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Research article summary (published 12 Dec 2001):

Delayed oxidant-induced cell death involves activation of phospholipase A2.

Full Abstract

Short-term (1 h) exposure of cells to a low steady-state concentration of H(2)O(2) 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.

 

Author information

Author/s: Zhao, M (M); Brunk, U T (UT); Eaton, J W (JW);

Affiliation: Division of Pathology II, Faculty of Health Sciences, Linköping University, Sweden. ming.zhao(-atsign-)inr.liu.se

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: FEBS letters (FEBS Lett), published in Netherlands. (Language: eng)

Reference: 2001-Dec; vol 509 (issue 3) : pp 399-404

Dates: Created 2001/12/25; Completed 2002/01/25; Revised 2007/11/15;

PMID: 11749963, status: MEDLINE (last retrieved date: 2/18/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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Associated Chemicals: Oxidants (0) ; Proto-Oncogene Proteins c-bcl-2 (0) ; Melitten (20449-79-0) ; Hydrogen Peroxide (7722-84-1) ; Phospholipases A (EC 3.1.1.-) ; Group II Phospholipases A2 (EC 3.1.1.4) ; Phospholipases A2 (EC 3.1.1.4)

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