Supplementation with vitamin E but not beta-carotene in vivo protects low density lipoprotein from lipid peroxidation in vitro. Effect of cigarette smoking.

Abstract

Several lines of evidence suggest that oxidatively modified low density lipoprotein (LDL) is atherogenic and that antioxidants may protect LDL against oxidation. In addition, cigarette smoking is known to induce oxidant stress. We have examined the effect of ingestion of the antioxidants D,L-ar-tocopherol (vitamin E) and 0-carotene and of smoking on the resistance of LDL against copper-mediated oxidation. Six healthy nonsmoking volunteers ingested 1,000 IU/day D,L-a-tocopherol acetate for 7 days. After vitamin E ingestion concentrations of or-tocopherol in plasma and LDL increased 3.0-and 2.4-fold, respectively. Simultaneously, the oxidation resistance of LDL was elevated significantly (+41%), and the rate of oxidation was decreased significantly (-19%). The increase in o-tocopherol content of LDL and the increase in resistance time were highly correlated (r,=0.89, p=0.014). Eight weeks after termination of the vitamin E intake, o-tocopherol concentrations in plasma and LDL and oxidation resistance of LDL had returned to baseline values. In smokers (n=46), plasma levels of vitamin C (-26%) and concentrations of 0-carotene (-44%, -43%) and total carotenoids (-23%, -29%) in plasma and LDL, respectively, were significantly lower compared with nonsmokers (n=23). No differences were found in o-tocopherol content of LDL and the susceptibility of LDL to lipid peroxidation in both groups. Supplementation of a group of smokers in a 14-week randomized, double-blind, placebo-controlled intervention trial witĥ -carotene resulted in a 16.6-and 5.0-fold increase of LDL /^-carotene and total carotenoid content, respectively. Similar increases were found in plasma without changes in other vitamins. Comparison of the changes in the length of the resistance time between the /J-carotene group (R=23) and the placebo group (n=23) showed no significant differences. We conclude that Ingestion of vitamin E strongly protects LDL against oxidative modification, whereas ^-carotene is not effective, and that smoking does not alter the oxidation resistance of LDL. (Arteriosclerosis and Thrombosis 1992;12:554-562) KEY WORDS • low density lipoprotein oxidation • vitamin E • /3-carotene • cigarette smoking E levated plasma levels of low density lipoprotein (LDL) are associated with an accelerated development of atherosclerotic lesions, which is one of the main causes of coronary artery disease.

Enhanced plasma level of lipid peroxidation in Iranians could be improved by antioxidants supplementation

“…However, we cannot exclude the possibility that carotenoids can moderately in¯uence the lag-time, as there was a signi®cant correlation between all carotenoids and lag-time after supplementation with b-carotene (r 2 0.714, P`0.017; Figure 2). Princen et al, 1992, have reported that any increase in LDL lag-time was observed, despite the massive increase in LDL b-carotene after supplementation. However, these healthy subjects also had a high basal lag-time (100 min) as was shown in this study.…”

“…Supplementation with a-tocopherol conferred the increased protection of LDL against in vitro oxidation (Jialal et al, 1995;Reaven et al, 1993). The supplementation with bcarotene did not reveal a substantial improved oxidation resistance after the supplementation (Reaven et al, 1993;Princen et al, 1992). However, in disease states associated with low resistance of LDL to oxidation such as cystic ®brosis, the supplementation with b-carotene resulted in a decrease in oxidation products (MDA) and an increased protection of LDL against in vitro oxidation (Winklhofer- Roob et al, 1995).…”

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

“…Smoking enhances oxidation for example by reducing antioxidant capacity (Dietrich et al, 2003). There are also studies, where a significant association between smoking and decreased lag phase of LDL oxidation was not found (Princen et al, 1992;Marangon et al, 1997).…”

“…Ex vivo measures of LDL resistance to oxidation have shown significant increases even at low doses of alpha-tocopherol (43-200 mg/day) (Princen et al, 1995;Maskarinec et al, 1999;Upritchard et al, 2003). Antioxidant supplementation or increased consumption of fruit and vegetables has been reported to reduce the susceptibility of LDL to oxidation also in smokers (Princen et al, 1992;Roberts et al, 2003). In fact, beneficial effects of vitamin E supplementation on atherosclerosis may be the most relevant to persons with initially low serum levels of vitamin E. In this study, the lag phase of LDL oxidation prolonged significantly in both the study groups, smokers and nonsmokers after 8 weeks supplementation of vitamin E. Moreover, the effect of vitamin E was greater in smokers than in nonsmokers, which has also been reported by Salonen et al (2003).…”

“…Smoking-derived free radicals promote peroxidation of lipids and proteins (Frei et al, 1991). Several studies have explored the relation between smoking and LDL oxidation (Harats et al, 1989;Princen et al, 1992;Marangon et al, 1997;Gouazé et al, 1998), but the results are conflicting.…”