ArticleHeliyon2020
Estrogens counteract tributyltin-induced toxicity in the rat islets of Langerhans.
Article in Heliyon, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Endocrine disruptors, insulin resistance, and diabetes.Turkish journal of medical sciences · 2025Review
- Azelaic acid reduces arsenic-induced toxicity and inflammation in the rat islets of langerhans.Iranian journal of basic medical sciences · 2025Article
- Male Reproductive Toxicity of Antifouling Chemicals: Insights into Oxidative Stress-Induced Infertility and Molecular Mechanisms of Zinc Pyrithione (ZPT).Antioxidants (Basel, Switzerland) · 2024Review
- Trimetazidine Preconditioning Potentiates the Effect of Mesenchymal Stem Cells Secretome on the Preservation of Rat Pancreatic Islet Survival and Function In Vitro.Applied biochemistry and biotechnology · 2023Article
- Application of In Vitro Models for Studying the Mechanisms Underlying the Obesogenic Action of Endocrine-Disrupting Chemicals (EDCs) as Food Contaminants-A Review.International journal of molecular sciences · 2023Review
- Screening of Metabolism-Disrupting Chemicals on Pancreatic α-Cells Using In Vitro Methods.International journal of molecular sciences · 2022Article
- In Vitro Assays to Identify Metabolism-Disrupting Chemicals with Diabetogenic Activity in a Human Pancreatic β-Cell Model.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTributyltin (TBT) is known as an endocrine disruptor able to interfere with estrogen receptors (ERs) leading to toxic effects on the related endocrine pathways. TBT is an obesogen, reported to disrupt glucose homeostasis leading to diabetes. The aim of this study was to assess the influence of TBT and β-estradiol on the pancreatic islets of Langerhans in simultaneous exposures. EXPERIMENTAL: Pancreatic islets of 15 male rat were isolated and exposed to TBT (10 μM), β-estradiol, and TBT plus β-estradiol for 24 h. Therewith, cellular viability, oxidative stress, apoptosis, and insulin secretion markers were investigated.
resultsTBT decreased the viability and increased the apoptosis, reactive oxygen species, and insulin secretion TBT led to increased amounts of apaptosis, reactive oxygen species (ROS), and insulin secretion in pancreatic islets; however, cellular viability was reduced. Co-exposure with β-estradiol ameliorated the entire mentioned variables near to the control level.
conclusionThese results showed that β-estradiol protect pancreatic islets of Langerhans against TBT-induced toxicity by counteracting oxidative stress and apoptosis as well as insulin secretion. In this way, it is postulated that pancreatic ER pathways particularly in β-cells might be the determinant target of toxic effects of xenoestrogens like TBT. Hence, evaluation of xenoestrogens-induced ER dysfunction in the endocrine pancreas can be helpful in diabetic risk assessment of these contaminants. Pharmacological modifications of ER pathway in the β-cells seems promising for better management of diabetes.
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Registered trials
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