作者: Kan-zhi Liu , Hamid Massaeli , Bram Ramjiawan , Grant N. Pierce
DOI: 10.1007/978-94-007-6513-9_7
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摘要: When LDL is oxidized by a free radical generating system, both cholesterol and fatty acyl moieties within the are modified. Oxidized low density lipoprotein (oxLDL) can induce alterations in Ca2+ transients isolated cardiomyocytes. It unclear if oxidation of chains (in phospholipids, triglycerides cholesteryl esters) or unesterified more important producing oxLDL-induced alteration cellular calcium transients. Therefore, we investigated possible role chain peroxidation effects on Cholesterol oxidase (CO) treatment produced plus H2O2. The H2O2 peroxidized chains, as indicated an increased malondialdehyde (MDA) content. cell systolic [Ca2+] was significantly after incubation with CO-treated LDL. Diastolic unchanged. MDA content correlated change treated cells. Catalase, scavenger H2O2, inhibited formation prevented increment A similar stimulatory effect transient observed cells were exposure to only not CO. Direct myocytes (without LDL) failed produce but caused diastolic Ca2+. Exposure CO alone significant this catalase. These results suggest that acid moiety than generation ox-LDL-induced increases Further, situ membrane will destroy integrity. Our data also underline importance adding extracellular lipid any study oxygen radicals function. Under conditions radiologic chemically-induced oxygen-derived radicals, cardiac dysfunction damage may be induced process.