Supplementation with β-carotene in vivo and in vitro does not inhibit low density lipoprotein oxidation Original Research Article

The inhibition of low density lipoprotein (LDL) oxidation has been postulated as one mechanism by which antioxidants may prevent the development of atherosclerosis. Available data on the ability of β-carotene to inhibit LDL oxidation are conflicting. We examined the role of in vivo and in vitro supplementation with β-carotene on metal ion-dependent (cupric ions, Cu2+) and metal ion-independent (2,2′-azobis[2-amidinopropane]dihydrochloride, AAPH) oxidation of LDL as measured by the formation of conjugated dienes (absorbance at 234 nm). Sixteen subjects were supplemented with 50–100 mg of β-carotene on alternate days for 3 weeks following a week-long loading dose of 100 mg/day. Plasma β-carotene levels rose 5.5-fold, while LDL β-carotene levels rose 8.5-fold. Oxidation of LDL by Cu2+ or AAPH was not significantly delayed after in vivo supplementation with β-carotene compared with baseline. For AAPH, the lag phase (in minutes) was 75 ± 8 at baseline and 83 ± 14 after supplementation (P = 0.07). For Cu2+, the lag phase was 172 ± 41 at baseline and decreased to 130 ± 24 after supplementation (P < 0.01). Similarly, no protective effect against Cu2+-induced oxidation was observed when β-carotene was added to LDL in vitro. Supplementation of plasma with β-carotene in vitro prior to LDL isolation also did not enhance LDLʹs resistance to Cu2+- or AAPH-induced oxidation, despite a 5-fold increase in LDL β-carotene levels over vehicle control. These data indicate that supplementation with β-carotene in vivo or in vitro does not enhance the protection of LDL against metal ion-dependent and -independent oxidation; rather, in vivo β-carotene supplementation may lead to a shortening of the lag phase of Cu2+-induced lipid peroxidation in LDL.