Neural specificity of acrylamide action upon enzymes associated with oxidative energy-producing pathways. I. Histochemical analysis of NADH-tetrazolium reductase activity.
The mechanism by which acrylamide (ACR) produces a distal neurofilamentous axonopathy has not been determined. Our investigations are focused upon the effects of this toxicant on energy transformations; more specifically, on enzymes of oxidative metabolism. The current study determines the effects of ACR on NADH-tetrazolium reductase ( TR) activity (composite of primarily lipoamide and NADH dehydrogenases) in a variety of neural and non-neural tissues in order to test for a correlation between the neural specificity of enzyme inhibition with specific neurotoxicity. Quantitative histochemical assays demonstrate a significant inhibition of NADH- TR activity in ligated axons (-9.5%), Purkinje neurons (-17.3%) and dorsal root ganglion neurons (-17.8%) following a single ACR injection. Non-neural tissue enzymes were not significantly inhibited. A non-neurotoxic analogue, methylene-bis-ACR, had no effect upon these enzymes except in Purkinje neurons. The data supports, in general, the hypothesis that specific inhibition of neural NADH- TR activity by acrylamide is the primary site of action in producing the neuropathy. The neural specificity is attributed to lower levels of glutathione in neural tissues rather than specific inhibition of neural isoenzymes of NADH- TR.[1]References
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