Title:
Bisphenol S dysregulates thyroid hormone homeostasis; Testicular survival, redox and metabolic status: Ameliorative actions of melatonin

dc.contributor.authorAishwarya Sahu
dc.contributor.authorRakesh Verma
dc.date.accessioned2026-02-07T11:25:50Z
dc.date.issued2023
dc.description.abstractBisphenol S (BPS) is an incipient threat for reproductive health augmenting societal burden of infertility worldwide. In the present study, we investigated the mechanism of BPS induced testicular dysfunctions and protective actions of melatonin in mice. BPS (150 mg/kg BW) treatment reduced serum T3/T4, testosterone and elevated insulin levels along with adverse effect on thyroid and testicular histoarchitecture. Further, BPS treatment compromised sperm quality, reduced mRNA expression of steroidogenic (StAR/CYP11A1) markers, elevated oxidative load and disrupts metabolic status. However, melatonin (5 mg/kg BW) administration to BPS treated mice showed improved hormonal/histological parameters, enhanced thyroid hormone (TR-α/Dio-2)/melatonin (MT-1) receptor expressions. Further, melatonin treatment modulated the expression of testicular survival/redox (SIRT1/PGC-1α/FOXO-1, Nrf2/HO-1, p-JAK2/p-STAT3), proliferative (PCNA) and metabolic (IR/pAKT/GLUT-1) markers. Furthermore, melatonin treatment enhanced testicular antioxidant status and reduced caspase-3 expression. In conclusion, our results showed that BPS induces endocrine/oxidative and metabolic anomalies while melatonin improved male reproductive health. © 2023 Elsevier B.V.
dc.identifier.doi10.1016/j.etap.2023.104300
dc.identifier.issn13826689
dc.identifier.urihttps://doi.org/10.1016/j.etap.2023.104300
dc.identifier.urihttps://dl.bhu.ac.in/bhuir/handle/123456789/44190
dc.publisherElsevier B.V.
dc.subjectBPS/Melatonin
dc.subjectIR/pAkt/GLUT-1
dc.subjectp-JAK2/p-STAT3
dc.subjectSIRT1/PGC-1α/Nrf2
dc.subjectTestes
dc.subjectTR-α/Dio-2
dc.titleBisphenol S dysregulates thyroid hormone homeostasis; Testicular survival, redox and metabolic status: Ameliorative actions of melatonin
dc.typePublication
dspace.entity.typeArticle

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