9 
In fact, both Rosenfeld and Pringsheim (who did not, however, take 
into consideration the difference in the effect of alcohol upon the endo- 
genous and exogenous uric acid) attributed the increased excretion of 
uric acid, following the administration of alcohol, to an increased 
destruction of nucleic acid-containing proteids. In his striking way, 
Rosenfeld said that alcohol h}’pocritically spared the ordinary pro- 
teids that it might rage all the more fiercely among the nucleo- 
proteids without betraying itself in the nitrogen equilibrium.” 
This is mentioned simply to show that there seem to be no facts 
which necessarily point to alcohol, in small amounts, having an inhib- 
iting effect upon physiological oxidations. In fact, as our knowledge 
concerning specific cases of oxidation in the body increases, it becomes 
more and more apparent that the commonly used expressions that a 
substance ‘‘accelerates” or “retards” physiological oxidation are far 
too general. 
Thus there is more and more a tendency to discuss the effects of sub- 
stances upon specific cases of oxidation, and I have been led to believe 
that alcohol probably causes increased oxidation in some cases. The 
substance with which I have chiefiy experimented in this connection 
is acetonitrile. This substance may seem at first to have a purely 
theoretical interest, but from a long series of experiments with it I 
have been led to the conclusion that a thorough study of its conduct 
in the animal body may throw light upon a number of obscure proc- 
esses of metabolism.® Ghemicall}^, acetonitrile (GH3GN), or methyl 
cyanide, may be considered as hydrocyanic acid in winch the hydro- 
gen atom has been replaced by the methyl group. Both chemically 
and physiologically, however, acetonitrile is very different from hydro- 
cyanic acid, although it is almost certain that its physiological action 
is due to the slow liberation of hydrocyanic acid in the body. 
So far as I am aware acetonitrile has never been found in nature, 
although it has long been supposed that analogous compounds occur 
in living protoplasm, and importance has been attributed to them in 
certain disorders of metabolism. 
« The thyroid, for example, is quite generally supposed to have the power of effecting 
the neutralization of certain poisons of metabolic origin. These poisons are, however, 
purely hypothetical, and the only known poison toward which the thyroid has been 
shown to have an antidotal action is acetonitrile. In a previous paper (Journ. Biolog. 
Chem., vol. 1, p. 33; 1905) I have shown that animals to which small doses of thyroid 
have been administered for a short time will survive the injection of several times the 
fatal dose of acetonitrile. The explanation of this action is not known; if it were it 
would almost certainly throw much light on the physiology of the thyroid. It may 
also be noted in this connection that the feeding of parathyroids does not have such 
an effect; on the contrary, it slightly increases the susceptibility to acetonitrile. This 
affords another illustration of the fact that the thyroid and parathyroids have, in some 
respects at least, very different physiological effects. 
