Mechanistic assessment of cadmium toxicity in association with the functions of estrogen receptors in the Langerhans islets | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 16، دوره 22، شماره 4، تیر 2019، صفحه 445-451 اصل مقاله (640.16 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2019.33939.8076 | ||
| نویسندگان | ||
| Perham Mohammadi1؛ Mahban Rahimifard2؛ Maryam Baeeri2؛ Mohammad Abdollahi2، 3؛ Sara Mostafalou* 1 | ||
| 1Department of Pharmacology and Toxicology, School of Pharmacy, Ardabil University of Medical Sciences, Ardabil, Iran | ||
| 2Toxicology and Diseases Group, The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran | ||
| 3Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran | ||
| چکیده | ||
| Objective(s): Diabetes is a metabolic disease with an increasing prevalence for which finding new and efficient therapeutic approaches has always been a challenge. Preserving integrity and functionality of pancreatic β-cells as the only source of insulin in the body is such a case. To achieve this goal different cellular targets have been proposed among which pancreatic estrogen receptors have gotten much attention. In this work, we evaluated the integrity and function of islets of Langerhans under the influence of factors known to intervene with estrogen receptors. Cadmium, a toxic heavy metal, has been recently shown to interact with estrogen receptors but its toxicity in the pancreatic islets regarding this mechanism remains unclear. Materials and Methods: Isolated islets of Langerhans from the pancreas of rats were grouped and treated with cadmium chloride and also cadmium chloride plus β-estradiol. After 24 hr incubation, parameters of cellular viability, oxidative stress, apoptosis, and insulin secretion were measured. Results: The results indicated that cadmium reduced viability of the islets along with an increase in the formation of reactive oxygen species and apoptosis markers, and β-estradiol, in turn, was able to alleviate these disturbances to some extent, implicating the protective role of β-estradiol against pancreatic toxicity of cadmium. Conclusion: It can be concluded that modification of estrogen receptors in the endocrine pancreas and especially β-cells may be a promising target to find a new therapeutic strategy for diabetes and even uncovering mechanisms of environmental toxicants that have been known as risk factors of diabetes. | ||
| کلیدواژهها | ||
| Cadmium؛ Diabetes mellitus؛ Estradiol؛ Estrogen receptors؛ Insulin؛ Islets of langerhans Pancreas | ||
| مراجع | ||
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1. Bahadar H, Mostafalou S, Abdollahi M. Growing burden of diabetes in Pakistan and the possible role of arsenic and pesticides. J Diabetes Metab Disord 2014; 13:117-124. 2. Maqbool F, Mostafalou S, Bahadar H, Abdollahi M. Review of endocrine disorders associated with environmental toxicants and possible involved mechanisms. Life Sci 2016; 145:265-273. 3. Mostafalou S. Persistent organic pollutants and concern over the link with insulin resistance related metabolic diseases. Rev Environ Contam Toxicol 2016; 238:69-89. 4. Mostafalou S, Abdollahi M. Pesticides and human chronic diseases: evidences, mechanisms, and perspectives. Toxicol Appl Pharmacol 2013; 268:157-177. 5. Mostafalou S, Abdollahi M. Pesticides: an update of human exposure and toxicity. Arch Toxicol 2017; 91:549-599. 6. Chen YW, Yang CY, Huang CF, Hung DZ, Leung YM, Liu SH. Heavy metals, islet function and diabetes development. Islets 2009; 1:169-176. 7. Mostafalou S, Abdollahi M. Environmental pollution by mercury and related health concerns: renotice of a silent threat. Arh Hig Rada Toksikol 2013; 64:179-181. 8. Byrne C, Divekar SD, Storchan GB, Parodi DA, Martin MB. Cadmium--a metallohormone? Toxicol Appl Pharmacol 2009; 238:266-271. 9. Tiano JP, Mauvais-Jarvis F. Importance of oestrogen receptors to preserve functional [beta]-cell mass in diabetes. Nat Rev Endocrinol 2012; 8:342-351. 10. El Muayed M, Raja MR, Zhang X, MacRenaris KW, Bhatt S, Chen X, et al. Accumulation of cadmium in insulin-producing beta cells. Islets 2012; 4:405-416. 11. Bahadar H, Maqbool F, Mostafalou S, Baeeri M, Gholami M, Ghafour-Boroujerdi E, et al. The molecular mechanisms of liver and islets of Langerhans toxicity by benzene and its metabolite hydroquinone in vivo and in vitro. Toxicol Mech Methods 2015; 25:628-636. 12. Mostafalou S, Baeeri M, Bahadar H, Soltany-Rezaee-Rad M, Gholami M, Abdollahi M. Molecular mechanisms involved in lead induced disruption of hepatic and pancreatic glucose metabolism. Environ Toxicol Pharmacol 2015; 39:16-26. 13. Moeini-Nodeh S, Rahimifard M, Baeeri M, Abdollahi M. Functional improvement in rats’ pancreatic islets using magnesium oxide nanoparticles through antiapoptotic and antioxidant pathways. Biol Trace Elem Res 2017; 175:146-155. 14. Bahadar H, Maqbool F, Mostafalou S, Baeeri M, Rahimifard M, Navaei-Nigjeh M, et al. Assessment of benzene induced oxidative impairment in rat isolated pancreatic islets and effect on insulin secretion. Environ Toxicol Pharmacol 2015; 39:1161-1169. 15. Nili-Ahmadabadi A, Pourkhalili N, Fouladdel S, Pakzad M, Mostafalou S, Hassani S, et al. On the biochemical and molecular mechanisms by which malathion induces dysfunction in pancreatic islets in vivo and in vitro. Pest Biochem Physiol 2013; 106:51-60. 16. Panza S, Santoro M, De Amicis F, Morelli C, Passarelli V, D’Aquila P, et al. Estradiol via estrogen receptor beta influences ROS levels through the transcriptional regulation of SIRT3 in human seminoma TCam-2 cells. Tumour Biol 2017; 39:1010428317701642 17. Ortmann J, Veit M, Zingg S, Di Santo S, Traupe T, Yang Z, et al. Estrogen receptor-α but not -β or GPER inhibits high glucose-induced human VSMC proliferation: potential role of ROS and ERK. J Clin Endocrinol Metab. 2011; 96:220-228. 18. Llanos P, Contreras-Ferrat A, Barrientos G, Valencia M, Mears D, Hidalgo C. Glucose-dependent insulin secretion in pancreatic β-cell islets from male rats requires ca2+ release via ros-stimulated ryanodine receptors. PLoS One. 2015; 10:e0129238. | ||
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