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Literature DB >> 401474

Mitochondrial degeneration after organic phosphate poisoning in prosimian primates.

Abstract

The degenerative reaction of mitochondria to tricresylphosphate (TCP) poisoning in spinal ganglion cells of Slow Loris (Nycticebus coucang coucang) were studied with the electron microscope. In neurones of animals treated with TCP, mitochondria display various stages of alterations which confirm mitochondrial involvement in TCP poisoning. The role of degenerated mitochondria in the formation of neuronal lipofuscin is discussed. It is suggested that the lipofuscin granule is a metabolic product inherently related to mitochondrial degeneration, irrespective of the primary cause: ageing or intoxication.

Entities: Chemical Disease Species

Mesh：

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Year: 1977 PMID： 401474 DOI： 10.1007/bf00222412

Source DB: PubMed Journal: Cell Tissue Res ISSN： 0302-766X Impact factor: 5.249

19 in total

Review 1. CHEMICALLY (TCP) INDUCED FIBRE DEGENERATION IN THE CENTRAL NERVOUS SYSTEM, WITH REFERENCE TO CLINICAL AND NEUROPHARMACOLOGICAL ASPECTS.

Authors: P GLEES; H JANZIK
Journal: Prog Brain Res Date: 1965 Impact factor: 2.453

2. Observations on the morphology, submicroscopic structure and biological properties of satellite cells (s.c.) in sensory ganglia of mammals.

Authors: E PANNESE
Journal: Z Zellforsch Mikrosk Anat Date: 1960

8. The pathogenesis of dying-back polyneuropathies. I. An ultrastructural study of experimental tri-ortho-cresyl phosphate intoxication in the cat.

Authors: J Prineas
Journal: J Neuropathol Exp Neurol Date: 1969-10 Impact factor: 3.685

9. A note on the neuroglia in normal and tricresylphosphate (TCP) poisoned hen.

Authors: M M Ahmed
Journal: Acta Anat (Basel) Date: 1970

10. Synaptic morphology in the spinal cord of normal and tricresylphosphate (TCP) poisoned hen. An electron microscopic study.

Authors: M M Ahmed
Journal: Acta Neuropathol Date: 1971 Impact factor: 17.088

4 in total

Mitochondrial degeneration after organic phosphate poisoning in prosimian primates.

Review 1. CHEMICALLY (TCP) INDUCED FIBRE DEGENERATION IN THE CENTRAL NERVOUS SYSTEM, WITH REFERENCE TO CLINICAL AND NEUROPHARMACOLOGICAL ASPECTS.

2. Observations on the morphology, submicroscopic structure and biological properties of satellite cells (s.c.) in sensory ganglia of mammals.

3. The toxic effects of triortho-cresyl phosphate on the nervous system; an experimental study in hens.

4. The ultrastructure of tricresylphosphate poisoning in primates. 1. Studies on axonal alterations in the spinal cord.

5. Mitochondrial genesis of lipofuscin in the mesencephalic nucleus of the V nerve of aged rats.

6. Ultrastructure of tri-ortho-cresyl phosphate poisoning in the chicken. II. Studies on spinal cord alterations.

7. Neuronal aging in cultures. An electron-microscopic study.

8. The pathogenesis of dying-back polyneuropathies. I. An ultrastructural study of experimental tri-ortho-cresyl phosphate intoxication in the cat.

9. A note on the neuroglia in normal and tricresylphosphate (TCP) poisoned hen.

10. Synaptic morphology in the spinal cord of normal and tricresylphosphate (TCP) poisoned hen. An electron microscopic study.

1. Ultrastructural changes in the autonomic interneuron synapse activated during acetylcholinesterase suppression.

2. Changes in the ultrastructure of satellite cells of slow loris in tricresylphosphate poisoning.

3. Ultrastructural reactions of spinal ganglia to tri-ortho-cresyl-phosphate: effects of neurotoxicity.

4. The mode of mitochondrial degeneration in gliomas.