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Journal ArticleDOI

Carbon disulfide intoxication from overdosage of disulfiram.

Francis J. Kane
- 01 Nov 1970 - 
- Vol. 127, Iss: 5, pp 690-694
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TLDR
Clinical and experimental evidence bearing on the relationship between disulfiram and its metabolite, carbon disulfide, and similarities in the syndromes associated with the toxicity of each are reviewed.
Abstract
The author discusses a case of acute brain syndrome with depression, peripheral neuropathy, and transient parkinsonism following ingestion of large amounts of disulfiram. He reviews clinical and experimental evidence bearing on the relationship between disulfiram and its metabolite, carbon disulfide, and reviews similarities in the syndromes associated with the toxicity of each.

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Citations
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Journal ArticleDOI

Malnutrition and school progress

John Dobbing
- 01 Feb 1975 - 
Journal ArticleDOI

Peripheral Neuropathy Caused by Chemical Agents

Cavanagh Jb
TL;DR: In this article, the authors discuss peripheral neuropathy caused by chemical agents and propose a method to diagnose peripheral neuropathies caused by Chemical Agents, which they call Peripheral Neuropathy Caused by Chemical Agent (PNCA).
Journal ArticleDOI

A Critical Review of the Literature on Carbon Disulfide Toxicity

TL;DR: A critical review of the literature on carbon disulfide toxicity can be found in this article, with a focus on Carbon Disulfide Toxicity (CDT) as a potential carcinogen.
Journal ArticleDOI

Disulfiram toxicity and carbon disulfide poisoning

TL;DR: The results suggest that carbon disulfide is responsible for the behavioral and neurological side effects of disulfiram, and individuals receiving as little as 125 mg of dis sulfuriram per day may be at a three- to four-fold greater risk for arteriosclerotic cardiovascular disease than a comparable population not receiving the drug.
References
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Journal ArticleDOI

Biogenic Amines and Emotion

TL;DR: Although there does appear to be a fairly consistent relationship between the effects of pharmacological agents on norepinephrine metabolism and on affective state, a rigorous extrapolation from pharmacological studies to pathophysiology cannot be made, and confirmation of this hypothesis must ultimately depend upon direct demonstration of the biochemical abnormality in the naturally occurring illness.
Journal Article

The effect of disulfiram on catecholamine levels in the brain

TL;DR: In animals pretreated with the monoamine oxidase inhibitor pheniprazine, there was a closer correlation between the decrease in the norepinephrine content and the increase in the dopamine content in the hypothalamus and brainstem.
Journal ArticleDOI

Effects of disulfiram on tissue norepinephrine content and subcellular distribution of dopamine, tyramine and their β-hydroxylated metabolites

TL;DR: Disulfiram has been shown to markedly inhibit dopamine-β-Hydroxylase in vivo and to result in a decrease in norepinephrine content of tissues, presumably by making β-hydroxylation rate limiting.