Mitochondrial Changes in Axonal Dystrophy Produced by Vitamin E Deficiency

Schochet, Sydney S.

doi:10.1007/978-3-642-47449-1_7

Cited by 10 publications

(2 citation statements)

References 18 publications

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“…Dilatation of the ER cisternae sometimes followed by vacuolation was observed after axonal lesion (Pannese, 1963;Barron et al, 1967;Price & Porter, 1972), deafferentation (Glees, Hasan & Tischner, 1967;Ghetti et al, 1972), irradiation with protons (Andres, 1963) or X-rays (Masurovsky, Bunge & Bunge, 1967), and in ascorbic acid deficiency (Sulkin & Sulkin, 1967). Mitochondria1 changes similar to those described above were observed in nerve cells after administration of different agents, and during vitamin E deficiency (Schochet, 1971).…”

Section: Morphological Specificity Of the Degenerative Processsupporting

confidence: 80%

An Electron Microscopic Study of Cell Degeneration in Chick Embryo Spinal Ganglia

Pannese

1976

Neuropathology Appl Neurobio

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An electron microscopic study of cell degeneration in chick embryo spinal ganglia Cell degeneration which normally occurs during development was studied under the electron microscope in thoracic spinal ganglia of chicken embryos. Cells undergoing degeneration were often identified as primitive neuroblasts or transitional cells between the primitive and intermediate neuroblast, and sometimes as intermediate neuroblasts. Degeneration seems to begin with nuclear alterations (chromatin condensation and segregation of the nucleolar components) and ribosomal changes (polysomal disaggregation, and displacement of many membrane‐associated ribosomes). Soon the Golgi complex is no longer recognizable. Successively, large masses of finely granular material become prominent in the nucleus, the nuclear envelope breaks down, many mitochondria appear altered, many vacuoles with clear contents become evident, and ribosome crystals appear. At the end of the process the degenerated cell appears as a shrunken mass of granular debris and membrane fragments. Some neuroblastic processes contain clumped filaments and microtubules and/or polymorphic dense bodies. These structural changes are not unique to this degenerative process, but closely resemble those following other types of injuries of the nerve cell. A drastic reduction in the nuclear synthesis of RNA, and a profound impairment in protein synthesis are probably the main biochemical events which occur in these degenerating cells. Degeneration, which probably affects the neuroblasts which fail to establish appropriate connections with the periphery, seems to be one of the major factors controlling cell number in the spinal ganglia.

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Section: Morphological Specificity Of the Degenerative Processsupporting

confidence: 80%

An Electron Microscopic Study of Cell Degeneration in Chick Embryo Spinal Ganglia

Pannese

1976

Neuropathology Appl Neurobio

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“…Morphological alterations in the mitochondria from gracile and cuneate nuclei were reported by Schochet a number of years ago (13). Vitamin E deficient mitochondria were enlarged and pleomorphic; they underwent a characteristic non-autophagic dissolution leading to accumulation of masses of granular dense material.…”

Section: Mitochondria and Vitamin Ementioning

confidence: 95%

Impairment of Brain Mitochondrial Oxidative Phosphorylation Accompanying Vitamin E Oxidation Induced by Iron or Reactive Nitrogen Species: A Selective Review

Vatassery

2004

Neurochem Res

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Mitochondria are exposed to large fluxes of iron, and reactive oxygen and nitrogen species. Hence they are susceptible to oxidative stress, a process inhibited by vitamin E. Our investigations show that iron uncouples oxidative phosphorylation whereas peroxynitrite and nitrite are inhibitors of oxidative phosphorylation. Oxidation of mitochondrial vitamin E is accompanied by generation of lipid peroxidation products, altered enzyme activity and electrical conductance etc., and result in inefficient oxidative phosphorylation. Vitamin E is important for mitochondrial function because: (1) Prior investigations have shown that vitamin E is essential for maintaining mitochondrial respiration. (2) Vitamin E is the most potent, lipid-soluble antioxidant localized ideally in mitochondrial membranes. (3) The decline in respiratory control ratios (RCR) of rat brain mitochondria exposed to peroxynitrite closely paralleled the oxidative elimination of vitamin E. (4) Finally, iron is a strong uncoupler of oxidative phosphorylation in brain mitochondria from vitamin E deficient animals and not from controls.

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The Axon: Normal Structure and Pathological Alterations

Bilbao

Schmidt

2014

Biopsy Diagnosis of Peripheral Neuropathy

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Mitochondrial Changes in Axonal Dystrophy Produced by Vitamin E Deficiency

Cited by 10 publications

References 18 publications

An Electron Microscopic Study of Cell Degeneration in Chick Embryo Spinal Ganglia

An Electron Microscopic Study of Cell Degeneration in Chick Embryo Spinal Ganglia

Impairment of Brain Mitochondrial Oxidative Phosphorylation Accompanying Vitamin E Oxidation Induced by Iron or Reactive Nitrogen Species: A Selective Review

The Axon: Normal Structure and Pathological Alterations

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