Positive Health Online

Abstract

WITENBERG and colleagues, Department of Cell Biology and Histology, Sackler School of Medicine, Tel Aviv University, Israel studied the effect of ascorbic acid (vitamin C) loading upon apopto sis in the human myeloid leukaemia cell line HL-60 .

Background

Methodology

The human myeloid leukaemia cell line HL-60 transports the oxidised form of ascorbic acid, dehydroascorbic acid (DHA) and accumulates reduced ascorbic acid. The authors studied the effect of ascorbic acid loading on apoptosis induced by serum- and glucose-free culture and by oxidative stress induced by hydrogen peroxide (H2O2).

Results

Studies of uptake accumulation indicated that incubation of HL-60 cells with DHA resulted in the accumulation of intracellular ascorbic acid, which decreased when cells were incubated in DHA-free medium. Exposure of HL-60 cells to increasing concentrations of H2O2 resulted in dose-dependent intracellular accumulation of peroxides, accompanied by a decrease in intracellular ascorbic acid and an increase in apoptosis. There was a dramatic decrease in intracellular ascorbic acid when preloaded HL-60 cells were exposed to 150 microM H2O2; a dose-dependent protective effect of DHA was observed. Ascorbic acid loading also provided strong protection from apoptosis associated with serum- and glucose-free culture. Exposure of HL-60 cells to 150 microM H2O2 resulted in decreased Bcl-2 expression associated with enhance apoptosis. There was no significant variation of Bcl-2 expression following exposure of Hl-60 cells, loaded with ascorbic acid, to 150 microM H2O2, and only a slight increase in apoptosis.

Conclusion

These results demonstrate that ascorbic acid can inhibit apoptosis induced by oxidative stress in HL-60 cells .

References

Witenberg B et al. Inhibition by ascorbic acid of apoptosis induced by oxidative stress in HL-60 myeloid leukemia cells. Biochem Pharmacol 57(7): 823-32. Apr 1 1999.