Gomori‐positive astrocytes: Biological properties and implications for neurologic and neuroendocrine disorders
Identifieur interne : 005069 ( Main/Merge ); précédent : 005068; suivant : 005070Gomori‐positive astrocytes: Biological properties and implications for neurologic and neuroendocrine disorders
Auteurs : Evan W. Schipper [Canada]Source :
- Glia [ 0894-1491 ] ; 1991.
English descriptors
Abstract
Granule laden astrocytes exhibiting an affinity for chrome alum hematoxylin and aldehyde fuchsin (Gomori stains) have been described in the periventricular brain of all terrestrial vertebrate species examined to date including humans. The astrocytic inclusions are rich in sulfhydryl groups, emit an orange‐red autofluorescence, and stain intensely with diaminobenzidine, a marker of endogenous peroxidase activity. The distinct autofluorescence pattern and the absence of neutral lipid, acid phosphatase, and β‐glucuronidase activity exclude lipofuscin or lysosomes as components of these astrocytic granules. The emission of orange‐red autofluorescence and the nonenzymatic nature of the peroxidase activity implicate the presence of porphyrins and metalloporphyrins such as heme as major constituents of these cytoplasmic gliosomes. The role of Gomori‐positive astrocytes under normal and pathologic conditions is incompletely understood. In vivo, numbers of astrocytic granules increase as a function of advancing age, in response to chronic estrogen stimulation, and following X‐irradiation. In vitro, these cells accumulate with increasing time in culture and following exposure to the sulfhydryl agent, cysteamine. Gomori‐positive astrocytes may supply heme to neurons for the synthesis of cytochromes, catalases, and other heme enzymes. They may play a role in photostimulation of sexual cyclicity, the promotion of neuritic development, the degradation of toxic lipoperoxides, and the metabolism of various neurotransmitters. Conversely, these cells may contribute to the pathogenesis of several neurologic and neuroendocrine disorders. Examples of the latter include (a) augmentation of goldthioglucose neurotoxicity, (b) induction of hypothalamic anovulation and reproductive failure, (c) exacerbation of porphyric encephalopathy, and (d) potentiation of parkinsonism and other free radical‐related neurodegenerations.
Url:
DOI: 10.1002/glia.440040404
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Schipper</name><affiliation wicri:level="4"><country>Canada</country><wicri:regionArea>Department of Neurology, McGill University, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis‐Jewish General Hospital, Montreal, Quebec</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation><affiliation wicri:level="4"><country>Canada</country><wicri:regionArea>Dept. of Neurology, McGill University, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis‐Jewish General Hospital, 3755 Cote Ste. 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The astrocytic inclusions are rich in sulfhydryl groups, emit an orange‐red autofluorescence, and stain intensely with diaminobenzidine, a marker of endogenous peroxidase activity. The distinct autofluorescence pattern and the absence of neutral lipid, acid phosphatase, and β‐glucuronidase activity exclude lipofuscin or lysosomes as components of these astrocytic granules. The emission of orange‐red autofluorescence and the nonenzymatic nature of the peroxidase activity implicate the presence of porphyrins and metalloporphyrins such as heme as major constituents of these cytoplasmic gliosomes. The role of Gomori‐positive astrocytes under normal and pathologic conditions is incompletely understood. In vivo, numbers of astrocytic granules increase as a function of advancing age, in response to chronic estrogen stimulation, and following X‐irradiation. In vitro, these cells accumulate with increasing time in culture and following exposure to the sulfhydryl agent, cysteamine. Gomori‐positive astrocytes may supply heme to neurons for the synthesis of cytochromes, catalases, and other heme enzymes. They may play a role in photostimulation of sexual cyclicity, the promotion of neuritic development, the degradation of toxic lipoperoxides, and the metabolism of various neurotransmitters. Conversely, these cells may contribute to the pathogenesis of several neurologic and neuroendocrine disorders. Examples of the latter include (a) augmentation of goldthioglucose neurotoxicity, (b) induction of hypothalamic anovulation and reproductive failure, (c) exacerbation of porphyric encephalopathy, and (d) potentiation of parkinsonism and other free radical‐related neurodegenerations.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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