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Iron overload diminishes atherosclerosis in apoE-deficient mice

Show simple item record Kirk, Elizabeth A. en_US Heinecke, Jay W. en_US LeBoeuf, Renée C. en_US 2010-04-21T15:55:37Z 2010-04-21T15:55:37Z 2001-06-15 en_US
dc.identifier.citation Kirk EA, Heinecke JW, LeBoeuf RC. Iron overload diminishes atherosclerosis in apoE-deficient mice. J Clin Invest. 2001;107(12):1545-1553. en_US
dc.identifier.other 10.1172/JCI7664 en_US
dc.identifier.uri en_US
dc.description.abstract It has been proposed that elevated levels of tissue iron increase the risk for atherosclerosis, perhaps by favoring the formation of pro-atherogenic oxidized LDL. Working with apoE-deficient (apoE–/–) mice, which do not require a high-fat diet to develop atherosclerosis, we compared the effects of standard diet (0.02% iron) or a 2% carbonyl iron diet. After 24 weeks, mice fed the 2% carbonyl iron diet had twice as much iron in their plasma, a ninefold increase in bleomycin-detectable free iron in their plasma, and ten times as much iron in their livers as control mice. Dietary iron overload caused a modest (30%) rise in plasma triglyceride and cholesterol. Nevertheless, this regimen did not exacerbate, but rather reduced the severity of atherosclerosis by 50%, and it failed to elevate hepatic levels of heme oxygenase mRNA, which is induced by many different oxidative insults in vitro. Moreover, hepatic levels of protein-bound dityrosine and ortho-tyrosine, two markers of metal-catalyzed oxidative damage in vitro, failed to rise in iron-overloaded animals. Our observations suggest that elevated serum and tissue levels of iron are not atherogenic in apoE–/– mice. Moreover, they call into question the hypothesis that elevated levels of tissue iron promote LDL oxidation and oxidative stress in vivo. en_US
dc.description.sponsorship NIH grants DK-02456, HL-52848, AG-15013, DK-56341, and RR-00954, the American Heart Association, and the Pharmacia-Monsanto-Searle/Washington University Biomedical Program. en_US
dc.language.iso en_US en_US
dc.title Iron overload diminishes atherosclerosis in apoE-deficient mice en_US

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