EFFECT OF DEFICIENCY IN ANIMALS 



were produced. ; these were more acute when sulphasuxidine was also 

 added to the diet.^^o With sulphasuxidine alone, a normocytic 

 anaemia was produced which was cured by the administration of 

 pteroylglutamic acid. A more severe anaemia was produced by the 

 addition of a crude folic acid antagonist to the diet,^3«» ^^6 the effects 

 of which were overcome more effectively by a mixture of pteroyl- 

 glutamic acid and bio tin than by the former alone. 



Monkeys 



Vitamin M was the name assigned by Langston et al.^^ to a factor 

 in liver and yeast that relieved leucopenia and granulocytopenia in 

 monkeys (see page 460). These symptoms were partially relieved by 

 xanthopterine and completely by a pure specimen of the fermentation 

 L. casei factor,^^ and by synthetic pteroylglutamic acid.^^ 



Vitamin M deficiency is characterised by loss of weight, leuco- 

 penia, granulocytopenia, anaemia, bloody discharge, gingivitis, ne- 

 crosis of the gums, loss of appetite and susceptibility to dysentery. 

 Autopsy revealed ulcerated colon, liver damage and adrenal changes.^® 



Injection of 2 to 6 mg. of synthetic pteroylglutamic acid was 

 followed by a dramatic increase in the leucocyte and reticulocyte 

 counts. A prompt, but transient, increase in red blood cells occurred 

 within twenty-four hours, followed by a return to the previous low 

 levels and, several days later, by a more permanent increase. 



Folic acid, however, may not be the only factor responsible for 

 vitamin M deficiency, for Cooperman et al.,^'' in the course of an in- 

 vestigation into the effect of riboflavine deficiency, maintained rhesus 

 monkeys on a diet containing all the other members of the vitamin B 

 complex, including a norit eluate preparation from liver, and observed 

 a fall in the red and white blood cell count which was not restored to 

 normal by the administration of large doses of riboflavine. Addition 

 of whole liver to the diet restored the normal blood picture. When 

 monkeys were maintained on a similar diet containing adequate ribo- 

 flavine but no folic acid, growth was slow and white blood cell counts 

 become low. The addition to the diet of vitamin Be, vitamin Be 

 conjugate or L. casei factor only partially remedied the deficiency 

 symptoms. Concentrates of vitamin B^o and B^ had no effect. It 

 appeared that a deficiency of folic acid precipitated a deficiency of 

 the monkey anaemia factor ; this was characterised by lack of growth, 

 a low level of haemoglobin and a reversal of the lymphocyte-neutro- 

 phile ratio. The animals were cured by treatment with whole liver, 

 indicating the presence therein of an anti-anaemia factor additional 

 to folic acid. This was also present in raw milk and stimulated the 

 growth of 5. faecalis R.^^ In this respect it resembled the SLR 

 factor, but differed from it in being heat-labile. 



491 



