PHOSPHATIDYLSERINE SYNTHESIS IN RAT CEREBRAL-CORTEX - EFFECTS OF HYPOXIA, HYPOCAPNIA AND DEVELOPMENT

Citation
R. Mozzi et al., PHOSPHATIDYLSERINE SYNTHESIS IN RAT CEREBRAL-CORTEX - EFFECTS OF HYPOXIA, HYPOCAPNIA AND DEVELOPMENT, Molecular and cellular biochemistry, 126(2), 1993, pp. 101-107
Citations number
37
Categorie Soggetti
Biology
ISSN journal
03008177
Volume
126
Issue
2
Year of publication
1993
Pages
101 - 107
Database
ISI
SICI code
0300-8177(1993)126:2<101:PSIRC->2.0.ZU;2-8
Abstract
Phosphatidylserine, which is necessary for protein kinase C activity, is synthesized in mammalian tissues by the Ca2+ - dependent base excha nge enzyme. The synthesis of phosphatidylserine is greater in slices o r homogenates of rat cerebral cortex subjected to hypoxia by N-2 treat ment when compared with O-2 plus 5% CO2 An intermediate effect was obs erved when the treatment was done with N-2 plus 5% CO2. Incorporation rates were dependent on Ca2+ in Krebs-Henseleit Ringer bicarbonate med ium, being greater with 2 mM Ca2+ than with the same medium prepared w ithout Ca2+. The increase of phosphatidylserine synthesis, due to hypo xia, was, on the contrary, more evident in the medium lacking added Ca 2+. Similar results were obtained with the homogenates. This suggests that elevation of intracellular Ca2+, caused by hypocapnia and hypoxia , may be responsible for the greater incorporation of serine into phos phatidylserine. In both cerebrocortical slices and homogenate, [C-14]s erine incorporation decreased with development both in O-2 plus 5% CO2 and N-2-treated preparations. However, in younger rats (14-18 days) h ypoxia induced a lesser increase of phosphatidylserine than in 40 day old animals. We suggest that a regulatory mechanism for phosphatidylse rine synthesis is established during development and that N-2-treatmen t can increase phosphatidylserine synthesis by interfering with this r egulatory mechanism.