Membrane Fluidity Changes Are Associated with Benzo[ a ]Pyrene‐Induced Apoptosis in F258 Cells

 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.