365 



Comment on papers 34—35 



We calculated in paper 29 and the following papers the rate of renewal of phospha- 

 tides from the specific activity of the phosphatide phosphorus at the end of the 

 oxperiment, and of the moan specific activity of the cellular inorganic phosphorus 

 during the experiment. The latter is obtained from the specific activities of the 

 total inorganic P after correcting for the share of the extracellular phosphorus 

 in tlie total inorganic P activity. The possibility was considered in these studies 

 that it is not the cellular but the extracellular ^^p which participates in the synthe- 

 sis of the organic phosphorus compounds present in the tissues and that "It is 

 conceivable that some of the phosphatide molecules are renewed inside the cell 

 wall." Correspondingly, all turnover data were calculated, assuming once parti- 

 cipation of cellular 32 p and than of extracellular ^sp (paper 34). That phospliate 

 enters the cells, at least partly, by the formation of ATP and other intermediates 

 of the cycle on the cell membrane and that inorganic phosphate within the cell 

 arose from the dephosphorylating reactions of the cycle was shown later by 

 Sacks (1951). 



In paper 36 in which the calculation of the turnover rate is discussed we find 

 the following remark: " . . . If the incorporation of the phosphate radical into 

 the phosphatide molecules would be preceded by the formation of glycerophos- 

 phate and this process would be a comparatively slow one, in contrast to all other 

 steps involved in the synthesis of the phosphatide molecule, in this case the turnover 

 rate measured, using labelled phosphorus as an indicator, would be slower than 

 fotmd when using labelled fatty acids or labelled choline . . ." and that "the 

 question if and to what extent the rate of labelled phosphate incorporation into 

 the phosphatide differs, for example fiom that of the fatty acid incorporation 

 into the latter cannot be answered at the time being". The question thus raised 

 was answered by Chaikoff, Zilversmit, and their associates (1941) who demon- 

 strated that glycerophosphate is the pertinent precursor of phosphatide s,\Tithesis 

 and that the calculation of the turnover rate of phosphatides from the specific 

 activity of inorganic phosphorus leads to too low a value for the turnover rate. 

 In experiments with rats, taking 2 hi', the mean specific activity of the ortho- 

 phosphate phosphorus of the Uver was found to be three times that of the corre- 

 ponding value of glycerophosphate phosphorus (paper 35); thus, the turnover 

 rate calculated assuming the liver orthophosphate P to be the phosphatide pre- 

 cursor has to be multiplied by three to arrive at a correct turnover rate value. 

 The turnover rate of phosphatides present in the different sub-units of the liver 

 cell was found to differ markedly (paper 35 and Hevesy, 1947). Applying palmitic 

 acid — 1 — i^C as a precursor Chaikoff et al. could also demonstrate that the liver 

 is the principal site for the formation of fatty acid ester bonds of plasma phos- 

 phatide molecules. 



References 



O. Hevesy (1947) Ark. Kemi, A 24, No. 2C. 



J. Sacks (1951) Arch. Biochem. 30, 423. 



D. B. Zilversmit, C. Entenman, M. C. Fishler and I. L. Chaikoff (1941) 



J. Gen. Physiol. 26, 325. 

 D. S. Goldman, I. L. Chaikoff, W. O. Reinhardt, C. En^tenman and W. G. 



Datjben, (1950) ./. Biol. Chem. 184, 727. 



