Progressive Neuropathologic Lesions in Vitamin E-Deficient Rhesus Monkeys

Nelson, James S.; Fitch, Coy D.; Fischer, Vernon W.; Broun, G. O.; Chou, Albert C.

doi:10.1097/00005072-198103000-00008

Cited by 167 publications

(64 citation statements)

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“…20 Dystrophic axons may occur in either gray or white matter and are thought to develop as a result of an intrinsic or extrinsic (noxious agent) disturbance of the metabolism or function of the axoplasm or as a result of very chronic neuronal injury. 11,20 In animals, axonal dystrophy associated with the formation of spheroids occurring predominantly in the gray matter is associated with experimental and naturally occurring vitamin E deficiency, 25,28,31,39 locoweed poisoning, 14,42 some storage diseases, 7,21 primary heredofamilial neuroaxonal dystrophies 6,8 and various experimental toxicoses such as B,B'-iminodiproprionitrile (IDPN) 4,18 and sodium diethyldithiocarbamate poisoning 16 and as an incidental finding with advanced age. 10 In axonal dystrophy, spheroids are characterized by round, ovoid, or polymorphic masses that vary in diameter from 20 to 120 µm.…”

Section: Discussionmentioning

confidence: 99%

Neuroaxonal Degeneration in Sheep GrazingSorghumPastures

et al. 1995

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Abstract. During the fall of 1992, 250 (10%) of 2,500 Rambouilet cross feeder lambs grazing Sorghum bicolor developed neurologic signs including weakness, ataxia, head shaking, knuckling of the fetlocks, inability to rise, and opisthotonos. One hundred fifteen (46%) of the affected lambs died. Twenty of the surviving lambs exhibited residual neurologic signs of ataxia when stressed. At the same time, 275 (25%) of 1,100 ewes grazing a nearby sudex pasture (S. sudanese x S. bicolor) gave birth to lambs that were weak and unable to rise. Newborn lambs exhibited extensor rigidity and opisthotonos when assisted to a standing position. The dystocias that occurred were due to lambs with contracted limbs (arthrogryposis). All affected lambs died or were euthanized. Histologic examination of the brains of 3 feeder lambs and 9 newborn lambs revealed similar microscopic lesions. The predominant change was the presence of focal axonal enlargements (spheroids) in the proximal segments of axons, which were restricted to the nuclei of the medulla, cerebellum, and midbrain. In addition, the spinal cord contained spheroids in the ventral horn gray matter of the 6 newborns examined. Ultrastructurally, the spheroids were composed of aggregates of neurofilaments, mitochondria, vesicular bodies, and dense bodies bounded by a thin myelin sheath. There was mild gliosis in the more severely affected animals of both groups. There was minimal Wallerian degeneration in the white matter adjacent to affected nuclei in the brain and the ventromedial and dorsolateral funiculi of the spinal cord. This is the first detailed report of Sorghum toxicity in sheep.Ataxia, recumbency, and the birth of weak cystitis, urinary incontinence, or malformed offspring have been reported in pastures.

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Section: Discussionmentioning

confidence: 99%

Neuroaxonal Degeneration in Sheep GrazingSorghumPastures

et al. 1995

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“…1) Severe, chronic vitamin-E deficiency causes the progressive neurological syndrome ataxia in both humans and animals. [2][3][4][5][6][7] Among the eight forms of vitamin E, -tocopherol is transported into the circulation bytocopherol transfer protein (-TTP) with much higher efficiency than the others, which makes -tocopherol the most active form of vitamin E in mammals. Accordingly, -TTP knockout mice were recently used as a vitamin E-deficient animal model.…”

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confidence: 99%

Dietary Vitamin E Deficiency Increases Anxiety-Like Behavior in Juvenile and Adult Rats

Terada

Okura

Kikusui

et al. 2011

Bioscience, Biotechnology, and Biochemistry

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“…They have characteristics of both lysosomes and lipopigment granules. Many investigators believe that these inclusions result from intracellular peroxidation of phospholipids and unsaturated fatty acids (Swensen and Telford 1973;Nelson et al 1981;Guggenheim et al 1982;Neville et al 1983), though their exact genesis remains obscure.…”

Section: Electron Microscopic Findingsmentioning

confidence: 99%

Ultrastructural changes in skeletal muscle of a patient with familial intrahepatic cholestasis associated with vitamin E deficiency.

Kobayashi¹,

Tazawa

Nakagawa

et al. 1984

Tohoku J. Exp. Med.

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The skeletal muscle from a patient with familial intrahepatic cholestasis associated with vitamin E deficiency was studied by electron microscopy. The muscle fibers showed a variety of pathologic features including degenerative, necrotic and regenerative changes. Granule-like inclusions found in our biopsy specimens were similar in structure to those observed in vitamin E deficient animals. These inclusions were noted not only in the skeletal muscle fibers but also in endothelial cells of the intramuscular capillaries, Schwann cells and perineural cells. Disruption and disappearance of the plasma membrane, separation, disruption and pleats formation of the external lamina, and multilayered external laminae were observed in muscle fibers most frequently. The nerves among muscle fibers also showed degenerative features. These severely degenerative alterations of the muscle fiber have not so far been reported in vitamin E deficient patients. We discuss the process of cell damages caused by vitamin E deficiency. -vitamin E deficiency ; cholestasis ; inclusion body ; external lamina ; plasma membrane ; ultrastructure

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Progressive Neuropathologic Lesions in Vitamin E-Deficient Rhesus Monkeys

Cited by 167 publications

References 0 publications

Neuroaxonal Degeneration in Sheep GrazingSorghumPastures

Neuroaxonal Degeneration in Sheep GrazingSorghumPastures

Dietary Vitamin E Deficiency Increases Anxiety-Like Behavior in Juvenile and Adult Rats

Ultrastructural changes in skeletal muscle of a patient with familial intrahepatic cholestasis associated with vitamin E deficiency.

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