Native LDL (n-LDL), oxidized LDL (ox-LDL) and small dense LDL are involved in the endothelial dysfunction and may affect the endothelial-dependent vascular tone interacting with the L-arginine-nitric oxide (NO) pathway. HDL are known to play a protective role in atherogenesis. This study wanted to evaluate in endothelial cells the effect of LDL subtypes on NO and superoxide (O (2-)) production. Furthermore, we investigated if HDL could avoid the NO depletion and O (2-) increment observed during exposure to lipoproteins. Pre-treating the endothelial cells with increasing concentrations of n-LDL, ox-LDL and small dense LDL we established the lipoprotein concentrations that could identifie the L-arginine-NO function. Furthermore, cells were exposed to increasing concentrations of HDL without any change in NO levels. In n-LDL and ox-LDL treated cells, HDL increased NO production. HDL and L-arginine supplementation decreased O (2-) to almost 50 % of the level in n-LDL-treated cells. In ox-LDL-treated cells L-arginine completely blunted O (2-). In conclusion, HDL may play an anti-atherogenic role by improving NO release and decreasing O (2-) production in well functioning endothelial cells. L-arginine improves the NO pathway more than HDL in cells exposed to oxidative damage. The relationship between L-arginine-NO pathway and the lipoprotein composition and oxidation may be a crucial determinant for the initiation and progression of the early endothelial dysfunction.
Effect of different lipoprotein fractions on nitric oxide and superoxide production in endothelial cells
PASSARO, Angelina;FELLIN, Renato
1998
Abstract
Native LDL (n-LDL), oxidized LDL (ox-LDL) and small dense LDL are involved in the endothelial dysfunction and may affect the endothelial-dependent vascular tone interacting with the L-arginine-nitric oxide (NO) pathway. HDL are known to play a protective role in atherogenesis. This study wanted to evaluate in endothelial cells the effect of LDL subtypes on NO and superoxide (O (2-)) production. Furthermore, we investigated if HDL could avoid the NO depletion and O (2-) increment observed during exposure to lipoproteins. Pre-treating the endothelial cells with increasing concentrations of n-LDL, ox-LDL and small dense LDL we established the lipoprotein concentrations that could identifie the L-arginine-NO function. Furthermore, cells were exposed to increasing concentrations of HDL without any change in NO levels. In n-LDL and ox-LDL treated cells, HDL increased NO production. HDL and L-arginine supplementation decreased O (2-) to almost 50 % of the level in n-LDL-treated cells. In ox-LDL-treated cells L-arginine completely blunted O (2-). In conclusion, HDL may play an anti-atherogenic role by improving NO release and decreasing O (2-) production in well functioning endothelial cells. L-arginine improves the NO pathway more than HDL in cells exposed to oxidative damage. The relationship between L-arginine-NO pathway and the lipoprotein composition and oxidation may be a crucial determinant for the initiation and progression of the early endothelial dysfunction.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
