Abstract

On the basis of the assays reported above, the acute toxicity of thiourea to wild Norway rats is enhanced when a single aromatic radical is attached to one of the thiourea nitrogens. When there are 2 or more substituents, either on the same or both nitrogen atoms, the acute toxicity is lowered, as it also appears to be when substitution occurs on the sulfur atom, producing a thiopseudourea, or when the sulfur atom is replaced by an imido group to form a guanidine.

Pulmonary edema and pleural effusion resulted from acute poisoning with the N-substituted aromatic thioureas and with three of the thioamides, but were not produced consistently in lethal amounts by the other related compounds.

The results for domestic rats in general paralleled those obtained with wild Norways, differing markedly only in that the domestic rats exhibited a greater sensitivity to thiourea itself and to two aliphatic derivatives of low molecular weight.