N-methyl bases of ethanolamine prevent apoptotic cell death induced by oxidative stress in cells of oligodendroglia origin

A major reason for brain tissue vulnerability to oxidative damage is the hi gh content of polyunsaturated fatty acids (PUFAs). Oligodendroglia-like OLN 93 cells lack PUFAs and are relatively insensitive to oxidative stress. Wh en grown in serum-free defined medium in the presence of 0.1 mM docosahexae noic acid (DHA; 22:6 n-3) for 3 days, OLN 93 cells release in the medium 2. 6-fold more thiobarbituric acid-reactive substances (TBARS) after a 30-min exposure to 0.1 mM H2O2 and 50 mu M Fe2+. Release of TBARS was substantiall y decreased by similar to 20 and 30% on coincubation with either 1 mM N-mon omethylethanolamine or N,N-1-dimethylethanolamine (dEa), respectively. The protective effect of dEa was concentration- and time-dependent and was stil l visible after dEa removal, suggesting a long-lasting mechanism of protect ion. After 24 h following H2O2-induced stress, cell death monitored by cell sorting showed 16% of the cells in the sub-G, area, indicative of apoptoti c cell death. DHA-supplemented cultures showed 35% cell death, whereas cosu pplements with dEa reduced cell death to 12%, indicating cell rescue. Altho ugh 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.