Low-density lipoprotein (LDL) cholesterol participates in the atherosclerotic process only after oxidative modification (o-LDL). Persons with elevated body iron concentrations are at higher risk of atherosclerosis. Iron in vitro is capable of oxidizing LDL, but it is unknown whether or not high dietary iron concentrations alter LDL in vivo. The aim of this study was, therefore, to investigate (i) whether dietary iron concentrations cause LDL-cholesterol oxidation and (ii) whether antioxidants can prevent such changes.
Rats received diets differing only in iron concentration: 35 mg/kg, 150 mg/kg or 300 mg/kg diet. A LDL-VLDL particle was isolated and the following parameters measured: malondialdehyde and lipid hydroperoxide concentrations (as an indication for lipid peroxidation); alpha-tocopherol and retinol concentrations (as antioxidants); protein sulfhydryl and carbonyl concentrations (as an indication of protein modification); agarose gel electrophoresis and cholesterol/protein ratio.
Dietary iron increased LDL-VLDL lipid peroxidation (malondialdehyde and lipid hydroperoxide concentrations), protein modification (sulfhydryl concentration), agarose migration distance and band width as well as cholesterol/protein ratio. Increased quantities of dietary iron led to a higher degree of oxidative change in LDL-VLDL. Lipid peroxidation, as well as protein modification, occurred, suggesting apoB changes. This was probably due to diminished antioxidant concentrations of alpha-tocopherol and beta-carotene. Antioxidant supplementation (alpha-tocopherol - Vitamin E and beta-carotene), however, prevented all the above changes and could be helpful in the prevention of atherosclerosis.
