Maternal smoking-induced congenital heart and microvascular defects are closely associated with the impaired functioning of the in-utero feto-placental circulation system. Current groundbreaking facts revealed intimate crosstalk between circulating red blood cells (RBCs) and the vascular endothelium. Thus, RBCs have become the protagonists under varied pathological and adverse pro-oxidative cellular stress conditions. We isolated and screened fetal RBCs from the arterial cord blood of neonates, born to non-smoking (RBC-NS) and smoking mothers (RBC-S), assuming that parameters of fetal RBCs are blueprints of conditions experienced in-utero. Using atomic force microscopy and mass spectrometry-based shotgun lipidomics in the RBC-S population we revealed induced membrane stiffness, loss in intrinsic plastic activities and several abnormalities in their membrane-lipid composition, that could consequently result in perturbed hemodynamic flow movements. Altogether, these features are indicative of the outcome of neonatal microvascular complications and suggest unavailability for the potential rescue mechanism in cases of vascular endothelium impairment due to altered membrane integrity and rheological properties.

中文翻译：

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孕妇持续吸烟引起的胎儿红细胞膜理化性质的变化可能是血管合并症的早期标志。

孕妇吸烟引起的先天性心脏和微血管缺陷与子宫内胎盘胎盘循环系统功能受损密切相关。当前的突破性事实表明循环红细胞（RBC）与血管内皮之间存在密切的串扰。因此，在各种病理和不利的促氧化细胞应激条件下，红细胞已成为主角。我们假设胎儿​​红细胞的参数是宫内条件的蓝图，我们从非吸烟（RBC-NS）和吸烟母亲（RBC-S）出生的新生儿的动脉血中分离和筛选了胎儿红细胞。在RBC-S人群中使用原子力显微镜和基于质谱的shot弹枪脂质组学，我们揭示了诱导的膜硬度，内在塑性活动的丧失和其膜脂成分的一些异常，可能导致血液动力学流动的紊乱。总之，这些特征指示了新生儿微血管并发症的结果，并提示在由于膜完整性和流变特性改变而导致血管内皮损伤的情况下，潜在的抢救机制不可用。