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-hke 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 akeady dealt with in a previous topic, the haemolysins of venom are also 

 very stable, and it has been almost impossible to separate the haemolysins 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 haemolysins 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 haemolysins 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 haemolytic 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 susceptibihty to the haemolysins, 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 sequelae, if 

 any at all. It has been shown time and again that the direct application 

 of venom solution to the fourth ventricle in the meduUa 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. 



