Vitamin E Inhibits Anti-Fas-Induced Phosphatidylserine Oxidation but Does Not Affect Its Externalization during Apoptosis in Jurkat T Cells and Their Phagocytosis by J774A.1 Macrophages

Behice F. Serinkan, Yulia Y. Tyurina, Hareesh Babu, Mirjana Djukic, Peter J. Quinn, Alan Schroit, Valerian E. Kagan

Research output: Contribution to journalReview article

9 Scopus citations

Abstract

Apoptosis and phagocytosis of apoptotic cells provide for effective and harmless clearance of unwanted or damaged cells in the body. Preferential oxidation of one particular class of phospholipids, phosphatidylserine (PS), is a typical trait of both oxidant- and nonoxidant-induced apoptosis. PS oxidation is likely to play an important role in phagocytosis either by affecting PS externalization acting as an "eat me" signal or by more effective recognition of apoptotic cells by macrophage receptors. This implies that antioxidants effective in inhibiting PS oxidation may affect PS externalization and/or effective removal of apoptotic cells. Therefore, it is essential to determine whether vitamin E, the major lipid-soluble antioxidant of membranes, inhibits PS oxidation, and hence blocks apoptosis/phagocytosis. To test this, we studied the effects of vitamin E on PS oxidation and signaling using a model of anti-Fas-triggered apoptosis in Jurkat T cells. We found that incubation of cells with vitamin E (0.25-50 μM) resulted in its integration into cells to reach physiologically relevant concentrations. Using labeling of cell phospholipids with oxidation-sensitive and fluorescent cis-parinaric acid (PnA), we found that anti-Fas exposure caused significant and selective oxidation of PnA-PS in Jurkat T cells (22 ± 2.1% of its content in nonexposed cells). Vitamin E protected PnA-PS against oxidation in a concentration-dependent way such that at 25 μM and 50 μM, a complete inhibition of anti-Fas-induced PS oxidation was achieved. At all concentrations used, vitamin E had no effect on either biomarkers of anti-Fas-induced apoptosis (PS externalization, nuclear fragmentation) or phagocytosis of anti-Fas-induced apoptotic cells by J774A.1 macrophages. We conclude that vitamin E does not significantly interfere with extrinsic (death receptor-triggered) pathways of apoptosis and does not affect phagocytosis of anti-Fas-triggered apoptotic cells.

Original languageEnglish (US)
Pages (from-to)227-236
Number of pages10
JournalAntioxidants and Redox Signaling
Volume6
Issue number2
DOIs
StatePublished - Apr 2004

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

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