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Journal of Nutrition Vol. 102 No. 11 November 1972, pp. 1453-1463
Copyright © 1972 by American Society for Nutrition
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Metabolism of Carbonyl-labeled 14C-Biotin in the Rat1, 2,

Han-Min Lee, Lemuel D. Wright and Donald B. McCormick

Graduate School of Nutrition, and Section of Biochemistry and Molecular Biology, Cornell University, Ithaca, New York 14850

Ureido carbonyl-labeled 14C-biotin was injected intraperitoneally into young adult, male rats to study the excretion and degradation of the vitamin. After milligram quantities of the radioactive biotin were injected, the intact vitamin was found to be almost completely excreted in the urine within 24 hours. The initial excretion rate decreases with decreasing amounts of biotin administered. This initial decrease is even more marked with biotin-depleted rats. Biotin-depleted rats, treated with succinyl sulfathiazole and penicillin, were given a single injection of radioactive biotin (0.5 µg/100 g body weight). Urine was fractionated for radioactive biotin metabolites, four of which have been identified as follows: the d- and l-sulfoxides of biotin, bisnorbiotin, and a neutral ketone. No radioactive CO2 and urea could be detected. Also, liver homogenates were incubated with carbonyl-labeled biotin at 37° for 40 or 60 minutes, with or without aeration. Under O2-limiting conditions, the same four biotin metabolites were also found, but in different proportions. With aeration, the amount of biotin sulfoxides increased; also, trace amounts of radioactive CO2 and urea were detected. Therefore, the rat has the ability to metabolize the vitamin via at least partial ß-oxidation of the side chain and to effect some oxidation of the thioether sulfur to sulfoxides. Under physiological conditions, however, the metabolism of biotin in rats, unlike certain bacteria, does not include extensive cleavage of the ring structure of the molecule.


KEY WORDS: • biotin • bisnorbiotin • biotin sulfoxides

1 Supported in part by Public Health Service Research Grants AM-08721 and AM-12224 from the National Institute of Arthritis and Metabolic Diseases and in part by funds made available through the State University of New York.

2 Part of these data were included in a preliminary report presented at the meetings of the Federation of American Societies for Experimental Biology in Atlantic City, N. J., April, 1972.

Manuscript received 19 April 1972.





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