Effects of vitamin E on the toxicity of oxidized LDL on endothelial cells in vitro in smokers vs nonsmokers on diets rich in fish

Abstract

Objective: To clarify whether supplementation of vitamin E can alter the low density lipoprotein (LDL) oxidation properties and thereby affect endothelial cell function and prostacyclin production in smokers compared to nonsmokers on diets rich in fish in a pilot study. Design: The LDL of six smokers and six nonsmokers on habitual high fish diet was isolated before and after an 8-week supplementation of vitamin E (800 IU/day). LDL was oxidized by incubation with CuSO 4 . Cytotoxicity of LDL oxidized to different degrees on endothelial cells was investigated in vitro in these two groups. Setting: Helsinki University Central Hospital; Institute of Biomedicine, Pharmacology, University of Helsinki. Results: At baseline, the rate of oxidation was higher in nonsmokers than in smokers. The lag phase increased significantly after the supplementation of vitamin E both in smokers and nonsmokers. Native LDL dose dependently tended to reduce the viability of endothelial cells in vitro more markedly when isolated from smokers than from nonsmokers. Vitamin E supplementation had no beneficial effect on the cytotoxicity of oxidized LDLs in endothelial cell culture. On the other hand, simultaneous administration of Trolox s , the water-soluble analogue of vitamin E, attenuated the LDL cytotoxicity on endothelial cells. The vitamin E supplementation to LDL donors attenuated the increase in prostacyclin production both in smokers and nonsmokers. Conclusion: Supplementation of LDL donors (healthy male volunteers on habitual fish diet) with vitamin E increased the lag phase of LDL oxidation, but, on the other hand, did not influence in vitro cytotoxicity of LDL, or prostacyclin production.

Thiosemicarbazone derivate protects from AAPH and Cu2+-induced LDL oxidation

“…The increase in the lag phase for copper-induced LDL oxidation by antioxidants has already been described (Wen et al, 1999). Vitamin E, an endogenous antioxidant, is known to prevent LDL oxidation by donating the hydrogen atom of its phenolic hydroxyl group to a lipid peroxyl radical (Meydani, 1995;Seppo et al, 2005). Vigna et al (2003) showed that the increase in the lag phase and the reduction of the lipid peroxide formation are probably related to antioxidant properties or to mechanisms involving ion (Cu 2+ ) chelation.…”

Reduction of the Nailfold Capillary Blood Velocity in Cigarette Smokers

“…This might implicate oxLDL as a marker of acute vascular damage in smokers. Some previous intervention studies showed inconstancy in the changes of oxLDL and ICAM-1 in smokers,24,25) while more recently smoking intensity was reported to be associated with increased white blood cell count, but not C-reactive protein (CRP) levels, and smoking cessation did not reduce CRP. The relationship between CRP and smoking intensity might be masked by CRP's stronger relationship with adiposity 26)…”

How Safe is Vitamin E Supplementation?

“…Vitamin E works as an antioxidant, which prevents lowdensity lipoprotein-cholesterol (LDL-cholesterol) oxidation and subsequent damage to cell membranes, including the membranes of endothelial cells that line the blood vessels (Seppo, 2005). The vitamin works by donating a hydrogen atom from its phenolic hydroxyl group to a lipid peroxyl radical resulting in its conversion to a vitamin E radical.…”