SUPPLEMENTATION WITH BETA-CAROTENE IN-VIVO AND IN-VITRO DOES NOT INHIBIT LOW-DENSITY-LIPOPROTEIN OXIDATION

The inhibition of low density lipoprotein (LDL) oxidation has been pos tulated as one mechanism by which antioxidants may prevent the develop ment of atherosclerosis. Available data on the ability of beta-caroten e to inhibit LDL oxidation are conflicting, We examined the role of in vivo and in vitro supplementation with beta-carotene on metal ion-dep endent (cupric ions, Cu2+) and metal ion-independent (2,2'-azobis[2-am idinopropane]dihydrochloride, AAPH) oxidation of LDL as measured by th e formation of conjugated dienes (absorbance at 234 nm), Sixteen subje cts were supplemented with 50-100 mg of beta-carotene on alternate day s 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 ro se 8.5-fold. Oxidation of LDL by Cu2+ or AAPH was not significantly de layed after in vivo supplementation with beta-carotene compared with b aseline, For AAPH, the lag phase (in minutes) was 75 +/- 8 at baseline and 83 +/- 14 after supplementation (P = 0.07), For CU2+, the lag pha se was 172 +/- 41 at baseline and decreased to 130 +/- 24 after supple mentation (P < 0.01). Similarly, no protective effect against Cu2+-ind uced oxidation was observed when beta-carotene was added to LDL in vit ro. Supplementation of plasma with beta-carotene in vitro prior to LDL isolation also did not enhance LDL's resistance to CU2+- or AAPH-indu ced oxidation, despite a 5-fold increase in LDL beta-carotene levers o ver vehicle control. These data indicate that supplementation with bet a-carotene in vivo or in vitro does not enhance the protection of LDL against metal ion-dependent and -independent oxidation; rather, in viv o beta-carotene supplementation may lead to a shortening of the lag ph ase of Cu2+-induced lipid peroxidation in LDL.