Liberation of 14CO2 from [14C]adipic acid and [14C]octanoic acid by adult rats during riboflavin deficiency and its reversal
1990
Bates, C.J.
The purpose of the present study was to test the hypothesis that the already well-established mitochondrial lesion in fatty acid oxidation in riboflavin-deficient experimental animals, might be accompanied by an alteration in vivo in the kinetics of oxidation of labelled adipic acid. This dicarboxylic acid was chosen for testing as a metabolic probe because a block in its oxidation was already apparent from urine analysis of riboflavin-deficient animals, whereas the oxidation of medium- or long-chain monocarboxylic acids seemed to be little affected by deficiency in vivo. Female adult Norwegian hooded rats fed on purified diets containing either 15 mg riboflavin/kg diet (controls) or about 0.4 mg/kg (riboflavin-deficient) received an intragastric dose of either [1,6-14C]adipic acid or [1-14C]octanoic acid. Expired carbon dioxide was then collected in an alkaline trap over 3 h, for determination of radioactivity. This test was repeated at intervals for up to 2 weeks following riboflavin repletion of the deficient animals, and in riboflavin-dosed controls. Whereas the rate and extent of [14C]octanoic acid oxidation was not significantly affected by the deficiency or repletion, the extent of [14C]adipic acid oxidation was markedly and significantly increased during repletion of the deficient animals. The time-course indicated aA temporary overshoot, followed by a slow return to the control values over 1-2 weeks. Adipate oxidation was also much less affected by a preceding period of overnight starvation, than was octanoate oxidation. Thus, adipic acid (or a related metabolic probe) may have appropriate properties for the design of a functional test of fatty acid oxidation efficiency, during riboflavin deficiency or allied metabolic conditions in human subjects.
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