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Metabolism of [35S]Taurine in Man

John A. Sturman1,2,, Gershon W. Hepner3, Alan F. Hofmann and Paul J. Thomas

Department of Pediatric Research, Institute for Basic Research in Mental Retardation, Staten Island, New York 10314, and Gastroenterology Unit, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901

Taurine metabolism in man was defined by an isotope dilution technique during normal taurine intake (five subjects) or increased taurine intake (two subjects). A tracer dose of [35S]taurine was administered intravenously, and the amount and chemical form of radioactivity were determined in blood, urine, bile, and feces. Analysis of plasma specific activity decay curves indicated that taurine metabolism can be described by two exchangeable pools: a small (2 mmoles), rapidly exchanging pool (t1/2 rx 0.1 hour); and a large (98 mmoles), very slowly exchanging pool (t1/2 rx 70 hours). A small amount of [35S]isethionic acid was detected in urine, possibly the result of deamination of taurine by tissues; but otherwise no evidence of tissue biotransformation was obtained. Taurine was excreted predominantly (95%) in urine, about 70% as taurine and 25% as sulfate. The sulfate was considered to be formed in the intestine by bacterial degradation of taurine and then absorbed. Supplemental taurine (given orally) was well absorbed, caused a transient increase in plasma taurine levels, was excreted in urine without equilibration with the slowly exchangeable pool, and caused only a modest increase in total body taurine. Thus, taurine resembles other amino acids in having large tissue pools but differs strikingly in being metabolically inert with an extremely slow turnover rate.


KEY WORDS: • taurine • sulfate • compartmental analysis • cholyltaurine

1 This investigation was supported in part by the New York State Department of Mental Hygiene; Research grants AM-6908, AM-16770, and RR 585 from the National Institutes of Health, Public Health Service; and by grants-in-aid from the Share Foundation, the Mead Johnson Company, and the Ell Lilly Research Foundation.

2 Submitted for presentation at the 1975 meeting of the American Federation for Clinical Research and published in abstract form. Clin. Res. 23, 333a.

3 Present address: Department of Medicine, Milton S. Hershey College Medical Center, The Pennsylvania State University, Hershey, Pa. 17033.

Manuscript received 25 March 1975.


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