Control of Ehrlich cell division by zinc |
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Authors: | David H Petering Leon A Saryan |
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Institution: | (1) Department of Chemistry, University of Wisconsin-Milwaukee, 53201 Milwaukee, Wisconsin |
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Abstract: | The nutritional requirement for zinc in the proliferation of normal and malignant cells has been demonstrated in a number
of animal studies. A distinction is made between the effect of zinc status upon the host during carcinogenesis and tumor growth.
The present studies focus on the Ehrlich ascites tumor in mice fed a semipurified zinc-deficient diet along with defined concentration
of zinc in the drinking water. This model of zinc deficiency is compared with others in which chelating agents are used to
create zinc-deficient conditions or the microorganismEuglena gracilis is examined in a defined zinc-deficient medium. It is reported here that Ehrlich cells remain quiescent for several weeks
in severely deficient mice, suggesting their restriction to a G1 or G0 state of the cell cycle. The kinetics of thymidine and uridine uptake and incorporation into DNA and RNA in Zn-normal and
Zn-deficient tumors is consistent with the inhibition of thymidine kinase and DNA polymerase in the Zn-deprived system, but
with little effect on RNA synthesis. The concentration of metabolites of these labeled nucleosides in Ehrlich cells is also
consistent with a primary effect upon thymidine kinase. Although the ascites fluid Zn is depressed in Zn deficiency, total
cellular zinc and its distribution among cell fractions is not significantly affected. It is suggested that these effects
are specific in nature and not the result of a general lack of zinc for zinc metalloproteins and other binding sites in the
cell. |
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Keywords: | Zinc cell division control by DNA synthesis control by zinc RNA synthesis control by zinc Ehrlich cells zinc control of cell division |
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