Ca-ATPase Activity of Human Red Cell Ghosts: Preeclampsia, Lipid Peroxidation and MgSO₄

Abstract

The increased level of lipid peroxidation of red blood cells during preclampsia is considered to be responsible for the diminished Ca-ATPase activity in these cells. The level of lipid peroxidation and the Ca-ATPase activity of red blood cells from preeclamptic women, return to their normal values after in vivo and in vitro treatment with MgSO₄ for 24 h. In order to evaluate whether or not cell intactness is essential for these changes, we used either intact red blood cells or red cell ghosts from normotensive pregnant women. The intact red blood cells were treated with Fenton's reagent and then incubated with 4 mM MgSO₄. The red cells ghosts were irradiated with UV light and afterwards incubated with MgSO₄ at 4°C. Lipid peroxidation and Ca-ATPase activity were determined for all the preparations. Both, Fenton's reagent and UV irradiation increased the level of lipid peroxidation and diminished the Ca-ATPase activity of the red cell membranes. Incubation of the cells treated with Fenton's reagent, or the ghosts irradiated with UV, with 4 mM MgSO₄, returned Ca-ATPase activity and lipid peroxidation levels to normal values. The presence of MgSO4 blocked the effects in the ghosts of UV irradiation. MgSO₄ seems to better protect the red cell membrane against lipid peroxidation than other SO₄⁼ and Cl⁻ salts. These results indicate that the changes in the lipid peroxidation of the red cell ghosts and their Ca-ATPase activity are a result of changes to the cell membranes.

ACKNOWLEDGMENTS

Purified bovine brain calmodulin was generously supplied by Dr. Gustavo Benaim from the Universidad Central de Venezuela. We thank Dr. Matthew Turvey (University of Birmingham) for his valuable corrections. This research was supported in part by grant No. H9/181/R427, Project 96350, from the World Health Organization and by grant from FONACIT-Venezuela No. F-2005000222.

Declaration of Interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.