{"title":"双酚S失调甲状腺激素稳态；睾丸存活、氧化还原和代谢状态：褪黑素的改善作用。","authors":"Aishwarya Sahu , Rakesh Verma","doi":"10.1016/j.etap.2023.104300","DOIUrl":null,"url":null,"abstract":"<div><p><span>Bisphenol 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 </span>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.</p></div>","PeriodicalId":11775,"journal":{"name":"Environmental toxicology and pharmacology","volume":"104 ","pages":"Article 104300"},"PeriodicalIF":4.2000,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Bisphenol S dysregulates thyroid hormone homeostasis; Testicular survival, redox and metabolic status: Ameliorative actions of melatonin\",\"authors\":\"Aishwarya Sahu , Rakesh Verma\",\"doi\":\"10.1016/j.etap.2023.104300\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p><span>Bisphenol 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 </span>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.</p></div>\",\"PeriodicalId\":11775,\"journal\":{\"name\":\"Environmental toxicology and pharmacology\",\"volume\":\"104 \",\"pages\":\"Article 104300\"},\"PeriodicalIF\":4.2000,\"publicationDate\":\"2023-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Environmental toxicology and pharmacology\",\"FirstCategoryId\":\"93\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1382668923002429\",\"RegionNum\":3,\"RegionCategory\":\"环境科学与生态学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENVIRONMENTAL SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Environmental toxicology and pharmacology","FirstCategoryId":"93","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1382668923002429","RegionNum":3,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
Bisphenol S dysregulates thyroid hormone homeostasis; Testicular survival, redox and metabolic status: Ameliorative actions of melatonin
Bisphenol 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.
期刊介绍：
Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man.
Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals.
In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.
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