Section 10
Chapter 9,492

Supplementation with beta-carotene in vivo and in vitro does not inhibit low density lipoprotein oxidation

Gaziano, J.M.; Hatta, A.; Flynn, M.; Johnson, E.J.; Krinsky, N.I.; Ridker, P.M.; Hennekens, C.H.; Frei, B.

Atherosclerosis 112(2): 187-195


ISSN/ISBN: 0021-9150
PMID: 7772078
Accession: 009491214

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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 beta-carotene to inhibit LDL oxidation are conflicting. We examined the role of in vivo and in vitro supplementation with beta-carotene on metal ion-dependent (cupric ions, CU-2+) 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 beta-carotene on alternate days for 3 weeks following a week-long loading dose of 100 mg/day. Plasma beta-carotene levels rose 5.5-fold, while LDL beta-carotene levels rose 8.5-fold. Oxidation of LDL by CU-2+ or AAPH was not significantly delayed after in vivo supplementation with beta-carotene compared with base- line. For AAPH, the lag phase (in minutes) was 75 +- 8 at baseline and 83 +- 14 after supplementation (P = 0.07). For CU-2+, the lag phase was 172 +- 41 at baseline and decreased to 130 +- 24 after supplementation (P lt 0.01). Similarly, no protective effect against Cu-2+-induced oxidation was observed when beta-carotene was added to LDL in vitro. Supplementation of plasma with beta-carotene in vitro prior to LDL isolation also did not enhance LDL's resistance to Cu-2+ or AAPH-induced oxidation, despite a 5-fold increase in LDL beta-carotene levels over vehicle control. These data indicate that supplementation with beta-carotene in vivo or in vitro does not enhance the protection of LDL against metal ion-dependent and -independent oxidation; rather, in vivo beta-carotene supplementation may lead to a shortening of the lag phase of Cu-2+-induced lipid peroxidation in LDL.

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