SUPPLEMENTATION OF COCONUT OIL FROM DIFFERENT SOURCES TO THE DIET INDUCES CELLULAR-DAMAGE AND RAPID CHANGES IN FATTY-ACID COMPOSITION OF CHICK LIVER AND HEPATIC MITOCHONDRIA

Supplementation of 20% coconut oil from two commercial sources, pharma ceutical (''Pharmacy'') and cooking (''Pastry'') use, to the chick die t for 14 days produced a clear damage to the hepatic mitochondria, acc ompanied by an accumulation of glycogen and lipid droplets in the hepa tocyte cytoplasm. These effects may be accounted for the high proporti on of fat supplemented to the diets (20%). Pharmacy coconut oil induce d a high percentage of cellular death when administered for 14 days. F atty acid profiles in liver and hepatic mitochondria rapidly changed ( 24 hr) after both coconut oils supplementation to the diet. The accumu lation of shorter chain fatty acids (12:0 and 14:0) was always higher after Pharmacy than after Pastry diet feeding. This fact may contribut e, at least in part, to the cellular damage mentioned above especially after Pharmacy diet feeding. Mitochondrial ratios of saturated/unsatu rated and saturated/polyunsaturated fatty acids rapidly changed in par allel to these ratios in both diets. Most of the mitochondrial paramet ers measured tend to recuperate the control Values when diets were sup plied for 5-14 days. Nevertheless, the maintenance of the mentioned ra tios after 14-days Pharmacy diet feeding at significantly higher level s than those observed in control, seems to suggest the lack of the hom eostatic mechanism in these membranes and could be also related with t he high percentage of cellular death observed after this dietary manip ulation. (C) 1997 Elsevier Science Inc.