Biomedical subjects
Publications and source records attributed to A Goncerzewicz.
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Axon-myelin interrelationship was analysed morphometrically in developing optic nerves of Wistar rats maintained during the maturation on normal, lipid deficient and lipid enriched diets. The results obtained lead to the following conclusions: Myelinogenesis in the optic nerve of Wistar rats is severely retarded in animals maintained on a fatty acid deficient diet during the last period of intrauterine life and during their whole postnatal life. The axon diameter of the optic nerves in animals fed on a fatty acid deficient diet is normal in the first weeks of postnatal development, but it does not reach the values of normal ones in the young adult animals. The dietary deficit of fatty acids caused qualitative changes in the myelin-axon interrelationship in the course of myelinogenesis as indicated by an altered distribution of the ratios in the number of myelin lamellae to the axon diameter (the regression equation has changed from a linear to a parabolic one). Comparison of the morphometric and chemical studies of the developing myelin in the fatty acid deficiency experiments testify that the numerically normal myelin in young adult animals is still deficient in basic lipid classes.
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Wallerian degeneration of the rabbit optic nerve was produced by enucleation and the myelin output as well as its lipid composition were studied. In spite of the marked drop in the myelin mass, occurring very soon after enucleation the lipid composition of the corresponding myelin fractions did not change appreciably, phosphatidylcholine being the most resistant lipid species. However, from the very beginning of the degenerating process there appeared in the myelin lipid spectrum marked amounts of cholesteryl esters and phosphatidic acids and in the later period elevated amounts of lysophosphatidylcholine. Enhanced esterification of cholesterol could function as an early primary factor injuring the myelin membrane, the lysocompounds may be involved at a later stage in the pathomechanism of myelin decomposition in the central nervous system.
A histochemical study was performed on the activity of several phosphatases, esterases and oxidoreductases in the spinal cord of cat in the course of the myelinopathy provoked by the cerebrospinal fluid (CSF) exchange. The following results were obtained: 1. Neuroglial cells of the spinal cord react with a slight, focal increase of TPP-ase activity already during the early stage of myelinopathy evoked by repeated withdrawal and reinjecting of CSF into the Cisterna magna of experimental cats. 2. During the late stage of this experimental disease-- the oligo-and astroglia of the spinal cord dtsplay considerably increased activities of ATP-ase, acP, and of various oxidoreductases. 3. The observed morphological and functional (increased enzymic activity) changes of the oligodendroglia as well as the demonstrable damage of myelin sheath, seem to be the results of vasogenous edema. 4. The results of investigations performed did not yield any arguments, which would speak in favour of the assumption, that the changes of the oligodendroglia cells function as the primary cause in the myelinopathy provoked by the CSF exchange, affecting secondary the myelin sheaths. 5. The decissively increased lysosomal acP activity in oligodendroglial cells of the spinal cord investigated during the early stage of this myelinopathy, accompanied by an evidently damaged Golgi apparatus, may be explained when the Golgi zone is not necessarily the only cellular site where acid phosphatase may be performed.
The histoenzymic pattern of oxidative enzymes (G3PD, IDH, SD, G6PD,HBD, NADPH: dehydrogenase) was investigated in experimental allergic encephalomyelitis (EAE) produced in rats according to PATERSON [13]. The results obtained lead to following conclusions: (1) The neuroglia, including the white matter oligodendroglia of immunized rats, exhibits increased oxidoreductase activities; (2) The neuroallergic reaction induces some stimulation of the oxidoreductive metabolism of oligoden-droglia; (3) The enzymatic hyperactivity in EAE does not show any relation to the morphological signs of alterations of the myelin sheath.
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A case of adrenoleukodystrophy is reported in which the diagnosis was possible only after electron microscopic examination in view of absence of clinical signs of adrenocortical failure.
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