Gallo Giuseppe, Bruno Rosalinda, Taranto Adele, Martino Guglielmo
Department of Biology, Ecology and Earth Sciences, University of Calabria, Rende (CS), Italy.
Department of Pharmacy and Health Sciences and Nutrition, University of Calabria, Rende (CS), Italy.
Pharmacogn Mag. 2017 Oct;13(Suppl 3):S561-S566. doi: 10.4103/pm.pm_483_15. Epub 2017 Oct 11.
Increased levels of malondialdehyde (MDA) and 4-hydroxynonenal (HNE) are demonstrated in plasma of uremic patients. A study showed that the comparison of erythrocytes of healthy and diseased patients (obese, hypertensive, and Type 2 diabetics) with age is associated to a disturbed oxidant/antioxidant balance when obesity is associated with hypertension. 4-hydroxytyrosol is shown to significantly protect red blood cells (RBCs) from oxidative damage (4-HNE). In literature, there are partial discussions on the role of lipids and their oxidation products. The products of degradation of membrane proteins are observed as self-consisting products without interrelations with membrane lipids.
The aim of this study is to evaluate the role of polyunsaturated fatty acid (PUFA) metabolites on oxidative damage (4-hydroxy-alkenals) in RBCs of hypertriglyceridemic patients after membrane treatment with 4-hydroxytyrosol.
The authors optimize the isolation of RBC ghosts and spectrophotometric method to measure free 4-hydroxyalkenals in human RBC membranes and investigated the effect on oxidative damage in human erythrocyte membranes and 4-hydroxytyrosol treatment to evaluate the membrane lipids reducible by this phenol.
Plasma triglyceride levels in patients are clearly higher than in controls. Moreover, total membrane proteins data are similar to previous described. The normalized alkenals levels are significantly enhanced in hyperlipemic patients in comparison to normoglyceridemic controls. After the 4-hydroxytyrosol action, lipid metabolites substantially decrease. The ratio of oxidized lipids (MDA + HNE) and membrane proteins data are similar to previously described ones.
According to experimental data, the accumulation of the alkenals in RBC membrane could be produced either by partial PUFA oxidation contained in glycerides and plasma glycerides and by glycerides into plasma membrane recycled RBC.
Hypertriglyceridemia induces oxidative stress in human red blood cell (RBC) membranesOxidative stress causes increased plasma membrane total protein concentration and hydroxynonenal and malondialdehyde levelsThe authors optimize the isolation of RBC ghosts and spectrophotometric method to measure free 4-hydroxyalkenals in human RBC membranesAfter the reduction with 4-hydroxytyrosol, oxidized lipid concentration significantly decrease. RBC: Red blood cell; MDA: Malondialdehyde; HNE\HAE: 4-hydroxyalkenals; LPO: Lipid peroxidation; ROS: Reactive oxygen species; ORAC: Oxygen Radical Absorbance Capacity.
尿毒症患者血浆中丙二醛（MDA）和4-羟基壬烯醛（HNE）水平升高。一项研究表明，当肥胖与高血压相关时，健康患者与患病患者（肥胖、高血压和2型糖尿病患者）的红细胞随年龄增长的比较与氧化还原/抗氧化平衡紊乱有关。4-羟基酪醇被证明能显著保护红细胞（RBC）免受氧化损伤（4-HNE）。在文献中，对脂质及其氧化产物的作用有部分讨论。膜蛋白降解产物被视为独立的产物，与膜脂质无相互关系。
本研究旨在评估多不饱和脂肪酸（PUFA）代谢产物对高甘油三酯血症患者红细胞经4-羟基酪醇处理后氧化损伤（4-羟基烯醛）的作用。
作者优化了红细胞血影的分离方法和分光光度法，以测量人红细胞膜中游离的4-羟基烯醛，并研究了对人红细胞膜氧化损伤的影响以及4-羟基酪醇处理对可被该酚还原的膜脂质的影响。
患者血浆甘油三酯水平明显高于对照组。此外，总膜蛋白数据与先前描述的相似。与正常甘油三酯血症对照组相比，高脂血症患者中归一化的烯醛水平显著升高。4-羟基酪醇作用后，脂质代谢产物大幅减少。氧化脂质（MDA + HNE）与膜蛋白数据的比值与先前描述的相似。
根据实验数据，红细胞膜中烯醛的积累可能是由甘油酯和血浆甘油酯中所含的部分多不饱和脂肪酸氧化以及血浆膜中再循环红细胞中的甘油酯引起的。
高甘油三酯血症诱导人红细胞（RBC）膜氧化应激
氧化应激导致质膜总蛋白浓度以及羟基壬烯醛和丙二醛水平升高
作者优化了红细胞血影的分离方法和分光光度法，以测量人红细胞膜中游离的4-羟基烯醛
用4-羟基酪醇还原后，氧化脂质浓度显著降低。
红细胞；MDA：丙二醛；HNE\HAE：4-羟基烯醛；LPO：脂质过氧化；ROS：活性氧；ORAC：氧自由基吸收能力
