Strikingly rapid toxic symptoms of organic thiocyanates were repeatedly observed in various kinds of animals by Traubmann (1930)(1), von Oettingen et al. (1936)(2), Cameron
et al. (1939)(3), Ohashi and Kimizuka (1947)(4), though not confirmed by Moriki (1936)(5). Such a violent action as above, however, can not be expected in regard to inorganic thiocyanates, such as KSCN, clinically available as a sedative or a blood pressure depressant.
The SCN radical has a close similarity in its chemical property to halogens, which may be named “pseudohalogen”. Then, Traubmann naturally presupposed an ethyl chloride C
2H
5Cl-like narcotic action as a pharmacological property of alkyl thiocyanates, i.e. methyl thiocyanate CH
3SCN, ethyl thiocyanate C
2H
5SCN, or propyl thiocyanate C
3H
7SCN. But it was found that the animals poisoned either by these alkyl thiocyanates or by aromatic thiocyanates (phenyl thiocyanate C
6H
5SCN and aniline thiocyanate NH
2C
6H
4SCN) caused respiratory excitement and convulsions. Thus he came to a postulation for the toxic particularity of organic thiocyanates.
Von Oettingen and others noticed the following phenomena: hyperemia, hemorrhage and edema in internal organs, when animals succumbed to the acute poisoning by lower alkyl thiocyanates, respiratory excitement and a rise in blood pressure when methyl or ethyl thiocyanate was administered subcutaneously; appearance of a AgNO
3-consuming substance
in vitro when these thiocyanates were placed for 48 hours with pieces of liver. These observations gave the impression that hydrocyanic acid might be liberated from methyl and ethyl thiocyanates in living animals.
In order to scrutinize more carefully the above-mentioned assumption, the present study was designed with six compounds of organic thiocyanates* as listed in Table 1.
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