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 Drosphila cells: -a) the return to normoxia after 24 h anaerobiosis is suficient 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 transcrip-tional 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 ofoxygen, could trigger the onset of the stress (or 'heat shock' response. © 1991 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.