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Eur J Nutr. 2002 Feb;41(1):27-34.

Vitamin C and vitamin E antagonistically modulate human vascular endothelial and smooth muscle cell DNA synthesis and proliferation.

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Medizinische Poliklinik, University of Bonn, Germany.



Vitamin C and E are suggested to play a preventive role in the pathogenesis of atherosclerosis. They reduce oxidation of low density lipoproteins (oxLDL), thereby protecting human vascular arterial endothelial and smooth muscle cells from oxLDL induced damages.


Since vascular arterial endothelial and smooth muscle cells are both involved in atherosclerotic plaque formation, we simultaneously examined the effect of vitamin C, E and oxLDL on their DNA synthesis and proliferation to further elucidate their joint role in this process.


Human umbilical arterial endothelial cells (HUAEC) and human arterial smooth muscle cells (HUASMC) were incubated with "preventive concentrations" of vitamin C (60 microM) and E (30 microM) and with LDL (60 microg/ml) of increasing oxidation grade. Cell proliferation and DNA synthesis were determined by cell count and [3H]-thymidine uptake, respectively.


Vitamin C alone or in combination with E increased significantly cell number and [3H]-thymidine uptake in HUAEC. The combination exhibited the strongest effect. In contrast, cell number and [3H]-thymidine uptake in HUASMC were significantly decreased in the presence of vitamin C, vitamin E or its combination. OxLDL (60 microg/ml) inhibited cell number and [3H]-thymidine uptake in HUAECs, the latter in an oxidation-grade dependent manner. In HUASMC oxLDL promoted a higher cell number and [3H]-thymidine uptake. If induced by minimally oxLDL, this reduction or increase could be partially reversed by vitamin C alone or in combination with vitamin E.


Vitamin C and E, alone or in combination, modulate proliferation and DNA synthesis of human arterial endothelial and muscle cells and this modulation is antagonistic. Thus, vitamin C and E may act "preventive" on atherosclerotic plaque formation in two steps: first reendothelialisation is promoted, then HUASMC growth is inhibited.

[Indexed for MEDLINE]

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