Myelin lipids in ischemic stroke.

Slices of ischemic focus (infarct area) and of the contralateral frontal lobe were submitted to histological and biochemical studies. The obtained results indicate that in stroke cases the necrotic focus as well as contralateral brain hemisphere are characterized by a marked decrease of cholesterol and cerebrosides content and an increase of lysophosphatidylcholine and cholesterol esters in the myelin fraction. We conclude that ischemia as well as the degenerative aging process are both responsible for the abnormal lipid pattern in the myelin of the white matter in stroke cases. The long lasting hypoxia resulting from cerebral vessel atheromatosis contributes to biochemical changes in the myelin of the apparently healthy white matter of the contralateral hemisphere in brain infarction.

Pattern of myelin proteins in moderate hypoxia.

Myelin proteins isolated from the brain of Wistar rats subjected to moderate hypoxia (7% of oxygen in a respiration gaseous mixture) for 30 min were investigated. Among the various protein fractions Wolfgram protein happened to be most markedly affected, demonstrating considerably lowered percentages in all experimental groups, starting from 24 h after hypoxia. Our findings compared with those obtained in other experimental conditions lead to the conclusion that changes in the myelin protein pattern are characteristic for particular morbid processes evoked by various pathogenic factors. The demyelination is concomitant with severe loss of basic proteins, whereas myelin lesions of other types are connected with changes in protein of higher molecular mass.

Myelin lipids of the rat brain in experimental hypoxia.

The pattern of cerebral myelin lipids was studied in Wistar rats exposed to mild hypoxia (7% of oxygen in a respiratory mixture) for 30 min. The most pronounced change involved a marked increase in cholesterol esters and lysophosphatidylcholine content in the myelin fraction. The results obtained indicate that mild hypoxia induces a lesion of myelin membranes but does not provoke the reaction of lymphocytes and macrophages, which by production of myelinolytic factors, evoke demyelination.

Lipids of the oligodendroglial fraction in methylnitrosourea induced encephalopathy.

The investigations were performed on oligodendroglial cells isolated from the cerebral white matter of Wistar rats treated intravenously with a 3% solution of MNU at a dose of 60 mg/kg body weight. The oligodendroglial fraction showed a decrease of the sphingomyelin, phosphatidylserine and phosphoinositides content. The observed changes correlated with alterations of the lipid spectrum found in the myelin fraction of MNU intoxicated rats. This would indicate that MNU acting in the central nervous system affects in a similar way the lipid metabolism of both components of the oligodendroglia-myelin system.

The effect of transplacental intoxication with ethylnitrosourea on myelin proteins.

Pregnant mice at the 15th day of gestation were injected with a single intravenous dose of ENU/80 mg/kg of body weight). The protein composition of the myelin fraction isolated by means of differential centrifugation from brains of the offsprings was studied. The results obtained lead to the following conclusions: 1. The myelin protein spectrum of transplacentally intoxicated animals aged 40 days postnatal, shows decreased percentages of the Wolfgram protein and of the low molecular weight basic protein, whereas the proportions of the high molecular weight component of the myelin basic protein as well that of the Agrawal's protein are elevated. 2. The alterations in the profile of myelin proteins obtained from experimental mice aged 70 days postnatal are less severe and consist in a decline of the percentage of Wolfgrams protein and elevation of the Agrawal's protein content. 3. The intraplacental intoxication of mouse fetuses leads to development of animals defective with respect to the protein composition of the central myelin.

Activity of acid: Co A ligase (AMP) in the course of experimental allergic encephalomyelitis.

In studies concerned with the activation of fatty acids, a metabolic step initiating the biosynthesis of fatty acids rendering them suitable for elongation, desaturation, esterification or degradation, we have demonstrated that the activity of acid: Co A ligase (AMP) -- E.C.6.2.1.3. is declined throughout the whole investigated period of experimental allergic encephalomyelitis (EAE). This observation clearly indicates that in this experimental disease it is not only the increased catabolism of lipid constituents furnishing the various membraneous structures, including myelin sheats, but also an overall impaired capacity of synthesing new lipids by the diseased cells of the nervous system which must be taken into consideration.