Glucocorticoid regulation of amino acid transport in anucleate rat hepatoma (HTC) cells.

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Abstract
The transport of .alpha.-aminoisobutyric acid (AIB) by rat hepatoma tissue culture (HTC) cells is rapidly and reversibly inhibited by dexamethasone and other glucocorticoids. To investigate the role of the nucleus in the regulation of transport and to determine whether steroid hormones or steroid-receptor complexes may have direct effects on cytoplasmic or membrane functions, the regulation of transport by dexamethasone was examined in anucleate HTC cells. Cytoplasts prepared from suspension cultures of HTC cells fully retain active transport of AIB with the same kinetic properties as intact cells. The uptake of AIB is not inhibited by dexamethasone or other corticosteroids. The inhibited rate of transport, manifested by cytoplasts prepared from dexamethasone-treated cells, is not restored to normal upon removal of the hormone. Anucleate cells exhibit specific, saturable binding of [3H]dexamethasone; the binding is reduced compared with that of intact cells. The nucleus is thus required for the glucocorticoid regulation of amino acid transport in HTC cells.