α-Naphthylthiourea is metabolized by rat liver and lung microsomes to α-naphthylurea (ANU), which is essentially nontoxic to rats with an ( > 800 mg/kg). Conversion of<unk>  to ANU requires NADPH. Carbon monoxide inhibits the reaction. There are some evidence of cytochrome P450 being responsible for the bioactivation of<unk> . Therefore, the toxicity of<unk>  cannot be explained with the activity of ANU. There are subproducts of this reaction which play an important role in toxicity: atomic sulfur and a metabolic reactive containing the carbon carbonyl of<unk> . The loss of cytochrome P-450 and monooxygenase activity seen on incubation of liver microsomes with<unk>  is likely the result of the covalent binding of atomic sulfur to cytochrome P-450. The available evidence suggests that the pulmonary toxicity of<unk>  results, at least in part, from the covalent binding of a cytochrome P-450 monooxygenase catalyzed metabolite of<unk>  to pulmonary macromolecules. This metabolite is most likely atomic sulfur or alternatively, the one containing the carbonyl carbon of<unk> . However, it is possible that the binding of both metabolites may be responsible for the lung toxicity.
Alpha-Naphthylthiourea
Arabinopyranosyl-N-methyl-N-nitrosourea
Trenbolone hexahydrobenzylcarbonate
Gadobenic acid
Penicilloic acid
Dimethyl methylphosphonate
Silver diammine fluoride
Tienilic acid