Abstract
Fast axonal transport deficiencies as mechanisms of action of aoylamide in producing axonal degeneration are under evaluation. The current study determines the effects of acry- lamide 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. Clycidamide, 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,-C2saturated 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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 343-356 |
| Number of pages | 14 |
| Journal | Journal of Toxicology and Environmental Health |
| Volume | 42 |
| Issue number | 3 |
| DOIs | |
| State | Published - Jan 1 1994 |
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ASJC Scopus subject areas
- Toxicology
- Pollution
Cite this
Toxic neurofilamentous axonopathies and fast axonal transport. v. reduced bidirectional vesicle transport in cultured neurons by acrylamide and glycidamide. / Harris, C. H.; Gulati, Adarsh K; Friedman, M. A.; Sickles, D. W.
In: Journal of Toxicology and Environmental Health, Vol. 42, No. 3, 01.01.1994, p. 343-356.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Toxic neurofilamentous axonopathies and fast axonal transport. v. reduced bidirectional vesicle transport in cultured neurons by acrylamide and glycidamide
AU - Harris, C. H.
AU - Gulati, Adarsh K
AU - Friedman, M. A.
AU - Sickles, D. W.
PY - 1994/1/1
Y1 - 1994/1/1
N2 - Fast axonal transport deficiencies as mechanisms of action of aoylamide in producing axonal degeneration are under evaluation. The current study determines the effects of acry- lamide 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. Clycidamide, 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,-C2saturated 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.
AB - Fast axonal transport deficiencies as mechanisms of action of aoylamide in producing axonal degeneration are under evaluation. The current study determines the effects of acry- lamide 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. Clycidamide, 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,-C2saturated 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.
UR - http://www.scopus.com/inward/record.url?scp=0028175589&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028175589&partnerID=8YFLogxK
U2 - 10.1080/15287399409531884
DO - 10.1080/15287399409531884
M3 - Article
C2 - 7517455
AN - SCOPUS:0028175589
VL - 42
SP - 343
EP - 356
JO - Journal of Toxicology and Environmental Health
JF - Journal of Toxicology and Environmental Health
SN - 0098-4108
IS - 3
ER -