Acrylamide alters oxidative enzyme activity in rat motoneurons.
Acrylamide (ACR) produces a central-peripheral distal axonopathy, via an unknown mechanism. We have investigated the effects of ACR on the activity of enzymes responsible for the oxidation of NADH (NADH-tetrazolium reductase activity, NADH-TR) with quantitative histochemical techniques. Chronic (5- or 10-day) injection of ACR (50 mg/kg/day) resulted in a significant decrease in enzyme activity in soleus motoneurons, which normally have high NADH-TR activity. The NADH-TR activity in motoneurons with low oxidative metabolism was not significantly affected. Retrograde labeling of motoneurons with horseradish peroxidase was diminished by the acrylamide treatment. These data demonstrate an acrylamide-induced change in the oxidative metabolism of certain motoneurons; further study will determine whether oxidative metabolism is the primary site of action of ACR in producing the distal axonopathy.
D020106:Acrylamide; D000178:Acrylamides / Q000494:pharmacology*; D000818:Animals; D006651:Histocytochemistry; D006735:Horseradish Peroxidase; D009046:Motor Neurons / Q000187:drug effects* / Q000201:enzymology; D009246:NADH Tetrazolium Reductase / Q000037:antagonists & inhibitors*; D009247:NADH, NADPH Oxidoreductases / Q000037:antagonists & inhibitors*; D051381:Rats
D000178:Acrylamides; D020106:Acrylamide; D006735:Horseradish Peroxidase; D009246:NADH Tetrazolium Reductase; D009247:NADH, NADPH Oxidoreductases