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H₂O₂-induced block of glycolysis as an active ADP-ribosylation reaction protecting cells from apoptosis

Dipartimento di Biologia, Università di Roma Tor Vergata; 00133, Rome, Italy; and
^* Istituto di Biochimica G. Fornaini, Università di Urbino, Rome, Italy

¹Correspondence: Dipartimento di Biologia, Università di Roma Tor Vergata; via della Ricerca Scientifica, 00133, Roma. E-mail. ghibelli{at}uniroma2.it

H₂O₂ treatment on U937 cells leads to the block of glycolytic flux and the inactivation of glyceraldehyde-3-phosphate-dehydrogenase by a posttranslational modification (possibly ADP-ribosylation). Glycolysis spontaneously reactivates after 2 h of recovery from oxidative stress; thereafter cells begin to undergo apoptosis. The specific ADP-ribosylation inhibitor 3-aminobenzamide inhibits the stress-induced inactivation of glyceraldehyde-3-phosphate-dehydrogenase and the block of glycolysis; concomitantly, it anticipates and increases apoptosis. Exogenous block of glycolysis (i.e., by culture in glucose-free medium or with glucose analogs or after NAD depletion), turns the transient block into a stable one: this results in protection from apoptosis, even when downstream cell metabolism is kept active by the addition of pyruvate. All this evidence indicates that the stress-induced block of glycolysis is not the result of a passive oxidative damage, but rather an active cell reaction programmed via ADP-ribosylation for cell self-defense.—Colussi, C., Albertini, M. C., Coppola, S., Rovidati, S., Galli, F., Ghibelli, L. H₂O₂-induced block of glycolysis as an active ADP-ribosylation reaction protecting cells from apoptosis.

Key Words: NAD • oxidative stress • hydrogen peroxide • 3-aminobenzamide

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