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Acrylamide Neurotoxicity: Role of Oxidative Metabolism.

PB89129365

Publication Date	1987
Personal Author	Sickles, D. W.; Wrenn, R. W.; Goldstein, B. D.; Coles, M.; Keldahl, C.
Page Count	25
Abstract	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 and cytochrome-c-reductase agreed with the NADH-TR histochemical data, except for the kidney studies. In general the neural tissue enzymes were more significantly affected than nonneural. 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.
Keywords	Toxicity Neurons Metabolism Oxidoreductases Laboratory animals Axoplasmic flow Amides Acrylamide CAS 79-06-1
Source Agency	National Institute for Occupational Safety and Health
NTIS Subject Category	57Y - Toxicology 57B - Biochemistry
Corporate Authors	Medical Coll. of Georgia, Augusta.; National Inst. for Occupational Safety and Health, Cincinnati, OH.
Supplemental Notes	Sponsored by National Inst. for Occupational Safety and Health, Cincinnati, OH.
Document Type	Technical Report
Title Note	Final rept. 1 Aug 84-1 Jun 87,
NTIS Issue Number	198906

Acrylamide Neurotoxicity: Role of Oxidative Metabolism.

Acrylamide Neurotoxicity: Role of Oxidative Metabolism.
PB89129365

Publication Date	1987
Personal Author	Sickles, D. W.; Wrenn, R. W.; Goldstein, B. D.; Coles, M.; Keldahl, C.
Page Count	25
Abstract	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 and cytochrome-c-reductase agreed with the NADH-TR histochemical data, except for the kidney studies. In general the neural tissue enzymes were more significantly affected than nonneural. 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.
Keywords	Toxicity Neurons Metabolism Oxidoreductases Laboratory animals Axoplasmic flow Amides Acrylamide CAS 79-06-1
Source Agency	National Institute for Occupational Safety and Health
NTIS Subject Category	57Y - Toxicology 57B - Biochemistry
Corporate Authors	Medical Coll. of Georgia, Augusta.; National Inst. for Occupational Safety and Health, Cincinnati, OH.
Supplemental Notes	Sponsored by National Inst. for Occupational Safety and Health, Cincinnati, OH.
Document Type	Technical Report
Title Note	Final rept. 1 Aug 84-1 Jun 87,
NTIS Issue Number	198906