Whittaker P, Wamer W G, Chanderbhan R F, Dunkel V C
Center for Food Safety and Applied Nutrition, US Food and Drug Administration, Washington, DC 20204, USA.
Nutr Cancer. 1996;25(2):119-28. doi: 10.1080/01635589609514434.
The ability of dietary antioxidants to reduce lipid peroxidation induced by iron overload was examined in weanling male Sprague-Dawley rats. Animals were fed ad libitum a modified AIN-76A diet (control) or control diet with 0.5% alpha-tocopherol acid succinate, 0.5% crystalline trans-beta-carotene, or 0.5% alpha-tocopherol acid succinate + 0.5% trans-beta-carotene for four weeks. In the following four-week period, the animals received the above diets with 10,000 micrograms Fe/g; a control group continued to receive 35 micrograms Fe/g, and a high-iron group received 10,000 micrograms Fe/g with no antioxidants. After four weeks of dietary supplementation with alpha-tocopherol. Beta-carotene or alpha-tocopherol + beta-carotene, liver concentrations of alpha-tocopherol and beta-carotene increased significantly (p < 0.001). Liver lipid peroxidation, measured by the lipid-conjugated diene assay, increased significantly from 0.012 mumol/mg of lipid in the controls to 0.021 mumol/mg of lipid in animals receiving the high-iron diet. However, lipid peroxidation was significantly reduced in all animals fed the antioxidants, with the group fed alpha-tocopherol + beta-carotene having a lower level than the high-iron group. Total serum cholesterol was elevated in animals fed a high-iron diet and in animals fed the high-iron diet with alpha-tocopherol. In contrast, total serum cholesterol levels in the two groups of animals receiving the diets containing high iron with beta-carotene alone or high iron with beta-carotene + alpha-tocopherol were significantly reduced to the level of the control group. High-density lipoprotein cholesterol also decreased to baseline in the animals receiving beta-carotene alone. Modulation of lipid peroxidation by alpha-tocopherol or beta-carotene may be an important mechanism for reducing oxidative stress.
在断乳雄性斯普拉格-道利大鼠中研究了膳食抗氧化剂降低铁过载诱导的脂质过氧化的能力。动物随意进食改良的AIN-76A饮食（对照）或添加0.5%琥珀酸生育酚、0.5%结晶反式β-胡萝卜素或0.5%琥珀酸生育酚+0.5%反式β-胡萝卜素的对照饮食，持续四周。在接下来的四周期间，动物接受上述含10000微克铁/克的饮食；一个对照组继续接受35微克铁/克，一个高铁组接受10000微克铁/克且不添加抗氧化剂。在膳食补充生育酚、β-胡萝卜素或生育酚+β-胡萝卜素四周后，肝脏中生育酚和β-胡萝卜素的浓度显著增加（p<0.001）。通过脂质共轭二烯测定法测量，肝脏脂质过氧化从对照组的0.012微摩尔/毫克脂质显著增加到接受高铁饮食动物的0.021微摩尔/毫克脂质。然而，在所有喂食抗氧化剂的动物中脂质过氧化显著降低，喂食生育酚+β-胡萝卜素的组水平低于高铁组。喂食高铁饮食的动物和喂食含生育酚的高铁饮食的动物血清总胆固醇升高。相比之下，单独接受含高铁和β-胡萝卜素饮食或含高铁和β-胡萝卜素+生育酚饮食的两组动物的血清总胆固醇水平显著降低至对照组水平。单独接受β-胡萝卜素的动物中高密度脂蛋白胆固醇也降至基线水平。生育酚或β-胡萝卜素对脂质过氧化的调节可能是降低氧化应激的重要机制。
