VIII. EFFECTS OF DEFICIENCY IN ANIMALS 319 



quick fall in achvnal as('orl)i(' acid and a slower fall in cholesterol whereas 

 the levels of these substances in other tissues remained inichanged. These 

 workers suggested that the release of adrenal cortical hormone may he 

 invoh'cd in lowering the content of ascorbic acid and cholesterol in the 

 adrenals. Active study of these problems is continuing in several labora- 

 tories. 



(3) Fatty Acid Oxidations. Quastel and Wheatley^*' studied the effect of 

 the vitamin on fatty acid oxidations in the liver and concluded that the 

 vitamin is important in maintaining the metabolism of fatty acids at a 

 normal level. Rusch and Kline-*^ reported that ascorbic acid catalyzes the 

 oxidation of phospholipids in the liver, and Elliott and Libet-''* found that 

 the vitamin augmented the phospholipid stimulation of oxidation in sus- 

 pensions of brain tissue. Bernheim, Wilbur, and Fitzgerald-*^ reported that 

 brain protein, also that of several other organs, is combined with a com- 

 pound probably containing hydroxyl groups attached to a benzene ring. 

 Ascorbic acid acted as a catalyst in the oxidation of the compound and in 

 the reaction the protein was split ofT and aldehyde groups became exposed. 



Abramson-*^ measured the oxidation of unsaturated fatty acids in nonnal 

 and scorbutic guinea pigs by means of the thiobarbituric acid color reaction 

 of Kohn and Liversedge.-^^ He observed that in scurvy the oxidation was 

 decreased in brain, testes, medulla oblongata, adrenals, and kidneys but in 

 spleen and heart there was little difference from the normal. Bernheim, 

 Bernheim, and Wilbur-"^ found that the color obtained upon addition of 

 thiobarbituric acid to lecithins or compounds containing them are due to 

 a product of the oxidation of unsaturated fatty acids such as linolenic. 

 Ascorbic acid appeared to catalyze the oxidation of lecithin either in free 

 form or when combined with tissue protein. In the reaction the oxidation 

 could be followed quantitatively. 



d. Minerals 



The study of mineral metal)olism in scurvy has not been given the atten- 

 tion it deserves. Some of the problems undoubtedly should l)e reinvesti- 

 gated, using a dietary regime complete in all respects except for the lack of 

 ascorl)ic acid. On the basis of l)lood studies it would appear that mineral 

 metabolism is not greatly deranged in scur\'y. This does not signify, how- 

 3ver, that an increased turnover of minerals does not occur in the tissues. 



(1) Calcirim. It is impossible to state with any degree of finality whether 



2" J. 11. Quastel and A. II. M. Whoatloy, Biochem. J. 28, 1014 (1934). 



=«^ H. P. Rusch and B. K. Kline, Cancer Research 1, 465 (1941). 



285 F. Bernheim, K. M. Wilbur, and D. B. Fitzgerald, J. Gen. Physwl. 31, 195 (1947; 



288 H. Al)ramson, ./. Biol. Chem. 178, 179 (1949). 



=" H. Kohn and M. Liversedge, J. Pharmacol. Expll. Therap. 82, 292 (1944). 



