INVESTIGADORES
GIUSTO Norma Maria
artículos
Título:
Anoxia-induced production on methylate and free fatty acids in retina, cerebral cortex and white matter in vitro: comparison with triacylglycerol and with other tissues
Autor/es:
GIUSTO, N.M.; BAZÁN, N.
Revista:
Neurochemical Pathology
Editorial:
ISN
Referencias:
Año: 1983 vol. 1 p. 17 - 41
ISSN:
0734-600X
Resumen:
The content and composition of retinal free fatty acids (FFA)† was determined during in vitro anoxia. Anoxia induced a fourfold increase in FFA production, but these lipids were modified only slightly after aerobic incubation. An even greater increase in FFA occurred when BSA was present during anoxia. In the presence of BSA, the FFA pool remaining in the anoxic tissue was larger than that observed under aerobiosis. The addition of glucose during aerobic incubation yielded even higher levels of FFA, and free docosahexaenoic acid was released rapidly and displaced into the medium during aerobic incubation. Anoxia promoted an increased release of polyenoic FFA, notably of docosahexaenoic acid. Similar FFA profiles were found in slices of cerebral cortex and white matter. Negligible amounts of endogenous longchain fatty acid methyl esters (FAME) were observed in the neural tissues after aerobiosis. However, a remarkable increase in FAME occurred during anoxia. This phenomenon was reversed by aerobic reincubation. Glucose enhanced the triacylglycerol content in anoxic brain slices. During anoxia, retina and gray matter slices generated predominantly docosahexaenoate, arachidonate, stearate, and palmitate methyl esters, whereas white matter slices yielded other FAME. FAME that were present in liver and heart were not altered by anoxic incubation, even when FFA increased. It is concluded that FFA are derived from phospholipid deacylation, and that the in vitro retina is a more suitable CNS model for membrane lipid studies than brain slices, because it can maintain an almost constant FFA pool during short-term incubations under aerobic conditions. Also, the formation of FAME in the nervous system may be a defense mechanism aimed at lowering FFA levels when neurons are exposed to extreme oxygen deprivation.