© 1983 Oxford University Press
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Evaluation of Acrylamide Treatment on Levels of Major Brain Biogenic Amines, Their Turnover Rates, and Metabolites
Toxicology Program, Utah State University Logan, UT 84322
Evaluation of Acrylamide Treatment on Levels of Major Brain Biogenic Amines, Their Turnover Rates, and Metabolites. Aldous, C.N., Fair, C.H. and Sharma, R.P. (1983). Fundam. Appl. Toxicol. 3:182-186. Acrylamide, a widely used and chemically active substance, has caused delayed distal neuropathy in man and in experimental animals. Male rats administered 50 mg/kg/ day acrylamide for 5 days demonstrated ataxia in preliminary rotorod experiments. Additional groups of rats were dosed with 5, 15 or 50 mg/kg/day acrylamide for 5 days, then sacrificed on day 6 at various time intervals after iv injections of tritiated tyrosine (Tyr) or tryptophan (Trp). Brain levels of Tyr, Trp, norepinephrine(NE), dopamine(DA), serotonin(5-HT), and respective metabolites, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MOPEG-sulfate), 3,4-dihydroxyphenylacetic acid (DOPAC), and 5-hydroxyindoleacetic acid (5-HIAA) were assayed fluorometrically. Turnover rates of NE, DA and 5-HT were estimated by evaluating the rates of specific activity changes in neurotransmitters and precursor amino acids over time. A slight reduction of whole brain NE content was observed in rats administered 50 mg/kg/day acrylamide. Other neurotransmitter levels were not affected by acrylamide levels administered, nor were turnover rates affected. Levels of MOPEG-sulfate and DOPAC were unchanged at any dose tested. Increased levels of 5-HIAA were observed in rats receiving 15 and 50 mg/kg/day acrylamide. Results suggest that acrylamide neurotoxicity does not entail widespread damage to the neurons associated with these biogenic amines; however, the acid metaolite efflux from brain was significantly inhibited.