EFFECT OF DEFICIENCY IN ANIMALS 



deficiency, but this condition was not cured by pure riboflavine, and, 

 moreover, rats on a diet completely free from riboflavine, and con- 

 taining other members of the vitamin B complex, did not develop 

 cataract. 3 Only when rats were fed on a diet containing suboptimal 

 amounts of riboflavine, such as the Bourquin-Sherman diet, which 

 supplies an average of 0-5 /xg. of riboflavine per day, did they exhibit 

 a high incidence of cataract. Thus, whereas corneal opacity and 

 vascularisation * invariably resulted from a complete absence of the 

 vitamin, cataract formation only occurred with diets containing small 

 amounts of riboflavine. 



Changes in riboflavine intake were promptly reflected by changes 

 in its concentration in the cornea. ^ Intense visible or ultra-violet 

 light had no effect on the riboflavine concentration, and it was sug- 

 gested that this rather unexpected insensitivity to light might be due 

 to a combination of the flavine with an acceptor. 



Other symptoms associated with a severe deficiency of ribo- 

 flavine were a partial paralysis of the legs due to myelin degeneration 

 of the muscle sheaths, atrophy of the testes, early involution of the 

 thymus gland and structural alterations in the thyroid and adrenal 

 glands . ^ 



Prolonged deficiency of riboflavine also led * to neurological 

 abnormalities, such as loss of reflexes, myelin degeneration of peri- 

 pheral nerves and the posterior column of the spinal cord. 



Leucopenia, with both a relative and an absolute decrease in the 

 number of lymphocytes, appeared to be an early sign of aribofiavinosis, 

 and, in rats, occurred prior to changes in the lens and cornea of the 

 eye.'' Granulocytopenia was also observed ^ in rats maintained on a 

 purified diet deficient in riboflavine, but it was cured by folic acid 

 (see page 489) and not by riboflavine. An anaemia observed in some 

 of the animals was partially relieved by riboflavine but was not 

 affected by folic acid. 



At low oxygen tensions, the liver glycogen of ribofla vine-deficient 

 rats was not increased to the same degree as in normal rats, and the 

 deficient animals had a lower blood-sugar when fasted at sea-level 

 than had normal animals ; the riboflavine content of the liver de- 

 pended on the riboflavine intake.^ L-Cystine, DL-tryptophan, 

 L-tyrosine, L-histidine, glycine and D-glutamic acid were more toxic 

 to ribofla vine-deficient rats than to adequately nourished animals. ^° 



Effect in other Mammals 



The effects of riboflavine deficiency in mice were very similar to 

 the effects in rats, and were characterised by dermatitis, myelin de- 

 generation and keratitis .^^ Pigs on a ribofla vine-deficient diet fafled 



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