Abstract
Cadmium, an environmental pollutant, caused nephroptosis that was inhibitable by zinc. The mechanism of the antiapoptotic action of zinc is poorly understood. In this study, we found the stimulation of DNA synthesis, as assessed by bromodeoxyuridine incorporation, during prevention by zinc of apoptosis, suggesting that the proliferactive nature of zinc contributes to its inhibition of apoptosis. This finding was consistent with the result that the cells driven by dialyzed fetal bovine serum were resistant to apoptotic stimuli of cadmium. Furthermore, zinc activated the expression of endogenous Bcl-2 proteins. However, overexpression of Bcl-2 proteins by transfection did not facilitate zinc-mediated DNA synthesis. Thus, one possible role of zinc in the prevention of apoptosis is to promote DNA synthesis independently with activation of antiapoptotic proteins Bcl-2.
Footnotes
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Send reprint requests to: Dr. Masami Ishido, Regional Environment Division, National Institute for Environmental Studies, 16-2 Onogawa, Tsukuba, 305-0053. E-mail: ishidou{at}nies.go.jp
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↵1 This work was supported in part by research grants from the Ministry of Education, Science, and Culture of Japan and from Sumitomo Foundation.
- Abbreviations:
- FBS
- fetal bovine serum
- TUNEL
- terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling
- ELISA
- enzyme-linked immunosorbent assay
- BrdU
- bromodeoxyuridine
- IGF-1
- insulin-like growth factor-1
- PI3-kinase
- phosphoinositide 3-kinase
- Received January 21, 1999.
- Accepted April 9, 1999.
- The American Society for Pharmacology and Experimental Therapeutics
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