International journal of radiation biology, 74(5), 607-615.

Härtel, S., Ojeda, F., and H, Diehl. (1998).

Purpose: To evaluate the involvement of cholesterol induced variations of membrane dynamics in mouse thymocyte apoptosis. Materials and methods : Membranes of thymocytes of RK mice were enriched with cholesterol using methyl- beta -cyclodextrins as carriers. Spontaneous apoptosis was compared with apoptosis induced either by X-irradiation, by treatment with dexamethasone (DEX), and by phorbol-12-myristate-13-acetate (PMA). Apoptotic cells were quantified by means of flow cytofluorometry. Results: Small amounts of incorporated cholesterol enhance the cellular sensitivity for spontaneous apoptosis whereas larger amounts of incorporated cholesterol protect against spontaneous apoptosis and apoptosis induced by irradiation, DEX, or PMA. Conclusions: Cholesterol exerts specific rigidity effects on lipid membranes which have been shown to be involved in thymocyte apoptosis. The general effect of higher concentrations of cholesterol protecting against apoptosis hints towards a central protective mechanism. This study believes that either cholesterol paralyses great parts of the cell metabolism or that the apoptotic chain reaction is interrupted at a central point due to protection of membrane lipid regions from oxidative stress. Abbreviations AO is acridine orange, Bis-pyrene is 1,3-bis-(1-pyrenyl)propane (C35H24), DEX is dexamethasone (9- alpha -fluoro-16- alpha -methyl prednisolone), DPH is 1-6-diphenyl-1,3,5-hexatriene, LPO is lipid peroxidation, PKC is protein kinase-C, PMA is phorbol12-myristrate-13-acetate, p-(D)HPA is p-(di)hydrophenylic acid, ROS is reactive oxygen species.