The metabolism of 1-(14)C arachidonic acid in pyridoxine-deficient and pair-fed control rats.

The metabolism of 1-(14)C arachidonate was studied in pyridoxine-deficient and pair-fed pyridoxine-supplemented control rats. The studies included intestinal absorption, oxidation to(14)CO(2), organ uptakes and distribution of(14)C in the fatty acids of the various organs. Generally, pyridoxine deficiency resulted in little or no alteration of the metabolism of arachidonic acid 6 and 12 hrs after oral administration. A notable exception occurred in hearts of deficient animals in which the proportion of the incorporated(14)C activity found in fatty acids other than 20:4 was larger than that observed in hearts of pyridoxine-supplemented animals. A significant amount of(14)C activity in a water-soluble form was observed in hydrolysates of intestinal contents and of intestines of both groups. Pyridoxine-deficient rats had larger quantities than their respective pair-fed pyridoxine-supplemented controls. Most of the(14)C activity of fatty acids of various organs was present as arachidonic acid, but significant activity was present both in fatty acids of shorter and of longer retention time than 20:4. In brain about 20% of the(14)C activity in fatty acids was in a fraction tentatively identified as an 18:2 isomer. In lungs about 10% of the(14)C activity was in a fraction tentatively identified as a 22:2 isomer and a similar quantity was observed in a polyene tentatively identified as a 22:4.