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Bisphenols-enhanced platelet aggregation via TP, P2Y12, PAR1 and PAR4 receptors: a thrombotic legacy in a plastic-ubiquitous world.
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BPA and similar chemicals found in plastics (including "BPA-free" alternatives like BPF and BPS) made blood platelets clump together more intensely and for longer when tested with human blood samples—a process that can trigger dangerous clots linked to heart attacks and strokes. Even the substitutes marketed as safer alternatives to BPA showed this clot-promoting effect, and in some cases were even more potent, suggesting that swapping one bisphenol for another may not actually reduce health risks. While this research was done on blood samples rather than in living people, it adds to growing evidence that everyday plastic exposure could be qu
BACKGROUND: Cardiovascular diseases remain an urgent global health concern addressed by multiple clinical guidelines. Atherothrombosis is characterised by thrombus formation following disruption of atherosclerotic plaque, leading to major adverse cardiovascular events, such as myocardial infarction and stroke. Platelet hyperactivity is a key driver of these outcomes, leading causes of morbidity and mortality worldwide. Environmental xenobiotic exposure has been documented to contribute to atherosclerosis, endothelial dysfunction, and hypertension; however, its effects on thrombosis remain scarcely documented. In the present study, the effects of bisphenol A (BPA) and its most commonly used structural analogues on platelet aggregation were assessed using an model. analyses were also performed to identify potential receptors through which bisphenols may induce platelet aggregation. Additionally, our findings were contextualised within a systematic review spanning 10 years. METHODS: Platelet-rich plasma from healthy middle-aged men was incubated (30 min at 37°) with different bisphenols at concentrations ranging from 5 pM to 500 nM. Following incubation, platelet aggregation was induced with adenosine diphosphate (ADP) and measured with a Lumi-Aggregometer. Results were presented as standardised mean differences (SMD). A systematic review spanning 10 years was conducted to compare our findings. To explain our results, analyses were conducted to evaluate the binding affinity and interaction models of bisphenols at platelet receptors relative to their reference agonists and antagonists. Receptors were selected based on the structural similarity between their cognate agonist and bisphenols. Binding affinity was assessed for the thromboxane A (TP), the purinergic P2Y-subtype-12 (P2RY) and the protease-activated receptors 1 (PAR1) and 4 (PAR4). RESULTS: Bisphenols did not provoke platelet aggregation spontaneously. However, once ADP was added, they induced a strong and prolonged platelet aggregation (SMD: 1.90; CI: 1.68-2.11) in the model, with a potency ranking of BPF > TDF > BPS > BPA > BPAF. These findings were reinforced by the results from other studies in which human platelets were exposed to bisphenols. The analyses revealed that bisphenols exhibit favourable binding affinities for TP, which may explain the findings. Bisphenols also showed binding affinity for P2Y, PAR1, and PAR4. CONCLUSION: Our study demonstrated that exposure to bisphenols enhanced and prolonged ADP-induced platelet aggregation and, for the first time, illuminated their interactions with key receptors involved in this complex process. Nonetheless, bisphenols may also exert other pleiotropic effects that further contribute to platelet aggregation. These results highlight the remarkable toxicity of these xenobiotics and their significant impact on haemostatic balance.
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This review pulls together over a decade of research on how everyday plastic chemicals—like BPA, phthalates, and micro/nanoplastics—may make blood cells (platelets) more likely to clump together and form dangerous clots, a risk factor for heart attacks and strokes. While bisphenols (found in things like plastic bottles and food packaging) have the most evidence so far, the overall findings suggest plastic exposure could be an overlooked contributor to rising heart disease rates, especially in younger people. Since these chemicals are barely regulated, the researchers argue this evidence should prompt closer safety oversight and more stud
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