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Modification of acrylamide neuropathy in rats by selected factors.
Kaplan ML; Murphy SD; Gilles FH
Toxicol Appl Pharmacol 1973 Apr; 24(4):564-579
A modified rotarod technique is used to determine if dietary deficiencies in pyridoxine (65236) or thiamine (59438), bilateral adrenalectomy or cortisol (50237) treatment and pretreatment with microsomal enzyme inducers (DDT (50293) or phenobarbital (57307)) would modify the course of onset and recovery from functional acrylamide neuropathy in rats. Neither pyridoxine nor thiamine deficiency nor daily injections of cortisol is found to have any measurable effect on the cumulative dose of acrylamide required to produce functional impairment. Histologic studies of peripheral nerves from acrylamide treated rats reveal that at the time of onset of functional impairment young and phenobarbital pretreated adult rats have severe peripheral nerve damage. The total cumulative doses of acrylamide required to produce neurologic deficit in DDT pretreated and phenobarbital pretreated rats are 520 and 600 milligrams per kilogram, respectively, compared to 360 milligrams per kilogram for the controls.
NIOSH-Publication; NIOSH-Grant; Grants-other; Neurological-diseases; Endocrine-system; Amides; Amines; Adrenal-gland-disorders; Adrenal-cortex; Adrenocortical-hormones; Drugs; Corticoids; Vitamins; Pyridines
Physiology Harvard University 665 Huntington Ave Boston, Mass 02115
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Issue of Publication
Other Occupational Concerns; Grants-other
Toxicology and Applied Pharmacology
Harvard University, Boston, Massachusetts
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