Abstract
The riboflavin homolog 7-ethyl-8-methyl-10-(D-ribityl)isoalloxazine (7-ethyl-8-methyl-flavin; Fig. 1) 1 is able to serve as the sole flavin in the nutrition of the rat 2 . Females receiving only 7-ethyl-8-methyl-flavin, produce litters of the usual size consisting of normal appearing young, but the young die during the first 3 days after birth 3 .
Kim and Lambooy 4 have shown that 7-ethyl-8-methyl-flavin causes a reduction of succinic acid dehydrogenase (SDH) activity in tissues of healthy rats. The evidence 4 suggested that the coenzyme form of the homolog is able to replace riboflavin in the enzyme at a rate which is reasonably consistent with the half-life of the mitochondrion. These phenomena led to observations that the half-life of decay of rat liver SDH is approximately 14 days while that of the kidney is of the order of 100 days.
It might be argued that the large difference in the half-lives of SDH decay in the liver and kidney are not related to the reproductive cycle of the mitochondria in the tissues but rather that the homolog coenzyme forms a far more active holoenzyme with the apoenzyme of the kidney than with the apoenzyme of the liver.
The relatively slow rate of cell division in the brain reduces the need for new mitochondria to very low levels and it has been stated 5 that brain mitochondria grow and divide very slowly and may be stable for the lifetime of the cell. If the decay of SDH activity in the tissue of a rat receiving only the homolog is related to the rate of production of mitochondria, then the administration of the homolog as the sole flavin to rats and the determination of the SDH activity of the brains from weanling age well into adulthood should show an extremely slow rate of decay of the enzyme.
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