Abstract
Adrenal steroid hormones with glucocorticoid activity increase the uptake of Zn++ in certain mammalian cell cultures. Whereas in the absence of added hormones the Zn++ content of HeLa S3 cells is approximately 8- to 20-fold greater than that of an equivalent volume of medium, after growth in the presence of prednisolone the cellular Zn++ content doubles or triples. Kinetic studies suggest that cells must grow 8-12 hr in the presence of prednisolone before an increased Zn++ uptake becomes apparent. Accumulation of Zn++ is markedly depressed at low temperatures and in the presence of sulfhydryl-blocking agents. Inhibitors of either glycolysis or oxidative metabolism have little effect on Zn++ uptake. However, if both glycolysis and oxidative metabolism are inhibited, Zn++ accumulation is decreased. 65Z++ taken up by mammalian cells is readily exchangeable and is nearly all soluble in trichloracetic acid. Hormonal effects on Zn++ uptake are selective in that (a) only those steroid hormones with potent glucocorticoid effects stimulate Zn++ uptake while the degree of effectiveness of each hormone parallels its glucocorticoid activity; (b) susceptibility to hormone effects on Zn++ accumulation was confined to certain established "epithelium-like" cell lines; and (c) the uptake of several other cations, for example, 45Ca++ and 36Rb++, was not significantly enhanced by the steroid hormone, and a number of monovalent and divalent cations did not compete with 65Zn++. Certain effects of hydrocortisone on cells may be explained by an increase in the Zn++ content of cells.
ACKNOWLEDGMENTS This investigation was supported by Research Grant GM 15508 from the United States Public Health Service and Research Contract U-1296 with the Health Research Council of the City of New York. I wish to acknowledge the valuable technical assistance of Dr. Adriana Ruckenstein and Mrs. Maude Levy. I thank Drs. P. Elsbach, E. Simon, D. Schacter, M. J. Griffin, and J. King for their discussion and advice.
- Copyright ©, 1968, by Academic Press Inc.
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