254 
group, which renders it a dye. This is easily illustrated by the 
following example: — 
Azo-benzene (CgH3N = NCgH5), which contains the chromophor 
N — N, is coloured, but does not possess dyeing properties. It wily 
becomes a dye when tlie chromogenic group OH or NH, enters. 
Similarly, for example, oxyazo-benzene (OH.C,H^X = NC5H3) and 
amino-azobenzene (Il3N.Cgfl4N = NC^H5) are dyes. Their dyeing 
value increases with the number of chromogenic groups introduced. 
I'or this reason tri-amino-benzene (NH3.CgH5N = N.CgH3(NH2)2) is 
a much better dye than amino-azo-benzene. 
When wc apply the same theory to the therapeutics of Atoxyl,vre 
/ /OXa\ 
find that sodium-phenyl-arsenate ^CellsAsO^ J (which has 
been proved by Plimmer and Thomson'^, and also in this labora- 
toi'3', not to possess any curative effect), and also sodium-p-hydroxy- 
/ONa' 
)< 
phenyJ-arsenate ( OH.CeH^AsO 
\OH 
do not combine with the 
proteins, whilst atoxyl 
proteins and acts 
CH3CONH.C6HoAsO<^ 
\( 
/ONa\ _ . 
NH.C6H4AsO< 1 combines with the 
\ 0 H / 
on trypanosomes ; mono-acetylatcd atoxy! 
/ONa\ 
) com bines and is curative, while fully 
OH y 
/ CHgCOV 
>N.C6H5AsO< 
/ 
\ 0 H 
acetylated and benzoylated atoxyl ( 
, . . VCsHsCO 
does neither. 
Hence, we suggest that in Atoxyl the amido group (NHa-gro^p) 
and in mono-acetylated Atoxyl the imido group (NH-group) play 
same role as the chromogenic group in a dye. It has already been 
pointed out tliat the action of Atoxyl has generally been explained as 
being due to the arsenic, and the advantage of its use is that nior 
arsenic could be introduced in the organism in form of Atoxyl than 
in form of sodium arsenate; it might be argued from this poin^ ° 
view that the action of Atoxyl is as follows; — 
The Atoxyl attaches itself to the proteins ; the benzene nucleuses 
owly oxydised by the tissues and the arsenic is set free ; so 
