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Rat kidney cortical slices, during incubation in vitro, lose previously accumulated radiosulfur when exposed to conditions (e.g. addition to the medium of metabolic inhibitors) which normally depress the uptake of S(35). The extent of this loss is not affected significantly by the presence of phlorhizin, an agent which enhances markedly radiosulfate accumulation. On the other hand, when tissues are chilled to 1 degrees C., loss is slight or negligible even in the presence of metabolic inhibitors. These data, and observations on the effect of pre-incubation of kidney slices in S(35)-free media before the addition of radiosulfate, have been interpreted as evidence that S(35) accumulation in vitro may be resolved into at least two processes, namely (a) entrance of the isotope-labelled anion into the cells, by diffusion and/or active transport, and (b) complexing of S(35) (in ionic or other form) with an intracellular component. The postulated complex is stabilized, perhaps through inactivation of a specific enzyme, by chilling the tissue to 1 degrees C. Possible relationships are discussed among the observations noted above, sulfur metabolism in general, and aspects of the known in vivo transport mechanism for sulfate ion; i.e., renal tubular reabsorption.

FACTORS INFLUENCING THE UPTAKE AND LOSS OF RADIOSULFATE BY RAT RENAL CORTICAL TISSUE IN VITRO