Dietary iron elevates LDL-cholesterol and decreases plasma antioxidant levels: influence of antioxidants.

High body iron and LDL-cholesterol concentrations, and antioxidant deficiency, are regarded as risk factors for ischemic heart disease. Iron is well known for causing oxidative damage and antioxidants for their beneficial effects on radical scavenging. It is, however, unknown whether or not dietary iron causes depletion of plasma antioxidants; causes lipid peroxidation; alters HDL- and LDL-cholesterol, and triglyceride concentrations. Rats received diets differing only in iron concentration--15 mg/Kg, 35 mg/Kg, 150 mg/Kg or 300 mg/Kg diet. The second group of rats received antioxidants (alpha-tocopherol and beta-carotene) in their drinking water. Increasing dietary iron increased plasma lipid hydroperoxide and LDL-cholesterol concentrations, but did not affect HDL-cholesterol or triglyceride concentrations. It decreased antioxidants, alpha-tocopherol and retinol. Antioxidant supplementation inhibited the above changes.

Dietary iron concentration alters LDL oxidatively. The effect of antioxidants.

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 and beta-carotene), however, prevented all the above changes and could be helpful in the prevention of atherosclerosis.

Influence of ferritin levels on LDL cholesterol concentration in women.

Various researchers have observed a higher risk for atherosclerosis when body iron concentration is elevated. The exact mechanism, however, is not known, but probably occurs catalytically via iron. Whether or not body iron concentration has an effect on plasma lipoproteins is also unknown. The aim of this study was to investigate whether or not ferritin concentration within the normal range correlate with LDL-cholesterol (an atherosclerotic risk factor), HDL-cholesterol, apoB, triglyceride and the mobility of LDL particles. Blood was drawn from healthy female volunteers and the above parameters measured. LDL-cholesterol, apoB and the electrophoretic mobility of LDL particles were elevated with increasing ferritin concentrations. Both modified or oxidized LDL and elevated LDL concentration are regarded as risks for atherosclerosis and ischemic heart disease, suggesting that higher body iron is important in this process.