Evidence map›Paper›PMID 39968403›Full record

ArticleData in brief2025

Sub-network transcriptome dataset for diseases associated with exposure to bisphenol F and bisphenol S in human SH-SY5Y neuroblastoma cells.

Andrea Guzman, Christina L Sanchez, Emma Ivantsova, Jacqueline Watkins, Sara Sutton, Christopher L Souders, Christopher J Martyniuk

Abstract read
In one paragraph

Article in Data in brief, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Andrea GuzmanCenter for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, UF Genetics Institute, Interdisciplinary Program in Biomedical Sciences Neuroscience, University of Florida, Gainesville, FL 32611, USA.
Christina L SanchezCenter for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, UF Genetics Institute, Interdisciplinary Program in Biomedical Sciences Neuroscience, University of Florida, Gainesville, FL 32611, USA.
Emma IvantsovaCenter for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, UF Genetics Institute, Interdisciplinary Program in Biomedical Sciences Neuroscience, University of Florida, Gainesville, FL 32611, USA.
Jacqueline WatkinsCenter for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, UF Genetics Institute, Interdisciplinary Program in Biomedical Sciences Neuroscience, University of Florida, Gainesville, FL 32611, USA.
Sara SuttonCenter for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, UF Genetics Institute, Interdisciplinary Program in Biomedical Sciences Neuroscience, University of Florida, Gainesville, FL 32611, USA.
Christopher L SoudersCenter for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, UF Genetics Institute, Interdisciplinary Program in Biomedical Sciences Neuroscience, University of Florida, Gainesville, FL 32611, USA.
Christopher J MartyniukCenter for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine, UF Genetics Institute, Interdisciplinary Program in Biomedical Sciences Neuroscience, University of Florida, Gainesville, FL 32611, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bisphenol A replacement chemicals can result in toxicity to neuronal cells, however, the underlying mechanisms are not well characterized. Transcriptome analysis was conducted in the neuronal SH-SY5Y human cell line following exposure of cells to either bisphenol F (BPF) or bisphenol S (BPS) at a concentration of 0.1 nM. Transcriptome data were used to predict which diseases were associated with bisphenol exposure using sub-network enrichment analysis. There were 305 subnetworks perturbed by BPF and 279 subnetworks perturbed by BPS. Top gene sets altered by BPF included urticaria, gastric lesion, attention deficit disorder, familial Mediterranean fever, malocclusion, and lupus erythematosus while for BPS, top gene sets included chronic urticaria, polymyositis, genital herpes, and hypergammaglobulinemia. There were 164 common diseases identified between BPF and BPS datasets. These included protein regulators of androgen deficiency, cerebral toxoplasmosis, metabolic alkalosis, panic attack, T-helper lymphocyte infiltration and vitiligo. Data can be re-used in regulatory toxicology to characterize biomarkers of exposure and elucidate common molecular responses to bisphenol replacements.

Indexed as

Bisphenol replacementsInflammatory pathwaysNeurotoxicityProtein foldingProtein translation

Identifiers

PMID39968403
PMCPMC11833777

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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 OpenQuestion graph.