An associate and I1 previously found that if a hepatoxin, carbon tetrachloride, were given to dogs they could be made to excrete all instead of about half of a given dose of the sympathomimetic amine amphetamine. More recently I showed that if dogs were put on a maintenance dose of the amine, saturating the animals with vitamin C (ascorbic acid) would reduce the excretion of amphetamine to about one third of the amount normally excreted.2 This together with the in vitro deamination of the amine demonstrated the role of ascorbic acid in the detoxication of these compounds. However, to our surprise, if dogs saturated with vitamin C were given carbon tetrachloride orally, the excretion of amphetamine did not rise above normal.
These observations suggested that ascorbic acid might protect the animals against the toxic action of carbon tetrachloride on the liver. It was deemed more suitable to turn