Tedesco Idolo, Moccia Stefania, Volpe Silvestro, Alfieri Giovanna, Strollo Daniela, Bilotto Stefania, Spagnuolo Carmela, Di Renzo Massimo, Aquino Rita P, Russo Gian Luigi
a Institute of Food Sciences, National Research Council , Avellino , Italy ;
b Division of Onco-Hematology , S.G. Moscati Hospital , Avellino , Italy ;
Free Radic Res. 2016;50(5):557-69. doi: 10.3109/10715762.2016.1152629. Epub 2016 Mar 17.
In the present study, we report that polyphenols present in red wine obtained by a controlled microvinification process are able to protect human erythrocytes from oxidative stress and to activate Plasma Membrane Redox System (PMRS). Human plasma obtained from healthy subjects was incubated in the presence of whole red wine at a concentration corresponding to 9.13-73 μg/ml gallic acid equivalents to verify the capacity to protect against hypochlorous acid (HOCl)-induced plasma oxidation and to minimize chloramine formation. Red wine reduced hemolysis and chloramine formation induced by HOCl of 40 and 35%, respectively. PMRS present on human erythrocytes transfers electrons from intracellular molecules to extracellular electron acceptors. We demonstrated that whole red wine activated PMRS activity in human erythrocytes isolated from donors in a dose-dependent manner with a maximum at about 70-100 μg/ml gallic acid equivalents. We also showed that red wine increased glutathione (GSH) levels and erythrocytic antioxidant capacity, measured by 2,2-diphenyl-1-picrylhydrazyl (DPPH) quenching assay. Furthermore, we reported that GSH played a crucial role in regulating PMRS activity in erythrocytes. In fact, the effect of iodoacetamide, an alkylating agent that induces depletion of intracellular GSH, was completely counteracted by red wine. Bioactive compounds present in red wine, such as gallic acid, resveratrol, catechin, and quercetin were unable to activate PMRS when tested at the concentrations normally present in aged red wines. On the contrary, the increase of PMRS activity was associated with the anthocyanin fraction, suggesting the capacity of this class of compounds to positively modulate PMRS enzymatic activity.
在本研究中，我们报告称，通过可控微酿工艺获得的红酒中所含的多酚能够保护人类红细胞免受氧化应激，并激活质膜氧化还原系统（PMRS）。将从健康受试者获得的人血浆与全红酒一起孵育，红酒浓度相当于9.13 - 73μg/ml没食子酸当量，以验证其预防次氯酸（HOCl）诱导的血浆氧化以及使氯胺形成最小化的能力。红酒分别使HOCl诱导的溶血和氯胺形成降低了40%和35%。人类红细胞上存在的PMRS将电子从细胞内分子转移到细胞外电子受体。我们证明，全红酒以剂量依赖的方式激活从献血者分离出的人类红细胞中的PMRS活性，在没食子酸当量约为70 - 100μg/ml时达到最大值。我们还表明，红酒提高了谷胱甘肽（GSH）水平以及通过2,2 - 二苯基 - 1 - 苦基肼（DPPH）淬灭试验测定的红细胞抗氧化能力。此外，我们报告称GSH在调节红细胞中的PMRS活性方面起关键作用。事实上，红酒完全抵消了碘乙酰胺（一种诱导细胞内GSH耗竭的烷基化剂）的作用。红酒中存在的生物活性化合物，如没食子酸、白藜芦醇、儿茶素和槲皮素，在以陈酿红酒中通常存在的浓度进行测试时，无法激活PMRS。相反，PMRS活性的增加与花青素部分相关，表明这类化合物具有正向调节PMRS酶活性的能力。
