48 P-AMINOBENZOIC ACID 



is acetylated by the normal human. Although this high percentage may 

 appear at first sight to be at variance with the results of Tabor et al.,- two 

 points must be kept in mind: (1) the per cent of administered PABA ace- 

 tylated decreases with increase in the size of the dose (the small percentage 

 of acetylated PABA reported by Tabor et al. is associated with a dose of 

 6.2 g.); (2) Gershberg and Kuhl used the Bratton-Marshall reaction as 

 their method of assay, so that in actuality the "amount acetylated" repre- 

 sents not only acetyl PABA, but also acetyl PAHA, acetyl PABA glu- 

 curonide, and any other PABA derivatives in which the amino group is 

 involved. 



Gershberg and Kuhl included in their studies the "acetylation" of PABA 

 in subjects suffering from various metabolic disorders. A standard dose of 

 500 mg. of PABA was used in most experiments. Normal (control) in- 

 dividuals were found to "acetylate" 88 ± 1.9% of the standard dose. In 

 patients with severe liver disease acetylation is normal. The authors infer 

 that acetylation does not occur exclusively or necessarily primarily in the 

 liver but that other tissues also participate in acetylation. Acetylation is 

 normal in patients with rheumatoid arthritis, diabetes mellitus, hypo- 

 thyroidism, sprue, and leukemia. Patients with hyperthyroidism have a 

 diminished capacity to acetylate. This usually returns to within normal 

 limits as the hyperthyroidism is controlled. In two patients with hyper- 

 thyroidism the administration of sodium acetate was found to increase the 

 capacity to acetylate. The authors suggest that in hyperthyroidism there 

 is a decrease in available acetate, owing to its rapid utilization, which may 

 contribute to the decreased ability to acetylate PABA. 



Zilli and Di Ferrante^- found \'ery little difference between normal sub- 

 jects and patients with icterus and cirrhosis of the liver, in the rate at 

 which 1 g. of injected PABA is excreted, in the total excretion, or in the 

 proportions of free and acetylated PABA excreted. 



Although PABA has been reported to inhibit the in vitro conversion of 

 tyrosine and melanine by tyrosinase,^'' White et al?^ found that PABA 

 (20 g. daily) is without effect on the excretion of homogentisic acid by an 

 alcaptonuric. 



No data could be found in the literature concerning acetylation of PABA 

 in individuals in whom a pantothenic acid deficiency might be suspected 

 from a study of their nutritional history. It would appear to the present 

 reviewers that such a study could be instrumental in demonstrating the 

 essential nature of pantothenic acid in human nutrition. 



»2 E. Zilli and N. Di Ferrante, Acta Vitaminol. 2, 111 (194S). 



33 K. E. Paschkis, A. Cantarow, W. M. Hart, and A. E. RakofT, Proc. Soc. Expil. 



Biol. Med. 57, 37 (1944). 

 " A. G. White, J. G. Parker, and K. Block, J. Clin. Invest. 28. 140 (1949). 



