的贡献过氧化物减少glycoxidative血清白蛋白的抗氧化活性。
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坂田N,卫生部,Takebayashi年代
的贡献过氧化物减少glycoxidative血清白蛋白的抗氧化活性。
心脏血管。2002年11月,17 (1):22-9。
- PubMed ID
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12434198 (在PubMed]
- 文摘
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高血糖增加各组织氧化应激,导致糖尿病心血管并发症。血脂异常,如氧化低密度脂蛋白(LDL)的增加,是公认的糖尿病患者的高血糖。然而,高血糖导致增加LDL氧化的机理仍不清楚。白蛋白是循环,最丰富的蛋白质,可以作为一种抗氧化剂。因此,我们研究是否glycoxidative修改抑制蛋白的抗氧化活性,低密度脂蛋白氧化,澄清的机制这一修改可能抑制其抗氧化活性。人血清白蛋白(HSA)在磷酸盐与孵化,没有葡萄糖在37摄氏度长达8周在有氧条件下(称为glycoxidation (goHSA)和氧化(oHSA),分别)。金属chelator-treated nonoxidative HSA (chHSA)和刚做好HSA (fHSA)被用作控制。(N(ε))-羧甲基赖氨酸(CML) glycoxidative产品,是由酶联免疫吸附试验。氧化估计通过测量HSA的硫醇分子。Copper-mediated氧化低密度脂蛋白的存在与否进行修改在37摄氏度经营6天。 Malondialdehyde and negative charge of LDL were measured. To clarify the mechanism of reduced antioxidant activity of HSA, we examined firstly the binding activity of modified HSAs to copper, and secondly the effects of free radical scavengers on the formation of malondialdehyde. CML was formed in goHSA in a time- and concentration-dependent manner. Both goHSA and oHSA significantly decreased the contents of free thiol groups compared to ch- and fHSAs. The antioxidant activity of goHSA to LDL oxidation was the lowest among various modified HSAs. The oHSA showed a moderate decrease in antioxidant activity. The binding activity of go- and oHSAs to copper was lower than that of ch- and fHSAs. The formation of MDA from LDL oxidation in the presence of goHSA was completely inhibited by Tiron (1,2-dihydroxy-3,5-benzenedisulfonic acid) and superoxide dismutase. In contrast, catalase and mannitol had no effect. Our results indicate that in vitro glycoxidation of HSA induced a marked loss of antioxidant activity of this molecule to copper-mediated oxidation of LDL, which may be caused by the generation of superoxide.