RESUMEN
Feeding galactose to rats induces nerve conduction abnormalities, increased levels of nerve galactitol, endoneurial edema, elevated pressure and hypoxia of endoneurial fluid, and pathological abnormalities of nerve fibers. To investigate the cellular mechanisms of the fiber lesions and their possible relationship to alterations in the nerve microenvironment, rat peroneal nerves were morphometrically evaluated eight months after the commencement of galactose feeding. Whereas the density of neurofilaments (NF/micron2) in the transverse axonal area of myelinated fibers was not significantly different between the nerves of galactose-fed and control rats, axonal areas and the number of NF/axon, when related to myelin spiral length, were significantly less in nerves of galactose-fed rats. Myelin alterations, characteristic of axonal atrophy, were also significantly increased. The present data provide evidence of a proportionate decrease in axonal caliber and the number of NF/axon in myelinated fibers in experimental galactose neuropathy, suggesting that galactose induces fibers in experimental galactose neuropathy, suggesting that galactose induces either decreased NF synthesis, assembly or transport. The possible role of microenvironmental alterations, including endoneurial hypoxia and hyperosmolarity, in the production of this axonal atrophy is discussed.
Asunto(s)
Axones/patología , Citoesqueleto/ultraestructura , Galactosa/toxicidad , Filamentos Intermedios/ultraestructura , Conducción Nerviosa/efectos de los fármacos , Animales , Axones/efectos de los fármacos , Dieta , Microscopía Electrónica , Ratas , Ratas EndogámicasRESUMEN
A new synthetic pyrethroid, permethrin, has recently been granted a registration by the United States Environmental Protection Agency. Permethrin and a large number of other chemicals of its type are expected to receive widespread use in the environment in the near future. Since the mechanism by which these compounds exert their toxic effect in insects (and at higher doses in mammals) is by disruption of the normal function of nervous tissue, a detailed morphologic evaluation of the nervous system was performed on rats from two long-term feeding studies conducted on permethrin. In this evaluation, examination of central and peripheral nervous plus examination of extensive morphometric data and teased myelinated fibers of distal sural and tibial nerves and of the maxillary division of cranial nerve V did not reveal any changes which could be attributed to the feeding of the pesticide.
Asunto(s)
Enfermedades del Sistema Nervioso Central/inducido químicamente , Enfermedades del Sistema Nervioso Periférico/inducido químicamente , Piretrinas/toxicidad , Animales , Axones/efectos de los fármacos , Axones/patología , Enfermedades del Sistema Nervioso Central/patología , Femenino , Masculino , Fibras Nerviosas/efectos de los fármacos , Fibras Nerviosas/patología , Fibras Nerviosas Mielínicas/efectos de los fármacos , Fibras Nerviosas Mielínicas/patología , Enfermedades del Sistema Nervioso Periférico/patología , Permetrina , RatasRESUMEN
Fascicles of human sural nerve, fixed by immersion in isosmolar 2.5% glutaraldehyde solution and in isosmolar osmium tetroxide and embedded in epoxy, undergo a 10% shrinkage in area when compared with cryostal sections. By contrast, fascicles fixed in hyperosmolar solutions (whether 5.6% glutaraldehyde solution or 2.5% glutaraldehyde raised to the same level of hyperosmolality with sucrose) undergo a 43% shrinkage in area. Axis cylinders of myelinated fibers undergo a selective and severe shrinkage and assume noncircular shapes, the shapes allowing the transverse area to decrease when the perimeter remains unchanged. These studies raise the intriguing question of whether interstitial hyperosmolality in metabolic diseases, such as diabetes mellitus, or in uremia may cause osmotic axonal shrinkage, altered transverse fiber shape, and abnormality of function and structure of nerve.