Diphtheria  Antitoxin.  769 
one  half  hour,  and  heating  to  1400  C.  for  one  quarter  hour.36  No 
doubt  the  response  to  heat  will  depend  on  the  salts  present.  This 
has  been  found  to  be  true  in  the  case  of  certain  toxins,  etc.  Buchner 
found  that  alkali  sulphates  added  to  dilute  serum  increased  its  re- 
sistance to  heat  io°  C.  and  raised  its  activity.37 
Mellanby  found  that  acetic  acid  (5  per  cent.)  and  0.25  per  cent. 
HC1  have  no  deleterious  action  on  antitoxic  serum  at  room  tempera- 
ture, but  0.05  Cc.  n/10  HQ  added  to  1  Cc.  of  antitoxic  serum  weak- 
ened it.  Dilute  formic  acid  causes  a  precipitation  from  serum.38 
Weak  alkalies  dissolve  certain  antitoxic  precipitates.39  According 
to  v.  Groer  and  Kassowitz,  dilute  alkalies  activate  the  antitoxin, 
while  more  concentrated  alkalies  destroy  it.  Ba(OH)2  injures  anti- 
toxin.40 
Digestion  with  0.2  per  cent.  HQ  and  pepsin  causes  a  rapid  loss 
in  activity.41  It  is  slowly  destroyed  by  tryptic  digestion.42  The 
addition  of  Nad  in  solution  will  inhibit  pepsin*  from  digesting  cer- 
tain proteins.43 
After  saturation  of  the  diluted  (ten  times)  serum  with  C02,  the 
precipitate  contained  only  a  trace  of  antitoxin.44  Brieger  and  Krause 
passed  C02  into  a  solution  of  antitoxin  containing  NaCI,  (NH4)2S04 
and  glycerol,  but  the  precipitate  contained  no  antitoxin,  while  the 
filtrate  was  active.45 
Chloroform,  in  1  per  cent,  solution,  is  used  as  a  preservative  for 
antibodies,  but  causes  a  precipitate.  Diphtheria  antitoxin  and  toxin 
are  very  resistant  to  ether.46  V.  Groer  and  Kassowitz  shook  out 
antitoxic  serum  with  ether  and  found  that  the  serum  retained  its 
activity.  This  would  suggest  that  the  antitoxic  agent  was  not  a  free 
lipoid.  Antitoxin  is  not  precipitated  from  serum  by  25  per  cent, 
alcohol.    Higher  percentages  precipitate  antitoxin  according  to  the 
36  Camus,  M.  L.,  Soc.  de  Biol,  Vol.  50,  p.  235,  1898. 
37  Buchner,  H.,  Archiv  f.  Hyg.,  Vol.  17,  p.  138,  1893;  Ferrata,  A.,  Berl. 
klin.  Woch.,  Vol.  44,  p.  366,  1907. 
38  Brieger,  L.,  and  Krause,  M.,  Berl.  klin.  Woch.,  p.  946,  1907. 
39Aronson,  H.,  Berl.  klin.  Woch.,  Vol.  31,  p.  453,  1894. 
40  Freund,  E.,  and  Sternberg,  C,  Zeits.  f.  Hyg.,  Vol.  31,  p.  429,  1899. 
41  Mellanby;  also  Brieger,  L.,  and  Krause,  M.,  ibid. 
42  Mellanby;  v.  Groer  and  Kassowitz,  p.  449. 
43  Hamburger,  W.  W.,  Arch.  Intern.  Med.,  Vol.  16,  pp.  341,  508. 
44  Dieudonne,  Arb.  d.  Kais.  Ges.  Ami.,  Vol.  13,  p.  293,  1897. 
45  Brieger,  L.,  and  Krause,  M.,  Berl.  klin.  Woch.,  1907,  p.  946.  See  also 
Hiss,  P.  H.,  and  Atkinson,  J.  P.,  Journ.  Exper.  Med.,  Vol.  5,  p.  49,  1900-1. 
46  Pick,  E.  P.,  and  Schwarz,  O.,  Biochem.  Zeits.,  Vol.  17,  p'.  491,  1909. 
Am.  Tour.  Pharm.  \ 
Nov.,  iqi8.  J 
