Giant axonopathy characterized by intermediate location of axonal enlargements and acceleration of neurofilament transport

Monaco, Salvatore; Wongmongkolrit, T.; Shearson, C.M.; Patton, A.; Schaetzle, B.; Autilio-Gambetti, L.; Sayre, Lawrence M.

doi:10.1016/0006-8993(90)90062-g

Cited by 32 publications

(20 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The neurofilamentous aggregates were initially noted at proximal paranodes (the portion of the axon just proximal to the narrowing of the node of Ranvier). In association with these swellings, there was thinning of the overlying myelin sheath, which led to paranodal demyelination ( Figure 5A, B Another myelinated fiber lesion that has engendered recent interest is axonal atrophy, a change that had been previously noted in hexacarbon-treated rats (72,73,80,91) and in vitro neuronal preparations (77). Recent (Figure 5C, D).…”

Section: P-bromophenylacetylureamentioning

confidence: 83%

Mechanisms of Toxic Injury in the Peripheral Nervous System: Neuropathologic Considerations

Jortner

2000

Toxicol Pathol

View full text Add to dashboard Cite

show abstract

Section: P-bromophenylacetylureamentioning

confidence: 83%

Mechanisms of Toxic Injury in the Peripheral Nervous System: Neuropathologic Considerations

Jortner

2000

Toxicol Pathol

View full text Add to dashboard Cite

show abstract

“…Proximal giant axonal swellings are also seen in 3,4-dimethyl-2,5-HD (DMHD) neurotoxicity [1,2,10,26] and neurofilament protein cross-linking by gamma-diketones is well established and accepted [4,10,12,16,34,38,43,44). The development of proximal axonal swellings filled with 10 nm neurofilaments in spinal cord and spinal roots of rodents repeatedly treated with 1,2-DAB approaches, matches or exceeds the high protein reactivity and neurotoxic potency of DMHD [16,18,39].…”

Section: Discussionmentioning

confidence: 99%

Axonopathy-Inducing 1,2-Diacetylbenzene Forms Adducts with Motor and Cytoskeletal Proteins Required for Axonal Transport

et al. 2007

View full text Add to dashboard Cite

The aromatic hydrocarbon 1,2-diacetylbenzene (1,2-DAB) is a protein-reactive gamma-diketone metabolite of the neurotoxic solvent 1,2-diethylbenzene (1,2-DEB). The effect of neurotoxic 1,2-DAB and its non-neurotoxic isomer 1,3-DAB has been studied on motor proteins and cytoskeletal proteins of rat spinal cord (SC). For in vitro studies, SC slices were incubated with 1, 2, 5, 10 mM of DAB isomers for 30 min at 37 degrees C. For in vivo studies, rats received (i.p.) 20 mg/kg/day of 1,2-DAB or 1,3-DAB, or vehicle (2% acetone in saline), 5 days a week for 2 weeks. Spinal cord and sciatic nerve proteins were subjected to Western blotting using monoclonal mouse antibodies to NF-M, kinesin, dynein, and tau. Proteins were quantified and paired mean comparisons performed to assess concentration-dependent changes in native protein bands. In vitro, 1,2-DAB produced a concentration-dependent decrease of motor and cytoskeletal proteins. While dynein and tau appeared similarly affected by 1,2-DAB, kinesin was most affected by the toxicant. In vivo, 1,2-DAB affected motor and cytoskeletal proteins of sciatic nerves and spinal cord differentially. In general, sciatic nerve proteins were much more affected than spinal cord proteins. The results show that motor proteins that drive axonal transport anterogradely (kinesin) and retrogradely (dynein), cytoskeletal protein NF-M, which is slowly transported in the anterograde direction, and microtubule-associated protein, tau, which is involved in axonal transport, are differentially impacted by 1,2-DAB. By contrast, non-neurotoxic isomer 1,3-diacetylbenzene (1,3-DAB), had no adverse effect on neural proteins either in vitro or in vivo. 2D-Differential in gel electrophoresis (2D-DIGE) of sciatic nerves from neurotoxic 1,2-DAB and non-neurotoxic 1,3-DAB treated rats revealed 197 and 304 protein spots, respectively.

show abstract

“…In peripheral axons, n-hexane and some of its metabolites cause alterations in the longitudinal axonal transport, aggregation of neurofilaments and, after heavy exposure, axon degeneration (Spencer et al 1980;Monaco et al 1990). Microtubular alterations in the Sertoli cells seem to be involved in testicular degeneration (Boekelheide et al 1989).…”

Section: Mechanism Of Actionmentioning

confidence: 97%

“…Correspondence to: E Nyl6n alterations in the slow anterograde axonal transport, neurofilamentous accumulations, and axonodal swellings (Spencer et al 1980;Monaco et al 1990). Exposure to n-hexane or 2,5-hexanedione also causes testicular alterations in the rat (O'Donoghue et al 1978;Boekelheide 1987;Boekelheide et al 1989;Nyl6n et al 1989), which are seen as a degeneration of the seminiferous tubules and loss of germ cells.…”

Section: Htroductionmentioning

confidence: 99%

Effect of exposure to 2,5-hexanediol in light or darkness on the retina of albino and pigmented rats. II. Electrophysiology

Nylén

Bäckström²,

Hagman

et al. 1993

Arch Toxicol

View full text Add to dashboard Cite

Albino (Sprague-Dawley) and pigmented (Norwegian Brown) male rats were exposed to 2,5-hexanediol (H; 1%) in their drinking water for 5 or 8 weeks, respectively. Half of the rats of each strain were housed in light (average 30 cd/cm2 inside cage, 12 h/day); the other half was kept in constant darkness. Control groups were studied in parallel under identical conditions but without H. Electrophysiological recordings were made 2-5 days and 13 weeks after the end of the exposure to H. Alterations in the visual system, as measured by electroretinography and visual evoked response, were found in groups of albino rats exposed to H and/or light. The pupillary diameter was enlarged in the albino group exposed to both H and light. Among the pigmented rats, alterations were recorded only in the visual evoked response of the H exposed groups. The results demonstrate that simultaneous exposure to H and light can lead to alterations in visual function that are more severe than those induced by each agent alone, and may exceed a simple summation.

show abstract

Giant axonopathy characterized by intermediate location of axonal enlargements and acceleration of neurofilament transport

Cited by 32 publications

References 37 publications

Mechanisms of Toxic Injury in the Peripheral Nervous System: Neuropathologic Considerations

Mechanisms of Toxic Injury in the Peripheral Nervous System: Neuropathologic Considerations

Axonopathy-Inducing 1,2-Diacetylbenzene Forms Adducts with Motor and Cytoskeletal Proteins Required for Axonal Transport

Effect of exposure to 2,5-hexanediol in light or darkness on the retina of albino and pigmented rats. II. Electrophysiology

Contact Info

Product

Resources

About