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H 2 O 2 ‐induced block of glycolysis as an active ADP‐ribosylation reaction protecting cells from apoptosis
Author(s) -
Colussi C.,
Albertini M.C.,
Coppola S.,
Rovidati S.,
Galli F.,
Ghibelli L.
Publication year - 2000
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.00-0074com
Subject(s) - glycolysis , apoptosis , glyceraldehyde 3 phosphate dehydrogenase , chemistry , biochemistry , programmed cell death , microbiology and biotechnology , nad+ kinase , hexokinase , flux (metallurgy) , dehydrogenase , metabolism , biology , enzyme , organic chemistry
H 2 O 2 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. H 2 O 2 ‐induced block of glycolysis as an active ADP‐ribosylation reaction protecting cells from apoptosis. FASEB J . 14, 2266‐2276 (2000)