Abstract
1) Frog Rana nigromaculata died at 80% mortality level by the intrapertioneal injection of chlordimeform hydrochloride (CD; 300mg/kg). Metabolites of CD, N-formyl-4-chloro-o-toluidine (NF) and 4-chloro-o-toluidine (CT), required more high doses to produce the mortalities at the same level as CD.
2) All of CD and its metabolites, N′-(4-chloro-o-tolyl)-N-methylformamidine (DM), NF and CT, produced the contraction of frog rectus abdominis muscle at the concentration of 10-4-10-3M.
3) CD and DM strongly inhibited the Ach-induced contraction of frog rectus abdominis muscle, whereas both of NF and CT were inactive to the Ach-induced contraction at the concentration of 10-3M.
4) A correlation can be found between the inhibition of Ach-induced contraction of frog muscle and toxicity for several organisms among CD and its metabolites.
5) An MAO-specific inhibitor, Iproniazid phosphate (IP), was not toxic for frog and was inactive to the Ach-induced contraction of frog rectus abdominis muscle.
