Abstract
The Biochemical Evaluation of Neurotoxic Damage. BONDY, S. C. (1986). Fundam. Appl. Toxicol. 6, 208–216. The specific problems related to the study of chemicals that damage the nervous system are discussed. Such damage may be direct or may occur by a series of sequential events. Such a series of events may involve other organs and biochemical targets not confined to nerve tissue. The complexity of investigation of the mode of action of rather nonspecific toxic agents requires that a circumscribed objective be defined and examples of such goals are given. One of these is to attempt to determine which neuronal circuits are damaged by a given toxic agent and how this might cause alterations of behavior. Acrylamide and triethyl lead are used to exemplify the application of neurotransmitter receptor analysis to correlation of deranged nerve activity patterns with modulation of behavior. Such evaluation can set the stage for more detailed biochemical studies of neurotoxic mechanisms.
Highlights
Laboratory ofBehavioral and Neurological Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, P.O
In view of the especial vulnerability of the adult brain to anoxia, many chemicals interfering with normal oxidative metabolism, such as cyanide ions or carbon monoxide, can under certain circumstances appear selectively neurotoxic
We have examined the benzodiazepine binding sites at various times after a single injection of 7.9 mg/kg body wt of triethyl lead chloride (TEL) in adult male rats
Summary
Neurotoxic damage can be caused by many pharmacological agents and biological neurotoxins These types of compounds have an inherent man-made or evolutionary design and are generally harmful in rather selective ways. Unlike pharmacological agents and natural toxins such as snake venoms, many nonspecific toxic agents are industrial products not designed to affect biological function. They are likely to exert their effects by interacting with more than a single biological site. This potential multiplicity makes it difficult to identify the precise mechanisms by which damage to the organism is effected For this reason, sites of action of many toxic agents are generally less well understood than those of pharmaceutical agents. In view of the especial vulnerability of the adult brain to anoxia, many chemicals interfering with normal oxidative metabolism, such as cyanide ions or carbon monoxide, can under certain circumstances appear selectively neurotoxic
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