Dual effect of antimitotic drugs on steroid secretion in mouse adrenocortical Y-1 tumor cells.
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- Kotani Susumu
- Faculty of Computer Science and Systems Engineering, Kyushu Institute of Technology
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- Murofushi Hiromu
- Department of Biophysics and Biochemistry, Faculty of Science, University
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- Sakai Hikoichi
- Department of Biophysics and Biochemistry, Faculty of Science, University
抄録
Mouse adrenocortical Y-1 tumor cells were examined in a monolayer culture and their steroid secretion was measured. The Y-1 cells constantly released a small amount of steroids in the absence of adrenocor-ticotropin (ACTH). When synthetic ACTH (tetracosactide acetate) was added to the medium, an increase in the steroid secretion of approximately 5-fold was observed. The Y-1 cells also showed a typical cytoplasmic retraction in response to ACTH. Incubation of the cells with an antimitotic drug, colchicine, prior to ACTH-stimulation resulted in a 30-50% reduction in ACTH-induced steroid secretion. Under the conditions used in these experiments, viable numbers of cell and of total amount of protein per dish were not measurably changed, indicating that the condition was not lethal. Another antimitotic drug, colcemid, caused similar reactions, while lumicolchicine showed no effect. This suggests that the disruption of the microtubular system is the main cause of the inhibition. On the other hand, the ACTH-independent secretion was slightly enhanced by colchicine. The enhancement was also observed in prolonged incubation with colchicine, a condition which caused death in some of the cells.
収録刊行物
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- Cell Structure and Function
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Cell Structure and Function 13 (2), 171-177, 1988
日本細胞生物学会