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Estrogens Counteract Tributyltin-Induced Toxicity in the Rat Islets of Langerhans Publisher



Ghaemmaleki F1 ; Mohammadi P2 ; Baeeri M3, 4 ; Navaeinigjeh M3, 4 ; Abdollahi M3, 4 ; Mostafalou S1
Authors
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Authors Affiliations
  1. 1. Department of Pharmacology and Toxicology, School of Pharmacy, Ardabil University of Medical Sciences, Iran
  2. 2. Department of Physiology and Pharmacology, School of Medicine, Ardabil University of Medical Sciences, Iran
  3. 3. Toxicology and Diseases Group, Pharmaceutical Sciences Research Center (PSRC), The Institute of Pharmaceutical Sciences (TIPS), Tehran, Iran
  4. 4. Department of Toxicology and Pharmacology, School of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran

Source: Heliyon Published:2020


Abstract

Background: Tributyltin (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. Results: TBT 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. Conclusion: These 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. © 2020; β-estradiol; Diabetes; Estrogen receptors; Islets of Langerhans; Tributyltin; Endocrinology; Health sciences; Pharmacology; Reproductive system; Toxicology © 2020
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