Distal axonopathies caused by chronic exposure to acrylamide and certain Gamma-diketones are a known occupational health hazard. Previous studies from this laboratory have demonstrated that neuron-specific enolase (NSE) is selectively inactivated in animals with acrylamide neuropathy.
The aims of this proposal are to determine both the enzymatic activity and tissue levels of NSE by radioimmunoassay in brain regions and peripheral nerve of acrylamide intoxicated rats. Comparisons will be made to similar data obtained from nerve crush experiments to evaluate the response of the enzyme to two different kinds of injury: chemical and mechanical. In conjunction with these studies is the determination of the in vivo binding of (14C)acrylamide to NSE and to non-neuronal enolase. The latter enzyme serves as a control since its activity in unaffected in acrylamide intoxication. Immunoprecipitation by a double antibody method will be used for isolation and subsequent scintillation counting of these proteins from other soluble proteins in both brain regions and proximal and distal portions of peripheral nerve. In addition proteins from the soluble fraction of peripheral nerve will be separated by 2-dimensional polyacrylamide gel electrophoresis and labelled proteins will be identified by fluorography of the gels. Fluorographs are expected to demonstrate whether or not acrylamide binds uniformally to soluble proteins of nerve.
| Howland, R D; Alli, P (1986) Altered phosphorylation of rat neuronal cytoskeletal proteins in acrylamide induced neuropathy. Brain Res 363:333-9 |
| Howland, R D (1985) Biochemical studies of acrylamide neuropathy. Neurotoxicology 6:7-15 |
