| Autor: |
Avrova, N.F., Zakharova, I.O., Tyruin, V.A., Tyurina, Y.Y., Gamaley, I.A., Schepetkin, I.A. |
| Předmět: |
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| Zdroj: |
Neurochemical Research; Aug2002, Vol. 27 Issue 7/8, p751, 9p, 5 Charts, 5 Graphs |
| Abstrakt: |
The metabolic effects of ganglioside GM1 were found to be quite different in brain synaptosomes and phagocytic cells. Incubation of rat brain cortex synaptosomes with GM1 was shown to decrease the production of reactive oxygen species induced by Fe[sup 2+]-H[sub 2]O[sub 2] system and measured by chemiluminometric method in the presence of luminol. Gangliosides GM1, GDla, and GTlb significantly diminished the induced accumulation of lipid peroxidation product in brain synaptosomes, but protein kinase inhibitor (polymyxin B) abolished this effect. Incubation with antioxidants or GM1 significantly diminished the increase of [sup 45]Ca[sup 2+ ]influx and oxidative inactivation of Na[sup +],K[sup +]-ATPase in brain synaptosomes exposed to glutamate, the effect of GMI was concentration-dependent in the range 10[sup -11]-10[sup -8] M. But the incubation of human neutrophils and mouse peritoneal macrophages with 10[sup -11]-10[sup 10] M GM1, on the contrary, increased several times the luminol-dependent chemiluminescence response of these cells to activation by low concentrations of 12-myristate-13-acetate phorbol ester. The opposite effects of GM 1 in the nerve endings and phagocytic cells seem to be protective in both cases as the inhibition of reactive oxygen species production in the nerve cells may enhance their viability in damaged brain, while the intensification of their production in phagocytic cells may promote the resistance of organism to infection. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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