[Mechanism of acute toxic effects of chlorocholine chloride and 2-chloroethyl phosphonic acid (Ethephon)].

An account is given of results obtained from animal experiments that had been conducted with the view of elucidating the mechanisms underlying acute toxic action of CCC and Etephon. CCC was found to have neuromuscular blocking actions and, consequently, to lead to respiratory arrest in a situation of acute intoxication. The neuromuscular block has by all characteristics of a block by depolarisation. Acute toxicity of CCC was found to differ by species as well, which was attributable primarily to differentiated sensitivity of various species to depolarising neuromuscular blockers. The parasympathicomimetic effects of CCC were of secondary importance to acute toxicity of the compound. The toxicity of CCC could be reduced by small doses of atropine, but higher atropine doses proved to be unfavourable by aggravating respiratory paralysis. Reduction in acute CCC toxicity with concomitant administration of choline chloride was attributable to inhibition of the absorption rate of CCC. Long-term inhibition of plasma cholinesterase was recorded from rats and mice in after to oral administration of Etephon, but cholinesterases were not inhibited the erythrocytes and brain. All the cholinesterases studied, including those obtained from plasma, erythrocytes, and brain from rat and mouse, were inhibited in vitro by approximately identical Etephon concentrations. Inhibition of plasma cholinesteras was of no importance to acute toxic effects. Acid-borne corrosion was an established cause of deaths among rats and mice with acute Etephon intoxication.