The Effect of Zinc Deficiency and Food Restriction on Hepatic Zinc Proteins in the Rat

found in the response of the electron-capture detector for fatty acids of niicrosomal lipids from CC1,-treated rats (the latter peak is clearly a group of unresolved peaks). Since serum very-low-density lipoproteins derive directly from the hepatic cell and since the phospholipid fraction of such lipoproteins is believed to derive from the phospholipids of the endoplasmic reticulum, we investigated whether alterations like those observed in liver microsomal phospholipids could also be detected in the phospholipid fraction of very low-density lipoproteins (dc 1.006) after CCI, poisoning. Therefore fatty acid methyl esters of phospholipids of very-low-density lipoproteins from rats given CCI, 4 h earlier were analysed by use of the electron-capture detector. The response of the electron-capture detector showed one small peak only. This peak apparently corresponds to the second peak found in the response of the electron-capture detector for fatty acids of liver microsomal phospholipids of CC1,-treated rats. However, the first peak of the latter response is absent. It was deduced that the phospholipids of very-low-density lipoproteins are also daniaged by CCI,. However, the difference between the response of the electron-capture detector for phospholipids of very-low-density lipoproteins and that for phospholipids of liver microsomal fraction may mean that some of the CC1,-damaged molecular structures in the membranes of the endoplasmic reticulum are not available for the assembly of lipoproteins in CC1,-treated rats.