Imbalance in superoxide dismutase/thioredoxin reductase activities in hypercholesterolemic subjects: relationship with low density lipoprotein oxidation.
Imbalance in superoxide dismutase/thioredoxin reductase activities in hypercholesterolemic subjects: relationship with low density lipoprotein oxidation.
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DOI：
10.1186/1476-511x-11-79
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发表时间：
2012-06-21
影响因子：
4.5
通讯作者：
Emanuelli T
中科院分区：
文献类型：
--
作者：
Augusti PR;Ruviaro AR;Quatrin A;Somacal S;Conterato GM;Vicentini JT;Duarte MM;Emanuelli T
高胆固醇血症、氧化应激和炎症在动脉粥样硬化形成中有一定的关系。因此，本研究的目的是评估不同低密度脂蛋白(LDL)水平受试者的对氧磷酶(PON1)、超氧化物歧化酶(SOD)和硫氧还蛋白还原酶(TrxR-1)活性及其与血脂、氧化应激和炎症的关系。根据低密度脂蛋白水平分为低密度脂蛋白胆固醇组( <； 100 mg/dL，n = 23)、中低密度脂蛋白脂组(LD100-160 mg/dL，n = 50)和高低密度脂蛋白胆固醇组(L DL >； 160 mg/dL，n = 43)，测定血脂、高脂蛋白氧化、氧化低密度脂蛋白和自身抗体的水平及酶活性。与低低密度脂蛋白胆固醇组相比，高低密度脂蛋白胆固醇组的低密度脂蛋白胆固醇和超敏C反应蛋白水平升高(分别为2.7倍和3.7倍)，而中低密度脂蛋白胆固醇组和高密度脂蛋白胆固醇组的低密度脂蛋白胆固醇水平分别增加2.2倍和3.1倍(p <； 0.0 5)。同样，与低低密度脂蛋白胆固醇组相比，中低密度脂蛋白胆固醇组和高低密度脂蛋白脂组的超氧化物歧化酶活性、动脉粥样硬化指数(AI)和蛋白质氧化程度也更高(p <； 0.05)。与低低密度脂蛋白胆固醇组相比，只有高低密度脂蛋白胆固醇组的脂质氧化和超氧化物歧化酶/TrxR-1比值增加(p <； 0.05)。超氧化物歧化酶/TrxR-1比值与TBARS(r = 0.23，p <； 0.05)、LDlox(r = 0.18，p <； 0.05)、LDLoxAB(r = 0.21，p <； 0.05)、低密度脂蛋白(r = 0.19，p <； 0.05)和AI(r = 0.22，p <； 0.05)呈正相关。各组间PON1和TrxR-1活性相似。当低密度脂蛋白水平达到临床可接受水平时，一些氧化事件就会发生。此外，高胆固醇血症患者体内存在与低密度脂蛋白氧化正相关的超氧化物歧化酶和TrxR-1活性失衡。
There is a relationship among hypercholesterolemia, oxidative stress and inflammation in the atherogenesis. Thus, the objective of the present study was to assess paraoxonase (PON1), superoxide dismutase (SOD) and thioredoxin reductase (TrxR-1) activities and their relationship with lipids, oxidative stress and inflammation in subjects with different low density lipoprotein-cholesterol (LDL) levels. Serum lipids, highly sensitive C-reactive protein (hs-CRP), lipid and protein oxidation, oxidized LDL (LDLox) and LDLox autoantibodies (LDLoxAB) levels and enzymes activities were measured in a total of 116 subjects that were divided into the following groups according to their LDL levels: low-LDL group (LDL < 100 mg/dL, n = 23), intermediate-LDL group (LDL 100–160 mg/dL, n = 50) and high-LDL group (LDL > 160 mg/dL, n = 43). The LDLox and hs-CRP levels increased in the high-LDL group (2.7- and 3.7- fold, respectively), whereas the intermediate and high-LDL groups had higher LDLoxAB (2.2- and 3.1-fold) when compared to low-LDL group (p < 0.05). Similarly, SOD activity, the atherogenic index (AI) and protein oxidation were also higher in the intermediate (1.3-, 1.3- and 1.2-fold) and high-LDL (1.6-, 2.3- and 1.6-fold) groups when compared to the low-LDL group (p < 0.05). Lipid oxidation and SOD/TrxR-1 ratio increased only in the high-LDL group (1.3- and 1.6-fold) when compared to the low-LDL group (p < 0.05). The SOD/TrxR-1 ratio was positively correlated to TBARS (r = 0.23, p < 0.05), LDLox (r = 0.18, p < 0.05), LDLoxAB (r = 0.21, p < 0.05), LDL (r = 0.19, p < 0.05) and AI (r = 0.22, p < 0.05). PON1 and TrxR-1 activities were similar among groups. Some oxidative events initiate when LDL levels are clinically acceptable. Moreover, hypercholesterolemic patients have an imbalance in SOD and TrxR-1 activities that is positively associated to LDL oxidation.