Data Sheet 1_Acrylamide and bisphenol A: two plastic additives increase platelet activation, via oxidative stress.zip

BackgroundSince the mid-20th century, the widespread use of plastics has led to the buildup of harmful byproducts in the environment—most notably acrylamide (AA) and bisphenol A (BPA). These chemicals are now commonly detected in human tissues, raising concerns about their potential health effects. While their presence as environmental pollutants is well known, their specific impact on platelet function and the associated cardiovascular risks remains poorly understood.
MethodsTo explore how AA and BPA affect platelet physiology, we performed in vitro assays to assess platelet activation and aggregation following exposure to these compounds. We also used bioinformatic tools to identify potential protein targets in human platelets and carried out molecular docking simulations to investigate how AA and BPA interact with key enzymes involved in platelet regulation.
ResultsBoth AA and BPA exposure led to a significant increase in platelet activation and aggregation, suggesting an elevated risk of thrombosis. Proteomic analysis identified around 1,230 potential protein targets, with 191 affected by AA and 429 by BPA. These proteins are primarily involved in oxidative stress, apoptosis, and signaling pathways regulated by protein kinase C (PKC), p38α-MAPK, and superoxide dismutase (SOD). Molecular modeling further revealed that AA and BPA form stable complexes with several of these enzymes, indicating direct interference with platelet function.
Discussion and ConclusionOur study shows that AA and BPA can enhance platelet reactivity and aggregation, which are key factors in the development of cardiovascular disease (CVD). By identifying specific molecular pathways and targets affected by these pollutants, we provide new insights into their potential role in promoting thrombotic conditions. These findings highlight the urgent need for greater public health awareness and stronger regulatory efforts to reduce human exposure to AA and BPA.

研究背景
自20世纪中期以来，塑料的广泛使用导致环境中有害副产物不断积累，其中最具代表性的为丙烯酰胺（acrylamide，AA）与双酚A（bisphenol A，BPA）。这类化学物质目前已在人体组织中被频繁检出，引发了学界与公众对其潜在健康危害的广泛担忧。尽管二者作为环境污染物的存在已得到广泛证实，但其对血小板功能的具体影响以及相关联的心血管风险仍有待深入阐明。
研究方法
为探究丙烯酰胺（AA）与双酚A（BPA）对血小板生理功能的调控作用，本研究开展体外实验以评估暴露于这两种化合物后血小板的活化与聚集水平。此外，研究团队借助生物信息学工具识别人血小板中的潜在蛋白靶点，并通过分子对接模拟，深入分析AA与BPA与血小板调控相关关键酶的相互作用模式。
研究结果
暴露于AA与BPA均可显著提升血小板活化与聚集水平，提示血栓形成风险升高。蛋白质组学分析共识别出约1230个潜在蛋白靶点，其中191个受AA调控、429个受BPA调控。这些蛋白主要参与氧化应激、细胞凋亡以及由蛋白激酶C（protein kinase C，PKC）、p38α-MAPK和超氧化物歧化酶（superoxide dismutase，SOD）调控的信号通路。分子建模进一步揭示，AA与BPA可与其中多种酶形成稳定复合物，表明二者可直接干扰血小板正常功能。
讨论与结论
本研究证实，AA与BPA可增强血小板反应性与聚集能力，而这二者是心血管疾病（cardiovascular disease，CVD）发生发展的关键危险因素。通过识别受这类污染物影响的特异性分子通路与靶点，本研究为其促进血栓形成的潜在机制提供了全新的科学见解。上述研究结果凸显了提升公众健康认知、加强监管力度以降低人体暴露于AA与BPA水平的迫切性。