Evidence map›Paper›PMID 40371341›Full record

ArticleFrontiers in pharmacology2025

Acrylamide and bisphenol A: two plastic additives increase platelet activation, via oxidative stress.

C F Burgos, D Méndez, S Quintana, S Gonkowski, A Trostchansky, M Alarcón

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

C F Burgos *Department of Physiology, Faculty of Biological Sciences, Universidad de Concepción, Concepción, Chile.
D Méndez *Thrombosis Research Center and Healthy Aging, Universidad de Talca, Talca, Chile.
S QuintanaDepartment of Physiology, Faculty of Biological Sciences, Universidad de Concepción, Concepción, Chile.
S GonkowskiDepartment of Clinical Physiology, Faculty of Veterinary Medicine, University of Warmia and Mazury in Olsztyn, Olsztyn, Poland.
A TrostchanskyDepartamento de Bioquímica and Center for Free Radical and Biomedical Research, Facultad de Medicina, Universidad de la República, Montevideo, Uruguay.
M AlarcónThrombosis Research Center and Healthy Aging, Universidad de Talca, Talca, Chile.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Since 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. Methods: To 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. Results: Both 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 Conclusion: Our 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.

Indexed as

acrylamidebisphenolcardiovascular diseasesmicroplasticsplateletsplatelets and cardiovascular diseases

Identifiers

PMID40371341
PMCPMC12075958

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.