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Kraker AJ, Petering DH. Tumor-host zinc metabolism the central role of metallothionein. Biol Trace Elem Res. 1983;5(4):363-74doi: 10.1007/BF02987220.
Kraker, A. J., & Petering, D. H. (1983). Tumor-host zinc metabolism the central role of metallothionein. Biological trace element research, 5(4), 363-74. https://doi.org/10.1007/BF02987220
Kraker, A J, and Petering, D H. "Tumor-host zinc metabolism the central role of metallothionein." Biological trace element research vol. 5,4 (1983): 363-74. doi: https://doi.org/10.1007/BF02987220
Kraker AJ, Petering DH. Tumor-host zinc metabolism the central role of metallothionein. Biol Trace Elem Res. 1983 Aug;5(4):363-74. doi: 10.1007/BF02987220. PMID: 24263573.
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Biol Trace Elem Res. 1983 Aug;5(4):363-74. doi: 10.1007/BF02987220.

Tumor-host zinc metabolism the central role of metallothionein.

Biological trace element research

A J Kraker, D H Petering

Affiliations

  1. Department of Chemistry, University of Wisconsin-Milwaukee, 53201, Milwaukee, Wisconsin.

PMID: 24263573 DOI: 10.1007/BF02987220

Abstract

Features of tumor and host zinc metabolism are described. Emphasis is placed on tumor-host interactions. Using the model of the Ehrlich ascites tumor in mice, one clear site of modulation of cellular zinc by the amount of nutrient zinc available in the host is a zinc-binding protein with the properties of metallothionein. The selective depletion of zinc from this protein is correlated with the loss of cell proliferation by tumors injected into zinc-deficient animals. The properties of isolated metallothionein are consistent with a role for it as a reactive pool of intracellular zinc which can be donated to apozinc proteins and other structures. The presence of the Ehrlich tumor in mice also perturbs their distribution of zinc: zinc leaves the plasma and is accumulated by liver in the form of newly synthesized zinc metallothionein. During host zinc deficiency, this redistribution is not observed. This may be caused not only by a lack of mobile plasma zinc, but also by an inhibition of the initiation of this host response at the site of the tumor in the peritoneum.

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