We report that N-oleoylethanolamine (NOE), widely employed as a ceramidase inhibitor, also inhibits glucosylation of naturally occurring ceramides. When CHP-100 neuroepithelioma cells were exposed for 18h to non-toxic NOE concentrations (i.e. up to 70 mu M), basal incorporation of labelled hexose into glucosylceramide (GlcCer) and higher order neutral glycosphingolipids was significantly inhibited. In cells treated with 30 mu M N-hexanoylsphingosine (C-6-Cer), NOE affected only marginally short-chain glucocerebroside accumulation, but markedly decreased accumulation of glucocerebrosides originating from glucosylation of a long-chain ceramide (Lc-Cer) pool produced upon C-6-Cer treatment. Evidence is provided that NOE effects neither are mediated by their effects on ceramidase nor are due to enhanced long-chain GlcCer (Lc-GlcCer) conversion to higher order glycosylated derivatives. NOE inhibition of Lc-GlcCer generation was accompanied by enhanced accumulation of Lc-Cer and by potentiation of apoptosis induced by C-6-Cer; the possible causal relationships between these two phenomena are discussed. (C) 1999 Academic Press.
Spinedi, A., DI BARTOLOMEO, S., Piacentini, M. (1999). N-oleoylethanolamine inhibits glucosylation of natural ceramides in CHP-100 neuroepithelioma cells: Possible implications for apoptosis. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 255(2), 456-459 [10.1006/bbrc.1999.0230].
N-oleoylethanolamine inhibits glucosylation of natural ceramides in CHP-100 neuroepithelioma cells: Possible implications for apoptosis
SPINEDI, ANGELO;DI BARTOLOMEO, SABRINA;PIACENTINI, MAURO
1999-01-01
Abstract
We report that N-oleoylethanolamine (NOE), widely employed as a ceramidase inhibitor, also inhibits glucosylation of naturally occurring ceramides. When CHP-100 neuroepithelioma cells were exposed for 18h to non-toxic NOE concentrations (i.e. up to 70 mu M), basal incorporation of labelled hexose into glucosylceramide (GlcCer) and higher order neutral glycosphingolipids was significantly inhibited. In cells treated with 30 mu M N-hexanoylsphingosine (C-6-Cer), NOE affected only marginally short-chain glucocerebroside accumulation, but markedly decreased accumulation of glucocerebrosides originating from glucosylation of a long-chain ceramide (Lc-Cer) pool produced upon C-6-Cer treatment. Evidence is provided that NOE effects neither are mediated by their effects on ceramidase nor are due to enhanced long-chain GlcCer (Lc-GlcCer) conversion to higher order glycosylated derivatives. NOE inhibition of Lc-GlcCer generation was accompanied by enhanced accumulation of Lc-Cer and by potentiation of apoptosis induced by C-6-Cer; the possible causal relationships between these two phenomena are discussed. (C) 1999 Academic Press.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
