Abstract: Object: To investigate the effects of different zinc sources and levels of addifion on apoptosis and their mechanism. Method: Dexamethasone was used to make the apoptosis model of thymocytes. Zinc sulfate and zinc methionine were added to the medium with the levels of 0, 50, 100, 500, 1000μmol/L. The activity AKP, Cu, Zn-SOD and intracellular calcium concentration and the percentage of apoptosis nuclei were determined. Result: Both ZnSO4 and Zn-Met could modulate apoptosis. They inhibited apoptosis and decreased DNA ladder formation; and the modulation would rely on the dose of zinc. Supple- mented with 50, 100μmol/L zinc, the ability of Zn-Met inhibiting apoptosis was less efficiency than ZnSO4 (p<0.05), and of no difference to modulate apoptosis when being added with 500 or 1000μmol/L to the medium (p>0.05). Intracellular calcium concentrations of cells cultured with Zn-Met were higher than those cultured with ZnSO4 of the same level. Zinc supplementation decreased the concentration of intracellular calcium significantly (p<0.05), but increased the activity of Cu, Zn-SOD (p<0. 05) in the extract of the cells, and AKP in the supernatant of the culture fluids (p>0.05). Conclusion: Both forms of zinc could modulate apoptosis of thymocytes induced by glucocorticoid. The mechanism might involve the exchange of intracellular calcium and the redox of cells.

Key words:  zinc sulfate, zinc methionine, apoptosis, dexamethasone, thymocytes