Summary:The synthetic all-trans isomer of ß-carotene was recently shown to possess antioxidant properties towards the formation of oxidized low density lipoprotein.| In the present study, the binding of the all-trans and the 9-cis isomers of ß-carotene to plasma lipoproteins was investigated, and the effect of these isomers on the susceptibility of plasma lipoprotein to lipid peroxidation and on macrophage uptake of oxidized LDL were studied. Both the synthetic all-trans isomer of ß-carotene and the natural ß-carotene from the algae Dunaliella Bardawil [which is composed of the all-trans (70%) and 1 the 9-cis (30%) isomers], were found to bind similarly to all plasma lipoproteins, following the incubation of ß-carotene with purified lipoproteins or with whole plasma.Incubation of the ß-carotene isomers with whole plasma, followed by separation of the lipoproteins, revealed substantial carotene binding to very low density lipoprotein (VLDL) and to LDL and limited binding to high density lipoprotein (HDL). Lipid peroxidation of VLDL and LDL were significantly inhibited by ß-carotene.The synthetic ß-carotene, however, was twice as effective as the Dunaliella ß-carotene in inhibiting LDL lipid | peroxidation (following LDL incubation with copper ions). Cellular degradation of oxidized lipoproteins | (mediated via the scavenger receptor) was decreased by 40% and 18%, respectively, when they were prepared by incubation in the presence of synthetic or natural ß-carotene; the control oxidized LDL was prepared in the absence of ß-carotene.ß-Carotene probably binds to the cholesteryl ester moiety of LDL, and causes changes in the physicochemical properties of the lipoprotein. The synthetic all-trans isomer of ß-carotene, but not the natural ß-carotene, reduced LDL electrophoretic mobility and increased the availability of free amino groups of lysine residues.We conclude that altough both the all-trans and the 9-cis isomers of ß-carotene can bind in vitro to plasma ! lipoproteins, they exert different effects of LDL atherogenicity; the all-trans isomer of ß-carotene is more effective in inhibiting the susceptibility of lipoproteins to lipid peroxidation and in reducing the cellular uptake of oxidized LDL by macrophages.
Gastrointestinal injury involves oxidative damage as the result of oxygen-derived free radicals which are formed during the inflammatory reactions. Chylomicrons which are synthesized by the intestine can thus be exposed to lipid peroxidation in celiac disease. Similarly, low-density lipoprotein (LDL) propensity to oxidation may be enhanced as a result of a direct or indirect effect of the oxidative process. To resolve these possibilities, plasma chylomicrons and LDL were isolated from a patient with celiac disease and from a control healthy subject before and 3 h after a fat-rich meal, and their propensity to copper-induced lipid peroxidation was then analyzed. The patient’s chylomicrons, its LDL that was obtained before the fat-rich meal and its LDL that was obtained after the meal demonstrated 220, 39 and 48% elevation in their content of thiobarbituric-acid-reactive substances in comparison with the control lipoproteins. After a complete recovery of the patient’s intestine, the susceptibility of the patient lipoproteins to in vitro oxidation returned toward normal levels. In the patient LDL fraction (obtained either before or after the fat-rich meal), but not in the patient’s chylomicrons, the carotenoid content was reduced by 70%, vitamin E by 45%, and the LDL content of arachidonic acid was increased by 70% in comparison with the control lipoproteins. On recovery of the patient and return of the intestine to its normal morphology, normalization of all of these constituents was achieved.
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