Tupe R S, Diwan A G, Mittal V D, Narayanam P S, Mahajan K B
Br J Biomed Sci. 2014;71(3):93-9; quiz 138. doi: 10.1080/09674845.2014.11669971.
This study examines the individual stages of plasma protein glycation, antioxidant status and their association with erythrocyte oxidative stress in patients with type 2 diabetes mellitus (T2DM). Study was carried out on blood from 70 patients with T2DM and 40 healthy age- and gender-matched volunteers. Biomarkers of plasma protein glycation (fructosamine, protein carbonyls, advanced glycation end products [AGEs], amyloid), antioxidant status (thiols, total antioxidant capacity and erythrocyte oxidative parameters), osmotic fragility, lipid peroxidation (LPO), reduced glutathione (GSH) and catalase were determined. Plasma glycation markers were higher in T2DM patients than in healthy volunteers: fructosamine 578 vs. 525 micromol/mL; carbonyl 21.23 vs. 18.84 nmol/mg protein (P < or = 0.01); AGEs 213.94 vs. 178.27 AU/mg protein (P < or = 0. 05); and amyloid 0.53 vs. 0.40 A530 nm (P < 0.01). Plasma antioxidant status was significantly reduced in patients with diabetes compared to the healthy volunteers, with lower plasma protein thiols (1.16 vs. 1.36 nmol/mg protein; P < 0.01) and total antioxidant capacity (26 vs. 34 micromol; P < 0.01). Erythrocytes from the patient group were found to show greater oxidative damage, with elevated numbers of fragile cells and increased LPO, and reduced GSH level. Among the glycation markers, positive correlations were evident between fructosamine and amyloid (r = 0.350, P < 0.001) and AGEs and amyloid (r = 0.070). Plasma glycation markers showed negative correlation with plasma antioxidant status while positive correlation was demonstrated between erythrocytes fragility and AGEs and amyloid. Erythrocyte LPO levels correlated positively with amyloid. These data suggest that increased levels of multiple plasma protein glycation products in T2DM patients play a key role in reduced plasma antioxidant status and amplified erythrocyte oxidative damage.
本研究探讨了2型糖尿病（T2DM）患者血浆蛋白糖化的各个阶段、抗氧化状态及其与红细胞氧化应激的关系。研究对象为70例T2DM患者和40例年龄及性别匹配的健康志愿者的血液。测定了血浆蛋白糖化的生物标志物（果糖胺、蛋白质羰基、晚期糖基化终产物[AGEs]、淀粉样蛋白）、抗氧化状态（硫醇、总抗氧化能力和红细胞氧化参数）、渗透脆性、脂质过氧化（LPO）、还原型谷胱甘肽（GSH）和过氧化氢酶。T2DM患者的血浆糖化标志物高于健康志愿者：果糖胺分别为578和525微摩尔/毫升；羰基分别为21.23和18.84纳摩尔/毫克蛋白（P≤0.01）；AGEs分别为213.94和178.27 AU/毫克蛋白（P≤0.05）；淀粉样蛋白分别为0.53和0.40 A530纳米（P<0.01）。与健康志愿者相比，糖尿病患者的血浆抗氧化状态显著降低，血浆蛋白硫醇含量较低（分别为1.16和1.36纳摩尔/毫克蛋白；P<0.01），总抗氧化能力较低（分别为26和34微摩尔；P<0.01）。患者组的红细胞显示出更大的氧化损伤，脆性细胞数量增加，LPO升高，GSH水平降低。在糖化标志物中，果糖胺与淀粉样蛋白之间（r = 0.350，P<0.001）以及AGEs与淀粉样蛋白之间（r = 0.070）存在明显的正相关。血浆糖化标志物与血浆抗氧化状态呈负相关，而红细胞脆性与AGEs和淀粉样蛋白呈正相关。红细胞LPO水平与淀粉样蛋白呈正相关。这些数据表明，T2DM患者多种血浆蛋白糖化产物水平升高在降低血浆抗氧化状态和放大红细胞氧化损伤中起关键作用。
