EFFECT OF DEFICIENCY IN ANIMALS 



of the protein content of the diet, but with a constant protein intake 

 the amount of pyridoxine in the tissues increased to a maximum 

 with increasing amounts of dietary pyridoxine up to 200 /xg. per day. 

 Storage was directly proportional to protein intake, and maximum 

 values were obtained with a pyridoxine intake of 25 /zg. per day. 

 On the other hand, Schweigert et al^^ found that the protein content 

 of the diet did not affect the storage or depletion of pyridoxine. 



Further evidence that a disturbance of normal protein metabolism 

 occurs in vitamin Bg deficiency is provided by the findings of Hawkins 

 et al^^ that, on a high protein diet, the fasting blood levels of urea 

 and non-protein nitrogen increased when rats were deprived of 

 vitamin Bg, and by the observation of G. J. Martin ^o that L-tyrosine 

 was less toxic to pyridoxine-deficient rats than to normal rats. 



Mice. The association between pyridoxine and protein metabolism 

 noted in rats was confirmed in experiments on mice. The reserves of 

 pyridoxine in the tissues of mice fed on a vitamin Bg-deficient diet 

 decreased much more rapidly when the diet contained 50 % of casein 

 than when it contained only 10 %,^^ whilst the mice on the high 

 protein diet lost more weight and had a higher mortality than those on 

 the low protein diet. The effects were not due to variations in 

 calorie intake, in the urinary excretion of pjnridoxine or in the tryp- 

 tophan content of the diet. The pyridoxine content of the tissues 

 increased as the pyridoxine content of the diet increased. At low 

 levels of pyridoxine intake, less pyridoxine was stored on the high 

 protein than on the low protein diet but at high levels the high protein 

 diet gave the higher pyridoxine storage. In young vitamin Bg-de- 

 ficient mice cartilage growth and bone formation were inhibited, the 

 effect being accentuated on a high protein diet .21 



Hamsters. When Syrian hamsters were fed on a vitamin Bg-de- 

 ficient diet, growth stopped in two or three weeks and food and water 

 intake diminished. Muscular weakness developed, changes in the fur 

 occurred and increased amounts of xanthurenic acid were excreted in 

 the urine. Deficient animals died after twelve or thirteen weeks, and 

 autopsy revealed a loss of fat tissue and atrophy of lymphoid tissues, 

 notably the thymus. Animals recovered after about nine weeks when 

 given daily injections of 50 jug. of pyridoxine. ^^^ 



Dogs. In addition to anaemia, deficient dogs also developed 

 cardiac embarrassment, dyspepsia, tachycardia, dilation and hyper- 

 trophy of the right ventricle and right auricle, accumulation of serous 

 fluid in the thorax and chronic passive congestion of the liver ; de- 

 generative changes were also found in the myelin sheaths of the peri- 

 pheral nerves and spinal cord.^ 



Dogs exhibited an increased urinary output of urea, ammonia, uric 

 acid and creatinine when maintained on a vitamin Bg-deficient diet.^^ 



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