PYRIDOXINE 



in restoring the activity of the apoenzyme. This finding may explain 

 the increased excretion of xanthurenic acid by rats and pigs fed a 

 vitamin Bg-deficient diet (page 330), since any indole not utilised in 

 the above reaction, by reason of the absence of pyridoxal phosphate, 

 would presumably be excreted as xanthurenic acid or kynurenine. 

 This hypothesis is supported by work with a pyridoxine antagonist, 

 desoxypyridoxine (see page 345) ; normal rats given desoxypyridoxine 

 together with tryptophan excreted more xanthurenic acid and kynur- 

 enine than animals receiving tryptophan alone. ^^ The effect was still 

 more noticeable with rats partially deficient in pyridoxine. The 

 addition of pyridoxine to the diet counteracted the effect of the 

 desoxypyridoxine. 



Pyridoxine was also shown to be essential for the metabolic con- 

 version of indole or anthranilic acid into tryptophan by L. arabinosus.^^ 

 Pyridoxal and pyridoxamine were much more active, and tryptophan 

 synthesis was increased by the addition of serine and acetate. 



Pyridoxal phosphate was also shown ^* to be the prosthetic group 

 of an enzyme, tryptophan ase, present in E. coli. This enzyme cata- 

 lyses the breakdown of tryptophan into indole, pyruvic acid and 

 ammonia and not, as might be expected by analogy with the Neurospora 

 enzyme, into indole and serine. 



Pyridoxine facilitates the conversion of tryptophan into nicotinic 

 acid. For example, when 100 mg. of DL-tryptophan were added to 

 the diet, more nicotinic acid and N^-methylnicotinamide were excreted 

 by rats fed pyridoxine than by rats maintained on a vitamin Bg-de- 

 ficient diet.^^ Pyridoxal and pyridoxamine were equally effective. 

 The increase in xanthurenic acid production in vitamin Bg deficiency 

 was not responsible for the decreased conversion of tryptophan into 

 nicotinic acid.^^ 



Whereas the pyridine nucleotide level of the erythrocytes of 

 vitamin Bg-deficient rats was not affected when L-tryptophan was 

 injected intravenously, an immediate increase was observed when the 

 injection was preceded by a subcutaneous injection of pyridoxine.^' 



Antianaemic Activity 



As already mentioned, the onset of anaemia is one of the most 

 constant results of vitamin Bg deficiency in several species of animals, 

 but attempts to establish a connection between pyridoxine and the 

 anti-pernicious anaemia factor on the one hand and Castle's extrinsic 

 factor on the other (page 323), were unsuccessful. Investigation 

 showed, however, that pyridoxine did not itself possess antianaemic 

 properties, but that the lactones of the corresponding acids, known as 

 a- and /S-pyracin (see page 344), were the effective agents. Either of 



336 



