Abstract
It has recently been proposed that the similar multifocal axonopathies caused by several industrial toxins are due to the inhibition of metabolic enzymes with sensitive sulfhydryl groups. We find that the neurotoxins acrylamide and methyl n-butyl ketone in millimolar concentrations irreversibly inhibit rat brain and rabbit muscle creatine kinase and brain adenylate kinase. Brain creatine kinase was more sensitive to the toxins than was muscle creatine kinase or brain adenylate kinase. The chemically related but “nonneurotoxic” agents, N,N′-methylene bisacrylamide and methyl isobutyl ketone, were somewhat less effective than the known toxins. Dithiothreitol protected the enzymes against the toxins. However, differences in the effects of temperature and the protection by dithiothreitol indicated complex enzyme -toxin -dithiothreitol interaction. Protection by dithiothreitol does not necessarily implicate enzyme sulfhydryl groups or the site of toxin action. The lack of of cificity of toxin action and the concentrations of toxin required make it unlikely that metabolic enzyme inhibition alone accounts for hydrocarbon axonopathy.
Published Version
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