The effects of thioctic acid on motor nerve terminals in acrylamide-poisoned rats.
Acrylamide causes a distal neuropathy by combining with and depleting glutathione and other sulphydryl-containing compounds in axons and nerve terminals. This results in damage to the axon membrane and impaired efficiency of synaptic vesicle recycling. The changes may be assessed by staining nerve terminals in muscle with zinc iodide and osmium, a technique which depends upon the presence of sulphydryl compounds for the development of the stain. The present experiments were designed to test whether thioctic acid, itself a sulphydryl-containing compound, could protect against acrylamide-induced damage of motor nerve terminals. In vitro and in vivo experiments on acrylamide-poisoned rats showed that thioctic acid was able to maintain the integrity of the nerve terminal membrane, as shown by the ability of the terminals to develop 'spontaneous' sprouts and to stain with the zinc iodide osmium technique. Thioctic acid treatment also enhanced recovery after partial denervation of muscles in both normal and acrylamide-poisoned animals. The results suggest that thioctic acid is itself able to react with the acrylamide before the latter has a chance to bind and deplete axonal and nerve terminal glutathione.
Kemplay
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S
Department of Anatomy and Human Biology, King's College London (KQC).
Martin
P
P
Wilson
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S
D020106:Acrylamide; D000178:Acrylamides / Q000506:poisoning*; D000818:Animals; D005260:Female; D009046:Motor Neurons / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009121:Muscle Denervation; D009416:Nerve Regeneration; D010525:Peripheral Nerves / Q000187:drug effects / Q000473:pathology* / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D008063:Thioctic Acid / Q000494:pharmacology*
D000178:Acrylamides; D020106:Acrylamide; D008063:Thioctic Acid