On the mechanism of action of H2O2 in the cellular stress.
We propose a hypothesis according to which the reactive and reduced species of oxygen could be the intracellular inducers of the stress (or "heat-shock") response. This hypothesis is based on the following observations on Drosophila cells: a) the return to normoxia after 24 h anaerobiosis is sufficient to induce the synthesis of the "heat shock" proteins without elevation of temperature together with a rapid increase of O2 consumption; b) hydrogen peroxide introduced in the culture medium induces the early transcriptional activation of the "heat shock" genes (maximal after 5 minutes); c) hydrogen peroxide added to cellular extracts in vitro (thus acting as an intracellular metabolite) activates instantaneously the binding capacity of a "heat shock" factor to a DNA "heat shock" regulatory element. Thus, hydrogen peroxide, and possibly other reactive reduced species of oxygen, could trigger the onset of the stress (or "heat shock") response.
Becker
J
J
Génétique Moléculaire et Cellulaire, Unité Associée au CNRS 1135, Université Pierre et Marie Curie, Paris, Frane.
Mezger
V
V
Courgeon
A M
AM
Best-Belpomme
M
M
D000818:Animals; D015687:Cell Hypoxia; D002478:Cells, Cultured; D004331:Drosophila melanogaster / Q000166:cytology; D005609:Free Radicals; D005786:Gene Expression Regulation; D006360:Heat-Shock Proteins / Q000096:biosynthesis*; D006358:Hot Temperature; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D008954:Models, Biological; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D012045:Regulatory Sequences, Nucleic Acid; D013312:Stress, Physiological / Q000378:metabolism*
D005609:Free Radicals; D006360:Heat-Shock Proteins; D006861:Hydrogen Peroxide