Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-8-4
pubmed:abstractText
Fast axonal transport deficiencies as mechanisms of action of acrylamide in producing axonal degeneration are under evaluation. The current study determines the effects of acrylamide and several analogues on the number of vesicles moving within the neurite processes of cultured rat embryonic neurons. Acrylamide produced severe, concentration-dependent (0.25-1.0 mM) and time-dependent (0-60 min) reduction in the quantity of vesicles translocated in both the anterograde and retrograde directions. Glycidamide, a potential neurotoxic metabolite of acrylamide, produced a time-dependent but not a concentration-dependent (in the 0.25-1.0 mM range) reduction in bidirectional transport. Based on inhibition at 60 min, glycidamide was estimated to be 4 times more potent than acrylamide in altering transport. Propionamide, a C1-C2 saturated nonneurotoxic acrylamide analogue, had no effect on axonal transport. While a tendency for methylene bisacrylamide (MbACR) to reduce vesicle transport was noted, at the concentration used no statistically significant differences from control were observed. The data support the correlation between toxicant-induced fast anterograde and retrograde axonal transport reductions and axonal degeneration produced by acrylamide and its analogues.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0098-4108
pubmed:author
pubmed:issnType
Print
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
343-56
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Toxic neurofilamentous axonopathies and fast axonal transport. V. Reduced bidirectional vesicle transport in cultured neurons by acrylamide and glycidamide.
pubmed:affiliation
Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta 30912-2000.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't