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Molecular and biochemical evidence on the role of zearalenone in rat polycystic ovary.

Authors :
Abbasian, Nakisa
Momtaz, Saeideh
Baeeri, Maryam
Navaei-Nigjeh, Mona
Hosseini, Rohollah
Abdollahi, Mohammad
Source :
Toxicon. Nov2018, Vol. 154, p7-14. 8p.
Publication Year :
2018

Abstract

Abstract Globally, food and animal feed contamination with mycotoxins is one of the most important challenges affecting human health. Zearalenone is a non-steroidal mycotoxin with estrogen-like activity that has been reported to induce reproductive dysfunctions including polycystic ovary in women. The aim of this study was to assess the possible impact of prolonged low dose zearalenone (0.1 mg/kg b.w.) exposure to increase the risk of developing polycystic ovary in rats. We found that zearalenone increases the plasma insulin, glucose, testosterone, progesterone and luteinizing hormone levels, while the plasma estradiol level was reduced. Zearalenone also incited tumor necrosis factor-α and the secreted frizzled-related protein-4 expressions. Histological examination showed atresia of follicles in the treated group. It is concluded that zearalenone intoxication intensely manipulates the plasma hormonal factors and the level of gene expressions related to the polycystic ovary in rats, thus increases the risk of its progression. Graphical abstract Image Highlights • ZEA potentially triggers the risk factors of PCO in rats upon 3 months exposure. • The estrogenic effects of ZEA on the reproductive system are proportional to the period and the dosage of application. • ZEA increases gluconeogenesis and insulin secretory functions. • ZEA promotes the level of plasma TNF-α and the expression of Sfrp4 in the period of 3 months. • ZEA causes predominant changes in the structures of follicles in the rat ovaries. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00410101
Volume :
154
Database :
Academic Search Index
Journal :
Toxicon
Publication Type :
Academic Journal
Accession number :
132390921
Full Text :
https://doi.org/10.1016/j.toxicon.2018.07.022