Intraluminal hydrogen peroxide induces a permeability change of the endoplasmic reticulum membrane

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Gulonolactone treatment of mice resulted in the elevation of hepatic ascorbate and hydrogen peroxide levels accompanied by transient liver swelling and reversible dilatation of endoplasmic reticulum cisternae. Although a decrease in glutathione (reduced form)/total glutathione ratio was observed in microsomes, the redox state of luminal foldases remained unchanged and the signs of endoplasmic reticulum stress were absent. Increased permeability of the microsomal membrane to various compounds of low molecular weight was substantiated. It is assumed that Gulonolactone-dependent luminal hydrogen peroxide formation in the endoplasmic reticulum provokes a temporary increase in non-selective membrane permeability, which results in the dilation of the organelle and in enhanced transmembrane fluxes of small molecules.

Original languageEnglish
Pages (from-to)4131-4136
Number of pages6
JournalFEBS Letters
Volume582
Issue number30
DOIs
Publication statusPublished - Dec 24 2008

Fingerprint

Endoplasmic Reticulum
Hydrogen Peroxide
Glutathione
Dilatation
Permeability
Membranes
Endoplasmic Reticulum Stress
Liver
Microsomes
Organelles
Oxidation-Reduction
Swelling
Molecular Weight
Molecular weight
Fluxes
Molecules
gulonolactone

Keywords

  • ER stress
  • Glutathione
  • Gulonolactone oxidase
  • Hydrogen peroxide
  • Membrane permeability
  • Oxidative protein folding

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Genetics
  • Molecular Biology
  • Structural Biology

Cite this

Intraluminal hydrogen peroxide induces a permeability change of the endoplasmic reticulum membrane. / Margittai, E.; Lőw, P.; Szarka, A.; Csala, M.; Benedetti, Angelo; Bánhegyi, G.

In: FEBS Letters, Vol. 582, No. 30, 24.12.2008, p. 4131-4136.

Research output: Contribution to journalArticle

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AU - Szarka, A.

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AU - Benedetti, Angelo

AU - Bánhegyi, G.

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