NEUROTOXINS OF SNAKE VENOM 145 
Radium emanation has a similar deteriorating effect upon the neurotoxic 
principle. 
Among the chemical agents which have distinct destructive effects upon 
the neurotoxins, chlorine, bromine, iodine (as trichloride), potassium. per- 
manganate, calcium chloride, calcium hypochlorite, potassium and sodium 
hydrates, and gold chloride may be mentioned. Silver nitrate, mercury bichlo- 
ride, iron chloride, copper sulphate, and certain acids like tannic acid or picric 
acid precipitate the neurotoxic principles together with all other proteins, but 
they are not sufficient to prevent death when the whole mixture is injected 
into animals. 
Various mineral and organic acids do not destroy the neurotoxin even 
when used in fairly strong concentration. On the contrary, they are found 
to exert a certain protective action upon this principle against the effect of 
high temperature. 
The physical and chemical properties of the neurotoxins of venom, as 
outlined above, show the high stability of these toxins in a very remarkable 
manner. These marvelously powerful toxin-like substances present an 
amazing contrast with various toxins of vegetable nature, namely, bacterial 
toxins and certain toxalbumins, because the latter group shows character- 
istic high lability against various physical and chemical reagents such as 
light, heat, acid, and alkali. 
As already dealt with in a previous topic, the hemolysins of venom are also 
very stable, and it has been almost impossible to separate the hzmolysins and 
neurotoxins through their physical and chemical properties. ‘These two sets 
of toxins of venom go hand in hand all through these treatments without 
losing their coexistence. It is no wonder, therefore, that Cunningham was 
erroneously led to ascribe all nervous symptoms caused by cobra venom, the 
venom which contains large amounts of the hemolysins and neurotoxins, to 
the primary alteration of the blood. 
A series of biological analyses, which affords a far more delicate interpreta- 
tion of the toxic effects produced by venom, has later brought out numerous 
evidences that the hemolysins are quite insignificant in the fatal issue of venom 
toxication under consideration. Thus there are certain animals, the ox, 
goat, sheep, etc., which are entirely insusceptible to the hemolytic toxins, 
yet highly sensitive to the paralytic effects of the venom; this can only be 
accounted for by the neurotoxic action of the latter. Even in the cases of 
animals which show susceptibility to the hemolysins, death is produced 
by a minute quantity of venom — scarcely enough to dissolve a small 
amount of the blood, the loss of which can have no serious sequel, if 
any at all. It has been shown time and again that the direct application 
of venom solution to the fourth ventricle in the medulla quickly produces all 
_ nervous symptoms which would follow the administration through any other 
channels, by the skin, blood vessels, peritoneum, or alimentary canal. Here 
the changes in the blood corpuscles are excluded from the possible cause of 
the nervous symptoms, much less of the fatal issue. 
