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Ishido, M. et al.

Ishido, Suzuki, Adachi, Kunimoto,

Zinc stimulates DNA synthesis during its antiapoptotic action independently with increments of an antiapoptotic protein, Bcl-2, in porcine kidney LLC-PK(1) cells.

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.[1]

References

Zinc stimulates DNA synthesis during its antiapoptotic action independently with increments of an antiapoptotic protein, Bcl-2, in porcine kidney LLC-PK(1) cells. Ishido, M., Suzuki, T., Adachi, T., Kunimoto, M. J. Pharmacol. Exp. Ther. (1999) [Pubmed]

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