Abstract
UNCOUPLING of oxidative phosphorylation in mitochondria from steatotic livers1 and in experimental thyrotoxicosis2 is known to be accompanied, among other changes, by a decrease in liver pyridine nucleotides which are of major importance in phosphate uptake during electron transport to molecular oxygen3. The pronounced lowering of liver and its mitochondrial vitamin B12 in hyperthyroidism4 as well as in carbon tetrachloride injury (unpublished results), together with the observed protection by the vitamin against both these stress conditions4,5, would point to a function for the vitamin in the maintenance of tissue-levels of pyridine nucleotides. This has now been ascertained by following the effect in mice of simple vitamin B12 deficiency induced by feeding on a high vegetable protein diet6 on the extent of incorporation in vivo of administered nicotinamide into liver pyridine nucleotides in a manner similar to that studied by Kaplan et al. 7, and the changes in liver pyridine nucleotides, 6 and 48 hr. after carbon tetrachloride injection to adult rats as described before5, without and with vitamin B12 protection. Total and oxidized pyridine nucleotides were determined fluorimetrically by the procedure outlined by Dianzani1.
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References
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NADKARNI, G., WAGLE, D. & SREENIVASAN, A. Vitamin B12 and the Metabolism of Pyridine Nucleotides. Nature 180, 659–660 (1957). https://doi.org/10.1038/180659a0
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DOI: https://doi.org/10.1038/180659a0
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