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N ‐Methyl Bases of Ethanolamine Prevent Apoptotic Cell Death Induced by Oxidative Stress in Cells of Oligodendroglia Origin
Author(s) -
Brand Annette,
Gil Shosh,
Yavin Ephraim
Publication year - 2000
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2000.0741596.x
Subject(s) - oxidative stress , ethanolamine , programmed cell death , apoptosis , oxidative phosphorylation , microbiology and biotechnology , cell , chemistry , apoptotic cell death , biochemistry , biology , neuroscience
A major reason for brain tissue vulnerability to oxidativedamage is the high content of polyunsaturated fatty acids (PUFAs).Oligodendroglia‐like OLN 93 cells lack PUFAs and are relatively insensitive tooxidative stress. When grown in serum‐free defined medium in the presence of0.1 m M docosahexaenoic acid (DHA; 22:6 n‐3) for 3 days, OLN 93 cellsrelease in the medium 2.6‐fold more thiobarbituric acid‐reactive substances(TBARS) after a 30‐min exposure to 0.1 m M H 2 O 2 and 50 μ M Fe 2+ . Release of TBARS was substantiallydecreased by ∼20 and 30% on coincubation with either 1 m M N ‐monomethylethanolamine or N,N′ ‐dimethylethanolamine(dEa), respectively. The protective effect of dEa was concentration‐ andtime‐dependent and was still visible after dEa removal, suggesting along‐lasting mechanism of protection. After 24 h followingH 2 O 2 ‐induced stress, cell death monitored by cellsorting showed 16% of the cells in the sub‐G 1 area, indicative of apoptotic cell death. DHA‐supplemented cultures showed 35% cell death, whereas cosupplements with dEa reduced cell death to 12%, indicating cell rescue. Although the exact mechanism for this protection is not known, the nature of the polar head group and the degree of unsaturation may determine the ultimate resistance of nerve cells to oxidative stress.