Affiliations 

  • 1 Research Center for Inland Seas (KURCIS), Kobe University, Fukaeminami-machi, Higashinada-ku, Kobe 658-0022, Japan. Electronic address: horie@people.kobe-u.ac.jp
  • 2 Graduate School of Maritime Science, Kobe University, Fukaeminami-machi, Higashinada-ku, Kobe 658-0022, Japan
  • 3 Research Center for Inland Seas (KURCIS), Kobe University, Fukaeminami-machi, Higashinada-ku, Kobe 658-0022, Japan; Department of Environmental Biotechnology, School of Environmental Sciences, Bharathidasan University, Tiruchirappalli 620024, India
  • 4 School of Human Sciences, Kobe College, 4-1 Okadayama, Nishinomiya, Hyogo, Iwate 662-8505, Japan
  • 5 Department of Biology, Faculty of Science, University Putra Malaysia, 43400 UPM Serdang, Selangor, Malaysia
  • 6 Research Center for Inland Seas (KURCIS), Kobe University, Fukaeminami-machi, Higashinada-ku, Kobe 658-0022, Japan
PMID: 36470400 DOI: 10.1016/j.cbpc.2022.109531

Abstract

Water pollution due to plasticizers is one of the most severe environmental problems worldwide. Phthalate plasticizers can act as endocrine disruptors in vertebrates. In this study, we investigated whether the non-phthalate bis(2-ethylhexyl) sebacate (DEHS) plasticizer can act as an endocrine disruptor by evaluating changes in the expression levels of thyroid hormone-related, reproduction-related, and estrogen-responsive genes of Japanese medaka (Oryzias latipes) exposed to the plasticizer. Following the exposure, the gene expression levels of thyroid-stimulating hormone subunit beta (tshβ), deiodinase 1 (dio1), and thyroid hormone receptor alpha (trα) did not change. Meanwhile, DEHS suppressed dio2 expression, did not induce swim bladder inflation, and eventually reduced the swimming performance of Japanese medaka. These findings indicate that DEHS can potentially disrupt the thyroid hormone-related gene expression and metabolism of these fish. However, exposure to DEHS did not induce changes in the gene expression levels of kisspeptin 1 (kiss1), gonadotropin-releasing hormone (gnrh), follicle-stimulating hormone beta (fshβ), luteinizing hormone beta (lhβ), choriogenin H (chgH), and vitellogenin (vtg) in a dose-dependent manner. This is the first report providing evidence that DEHS can disrupt thyroid hormone-related metabolism in fish.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.