Acrylamide neurotoxicity: role of oxidative metabolism.
Sickles-DW; Wrenn-RW; Goldstein-BD; Coles-M; Keldahl-C; Testino-A
Department of Anatomy, Medical College of Georgia, Augusta, Georgia, 1988 Jan; :1-23
The possible selective inhibition of oxidative enzymes in neural tissues by acrylamide (79061) (ACR) given intraperitoneally at dose levels of 50mg/kg/day for 5 or 10 days was investigated. A 17 to 20 percent reduction in NADH-tetrazolium-reductase (NADH-TR) activity in one motoneuron type was demonstrated along with a progressive decrease in retrograde transport of horseradish-peroxidase from the muscle to the motoneuron. Following an acute exposure, activity returned to control levels in 72 hours, indicating that ACR did not irreversibly damage the neuron oxidative metabolism. The nonneurotoxic analogue, methylene-bis-acrylamide was less effective in enzyme inhibition. A study of the effects of ACR and a nonneurotoxic analogue on the NADH-TR activity of neural and nonneural tissues indicated that ACR specifically inhibited neural specific NADH-TR activity. The effect of ACR on the specific enzymes lipoamide-dehydrogenase (LdPH) and cytochrome-c-reductase (CCR) in neural and nonneural tissues was examined. The results agreed with the NADH-TR histochemical data, except for the kidney studies. In general the neural tissue enzymes were more significantly affected than nonneural. In studies of axoplasmic transport and nerve high energy phosphates the depletion of high energy phosphate was determined not to be the causative factor for deficits in axoplasmic transport caused by any of the neurotoxicants under study.
NIOSH-Grant; Neurotoxic-effects; Laboratory-animals; Enzyme-activity; Metabolic-study
Anatomy Medical College of Georgia Laney-Walker Blvd. Augusta, GA 30912
Final Grant Report
NTIS Accession No.
Neurotoxic Disorders; Neurotoxic-effects
Department of Anatomy, Medical College of Georgia, Augusta, Georgia
Medical College of Georgia, Augusta, Georgia