The effect of endogenous formaldehyde on the rat aorta endothelial cells

Previous studies have demonstrated endogenous formaldehyde (FA) may be involved in endothelial damage, and may be a potential factor of vulnerability of atherosclerosis. However, the mechanism has not been characterized. The present studies examined DNA-protein cross-links (DPC) formation in rat aorta endothelial cells (RAECs) treated with formaldehyde, hydrogen peroxide (H2O2), or formaldehyde with equal molar concentration of H2O2, which is produced with formaldehyde in the body at the same time. Using a K+/SDS precipitation assay for DPC determination, concentration-dependent increases in DPC formation were observed 1.5 h after treatment of RAECs with 0.01-2mM FA, H2O2, or FA with equal molar concentration of H2O2. Time-dependent increases in DPC formation were also observed at 0.5-4 h time point after treatment of RAECs with 0.05 and 0.1mM FA, or 0.1mM FA with H2O2. The DPC levels reduced after treatment with FA and equal molar concentration of H2O2, compared with treatment with FA alone. FA may be less cytotoxic, as FA alone did not affect the cell viability even treating for 4h, until the treatment concentration reached 2mM. However, H2O2, and FA with H2O2 induced significant decreases of cell viability. These studies suggest that FA and H2O2 may injure endothelial cells synergistically, and low concentration of FA (0.05-0.1) may contribute to the endothelial injury in the body during aging.