The effect of endogenous formaldehyde on the rat aorta endothelial cells

Abstract

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 (H 2O 2), or formaldehyde with equal molar concentration of H 2O 2, 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 0.01–2 mM FA, H 2O 2, or FA with equal molar concentration of H 2O 2. Time-dependent increases in DPC formation were also observed at 0.5–4 h time point after treatment of RAECs with 0.05 and 0.1 mM FA, or 0.1 mM FA with H 2O 2. The DPC levels reduced after treatment with FA and equal molar concentration of H 2O 2, compared with treatment with FA alone. FA may be less cytotoxic, as FA alone did not affect the cell viability even treating for 4 h, until the treatment concentration reached 2 mM. However, H 2O 2, and FA with H 2O 2 induced significant decreases of cell viability. These studies suggest that FA and H 2O 2 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.