Abstract
The influence of drug treatment on CN − release from DNS both in vivo and in vitro has been investigated. Treatment of rats with phenobarbital, 3–4 benzopyrene did not modify cyanide liberation from DNS.CC1 4 administration almost completely abolished the generation of CN − and consequently strongly decreased the acute toxicity of DNS. On the contrary, acute or chronic ethanol treatment significantly increased CN − formation from DNS in rat liver slices, increasing the toxicity of the drug. Thus ethanol administration to mice lowered the ld 50 i.p. from 63 mg/Kg to 38 mg/Kg. These results suggest that the considerable increase of DNS toxicity is due to a stimulation of cyanide release and a substrate limitation incurred in detoxification.
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