Signalling steps in apoptosis by ether lipids.
作者： L. A. Smets , H. Van Rooij , G. S. Salomons
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摘要: We have investigated the mechanisms of induction apoptosis by antineoplastic ether lipid ET-18-OCH3 (ALP) in sensitive S49wt mouse lymphoma cells and ALP-resistant S49ar variants, both with wild-type p53, related L1210 mutated p53. Ether lipid-resistant were cross-resistant to extracellular stress factors (cold shock, heat H2O2, dimethylsulfoxide) radiation-induced but not physiological apoptotic signals (dexamethasone, growth factor deprivation, thapsigargin, C2-ceramide) expressed similar levels apoptosis-regulating proteins Bcl-2, Bcl-X, Bax, Bad Bak as did parent cells. The uptake [3H]-ALP was strongly reduced stress-resistant this associated significant differences membrane cholesterol:phospholipid content nor microviscosity. In activity antioxidant enzyme glutathione peroxidase (GSH-Px) increased 4-fold depletion drug L-buthionine-S-R-sulfoximine (L-BSO) lowered resistance ALP, ionising radiation. results indicate that lipids induce imposing a special form physico-chemical stress, mediated reactive oxygen species independent p53 status. capacity glutathione-dependent anti-oxidant defence appeared an important shared determinant sensitivity lipids, several types
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