The etiology of acrylamide neuropathy: possible involvement of neuron specific enolase.
The effect of monomeric acrylamide, a potent neurotoxic agent, on total and neuron specific enolase activity was studied in vitro and in vivo. Acrylamide (10 mM) completely inhibited total enolase activity of rat brain soluble fractions. The I50 concentration was 3.7 mM. In rats chronically treated with acrylamide (550 mg/kg total) and exhibiting marked symptoms of neurotoxicity, neuron specific enolase activity was not detectable in sciatic nerves and was only 60% of control activity in brain. Total enolase activity in both central and peripheral nervous tissues was unchanged from control. The results suggest that inhibition of neuron specific enolase may be an important factor in the development of acrylamide neuropathy by interfering with glycolysis in neuronal tissue.
D000178:Acrylamides / Q000633:toxicity*; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000201:enzymology; D004305:Dose-Response Relationship, Drug; D004734:Energy Metabolism / Q000187:drug effects; D007527:Isoenzymes / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000201:enzymology; D010751:Phosphopyruvate Hydratase / Q000378:metabolism*; D051381:Rats
D000178:Acrylamides; D007527:Isoenzymes; D010751:Phosphopyruvate Hydratase