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Membrane Fluidity Changes Are Associated with Benzo[ a ]Pyrene‐Induced Apoptosis in F258 Cells
Author(s) -
GORRIA MORGANE,
TEKPLI XAVIER,
SERGENT ODILE,
HUC LAURENCE,
GABORIAU FRANÇOIS,
RISSEL MARY,
CHEVANNE MARTINE,
DIMANCHEBOITREL MARIETHÉRÈSE,
LAGADICGOSSMANN DOMINIQUE
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1378.011
Subject(s) - apoptosis , chemistry , pyrene , intracellular , benzo(a)pyrene , membrane fluidity , membrane , microbiology and biotechnology , cytotoxicity , transporter , biophysics , biochemistry , biology , in vitro , organic chemistry , gene
Polycyclic aromatic hydrocarbons (PAHs) such as benzo[ a ]yrene (B[ a ]P) constitute a widely distributed class of environmental pollutants, responsible for highly toxic effects. Elucidating the intracellular mechanisms of this cytotoxicity thus remains a major challenge. Besides the activation of the p53 apoptotic pathway, we have previously found in F258 hepatic cells that the B[ a ]P (50 nM)‐induced apoptosis was also dependent upon the transmembrane transporter NHE1, whose activation might result from membrane alterations in our model. We here demonstrate that: (1) B[ a ]P induces a membrane fluidization surprisingly linked to NHE1 activation; (2) membrane stabilization by exogenous cholesterol protects cells from B[ a ]P‐induced apoptosis, via an effect on late acidification and iron uptake.