Delayed oxidant-induced cell death involves activation of phospholipase A2
2001 (English)In: FEBS Letters, ISSN 0014-5793, E-ISSN 1873-3468, Vol. 509, no 3, 399-404 p.Article in journal (Refereed) Published
Short-term (1 h) exposure of cells to a low steady-state concentration of H2O2 causes no immediate cell death but apoptosis occurs several hours later. This delayed cell death may arise from activation of phospholipases, in particular phospholipase A2 (PLA2), which may destabilize lysosomal and mitochondrial membranes. Indeed, the secretory PLA2 (sPLA2) inhibitor 4-bromophenacyl bromide diminishes both delayed lysosomal rupture and apoptosis. Furthermore, sPLA2 activation by mellitin, or direct micro-injection of sPLA2, causes lysosomal rupture and apoptosis. Finally, B-cell leukemia/lymphoma 2 (Bcl-2) over-expression prevents oxidant-induced activation of PLA2, delayed lysosomal destabilization and apoptosis. This supports a causal association between PLA2 activation and delayed oxidant-induced cell death and suggests that Bcl-2 may suppress apoptosis by preventing PLA2 activation.
Place, publisher, year, edition, pages
2001. Vol. 509, no 3, 399-404 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-27705DOI: 10.1016/S0014-5793(01)03184-2Local ID: 12443OAI: oai:DiVA.org:liu-27705DiVA: diva2:248257