Summary
This summary is machine-generated.

Classic galactosemia, a metabolic disorder, involves galactose-1-phosphate accumulation. This study reveals that phosphate depletion caused by this accumulation leads to toxicity, offering new treatment avenues.

Keywords:
Galactose-1-phosphateGalactosemiaLithiumPhosphate trappingSaccharomyces cerevisiaeUnfolded protein response

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Area of Science:

  • Biochemistry
  • Metabolic Disorders
  • Genetics

Background:

  • Classic galactosemia is an inherited metabolic disorder resulting from GALT gene mutations.
  • Elevated galactose-1-phosphate is implicated in galactosemia toxicity, but underlying molecular mechanisms are unclear.

Purpose of the Study:

  • To investigate the molecular consequences of galactose-1-phosphate accumulation in galactosemia.
  • To explore the role of inorganic phosphate levels in galactosemia pathogenesis.

Main Methods:

  • Utilized yeast models of classic galactosemia.
  • Measured intracellular inorganic phosphate and glycogen levels.
  • Assessed the impact of gene deletions (GAL1) and phosphate level manipulation.

Main Results:

  • Galactose exposure in yeast models led to decreased intracellular inorganic phosphate.
  • Phosphate depletion correlated with increased glycogen content.
  • Restoring phosphate levels ameliorated galactose toxicity and increased galactose tolerance.

Conclusions:

  • Galactose-induced inorganic phosphate depletion is a key mechanism driving toxicity in galactosemia.
  • Targeting phosphate levels presents a potential therapeutic strategy for galactosemia.