Citrus fruit supplementation reduces lipoprotein oxidation in young men ingesting a diet high in saturated fat: presumptive evidence for an interaction between vitamins C and E in vivo

Abstract

To determine the effects of vitamin C on cardiovascular risk factors, we studied dietary vitamin C enrichment in 36 healthy male students consuming a diet high in saturated fatty acids. After a 1-mo run-in period during which the subjects consumed approximately 50 mg ascorbic acid/d (low-C diet), half of the subjects were randomly assigned to receive 500 mg ascorbic acid/d for an additional 2 mo (high-C diet). Plasma ascorbic acid increased from 13.5 micromol/L with the low-C diet to 51.7 micromol/L with the high-C diet. Plasma cholesterol increased slightly with the high-C diet, but not above baseline concentrations. This increase was offset by an increase in the lag period of in vitro LDL oxidation, which correlated with plasma ascorbic acid concentrations (r = 0.735, P = 0.0012). Lipoprotein vitamin E concentrations were unchanged with the two diets. There were no effects on concentrations of fibrinogen or factor VII. The fact that ascorbic acid reduced the in vitro susceptibility of lipoproteins to oxidation provides presumptive evidence for an interaction between aqueous and lipophilic antioxidants (vitamins C and E ) in maintaining the integrity of LDL particles.

Does vitamin C supplementation influence the levels of circulating oxidized LDL, sICAM-1, sVCAM-1 and vWF-antigen in healthy male smokers?

“…In our study, the increase in mean plasma ascorbate was similar to the study of Harats et al (1990). The stronger increase in the other studies (Fuller et al, 1996;Harats et al, 1998) may partly be due to a low vitamin C diet and related low plasma ascorbate concentrations. Indeed, the baseline plasma ascorbate concentration in the present study (45720 mmol/l) was higher than that in the above-mentioned studies.…”

“…Further, the bioavailability was found to be incomplete for doses over 200 mg of vitamin C (Levine et al, 1996). The previous studies in healthy smokers on LDL susceptibility for oxidation applied daily doses of 500 mg (Harats et al, 1998), 1000 mg (Harats et al, 1990;Fuller et al, 1996) and 1500 mg (Harats et al, 1990) vitamin C, which resulted in 2.0-2.3-fold (Harats et al, 1990), 3.8-fold (Harats et al, 1998) to 3.9-fold (Fuller et al, 1996) increase in plasma ascorbate levels. In our study, the increase in mean plasma ascorbate was similar to the study of Harats et al (1990).…”

“…A number of 4-week supplementation studies in healthy smokers have indicated that vitamin C effectively reduced the in vitro susceptibility of LDL for oxidation (Fuller et al, 1996;Harats et al, 1998) and the concentration of plasma lipid peroxidation products such as conjugated dienes and TBARS (Harats et al, 1990(Harats et al, , 1998Fuller et al, 1996). A possible mechanism explaining why vitamin C might reduce the oxidative modification of LDL is by scavenging aqueous free radicals before they can attack and oxidize LDL.…”

“…Vitamin C supplementation (500-2000 mg per day) has been shown to reduce the in vitro LDL oxidation susceptibility and plasma lipid peroxidation products thiobarbituric acid-reactive substrates (TBARS) (Harats et al, 1990(Harats et al, , 1998Fuller et al, 1996). In addition, trials in which an infusion of 10-18 mg vitamin C/min (or total dose about 1000 mg) was given to chronic smokers provided promising results for improved endothelial-dependent vasodilation (Heitzer et al, 1996;Motoyama et al, 1997).…”

Antioxidants and lipoprotein metabolism

“…Diets rich in fruits and vegetables have been shown to increase the resistance of LDL to oxidation (Abbey et al 1995;Harats et al 1998). Recently, we have shown that increased consumption of a carotenoid-rich (i.e.…”