Oxidative stress and high-density lipoprotein function in Type I diabetes and end-stage renal disease
Oxidative stress and high-density lipoprotein function in Type I diabetes and end-stage renal disease
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DOI：
10.1042/cs20040312
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发表时间：
2005-06-01
期刊：
影响因子：
6
通讯作者：
Jenkins, AJ
中科院分区：
文献类型：
--
作者：
Kalogerakis, G;Baker, AM;Jenkins, AJ
在一项横断面研究中，通过测量血浆蛋白羰基和比较高密度脂蛋白(高密度脂蛋白)的抗氧化能力与对氧磷酶1(PONI)活性和体外清除过氧化脂质(LPO)来评估高血管疾病风险组(ESRD(终末期肾病)和I型糖尿病)的氧化应激。比较22例血液透析患者(ESRID组)、20例无血管并发症的I型糖尿病患者和23例健康体检者(对照组)。终末期糖尿病患者血浆蛋白羰基含量[0.16(0.050)nmol/mg蛋白；P=0.001；平均值(SD)]高于I型糖尿病患者[0.099(0.014)nmol/mg蛋白]和健康人[0.093(0.014)nmol/mg蛋白]。与健康受试者相比，糖尿病患者的血浆PONI活性较低，但ESRID患者与健康受试者相比无差异。在不校正高密度脂蛋白的情况下，血浆PONI活性在三组之间没有差异。终末期肾病患者血浆PONI活性与血浆蛋白羰基浓度呈负相关(r=-0.50，P<；0.05)。在体外试验中，终末期肾病患者的高密度脂蛋白对LPO的清除高于健康受试者的高密度脂蛋白(P<；0.01)，而I型糖尿病患者的高密度脂蛋白的效果较差(P<；0.01)。清除LPO的效果与血浆PONI活性、体外糖基化或轻度氧化无关，但受到显著氧化和糖氧化的影响。ESRID患者的蛋白质羰基水平升高，但在无并发症的I型糖尿病患者中不会。高密度脂蛋白抗氧化功能在终末期肾病患者中增强，这可能是对氧化应激增加的一种代偿反应，但在I型糖尿病患者中较低。高密度脂蛋白功能障碍与糖氧化有关，而与糖基化或PONI活性无关。
In a cross-sectional study, oxidative stress in high vascular disease risk groups, ESRD (endstage renal disease) and Type I diabetes, was assessed by measuring plasma protein carbonyls and comparing antioxidant capacity of HDL (high-density lipoprotein) as pertaining to PONI (paraoxonase 1) activity and in vitro removal of LPO (lipid peroxides). ESRID subjects on haemodialysis (n = 22), Type I diabetes subjects (n = 20) without vascular complications and healthy subjects (n = 23) were compared. Plasma protein carbonyls were higher in ESRID patients [0.16 (0.050) nmol/mg of protein; P = 0.001; value is mean (SD)] relative to subjects with Type I diabetes [0.099 (0.014) nmol/mg of protein] and healthy subjects [0.093 (0.014) nmol/mg of protein]. Plasma PONI activity, with and without correction for HDL-cholesterol, was lower in diabetes but did not differ in ESRID compared with healthy subjects. Plasma PONI activity, without correction for HDL, did not differ between the three groups. In ESRD, plasma PONI activity and plasma protein carbonyl concentrations were inversely related (r = -0.50, P < 0.05). In an in vitro assay, LPO removal by HDL in ESRD subjects was greater than HDL from healthy subjects (P < 0.01), whereas HDL from patients with Type I diabetes was less effective (P < 0.01). Efficacy of LPO removal was unrelated to plasma PONI activity, in vitro glycation or mild oxidation, but was impaired by marked oxidation and glycoxidation. Protein carbonyl levels are increased in ESRID but not in complication-free Type I diabetes. HDL antioxidant function is increased in ESRD, perhaps a compensatory response to increased oxidative stress, but is lower in Type I diabetes. HDL dysfunction is related to glycoxidation rather than glycation or PONI activity.