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Orally Administered 6:2 Chlorinated Polyfluorinated Ether Sulfonate (F-53B) Causes Thyroid Dysfunction in Rats

DC FieldValueLanguage
dc.contributor.author김성희-
dc.contributor.author남기택-
dc.date.accessioned2021-01-19T08:03:28Z-
dc.date.available2021-01-19T08:03:28Z-
dc.date.issued2020-09-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/181442-
dc.description.abstractThe compound 6:2 chlorinated polyfluorinated ether sulfonate (F-53B), a replacement for perfluorooctanesulfonate (PFOS) in the electroplating industry, has been widely detected in numerous environmental matrices, human sera, and organisms. Due to regulations that limit PFOS use, F-53B use is expected to increase. Therefore, in this study, we performed a subchronic oral toxicity study of F-53B in Sprague Dawley (SD) rats. F-53B was administered orally once daily to male and female rats for 28 days at doses of 5, 20, and 100 mg/kg/day. There were no toxicologically significant changes in F-53B-treated rats, except in the thyroid gland. However, F-53B slightly reduced the serum concentrations of thyroid hormones, including triiodothyronine and thyroxine, compared with their concentrations in the vehicle group. F-53B also induced follicular hyperplasia and was associated with increased thyroid hormone biosynthesis-associated protein expression. These results demonstrate that F-53B is a strong regulator of thyroid hormones in SD rats as it disrupts thyroid function. Thus, caution should be exercised in the industrial application of F-53B as an alternative for PFOS.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherMDPI AG-
dc.relation.isPartOfTOXICS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleOrally Administered 6:2 Chlorinated Polyfluorinated Ether Sulfonate (F-53B) Causes Thyroid Dysfunction in Rats-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentBioMedical Science Institute (의생명과학부)-
dc.contributor.googleauthorSo-Hye Hong-
dc.contributor.googleauthorSeung Hee Lee-
dc.contributor.googleauthorJun-Young Yang-
dc.contributor.googleauthorJin Hee Lee-
dc.contributor.googleauthorKi Kyung Jung-
dc.contributor.googleauthorJi Hyun Seok-
dc.contributor.googleauthorSung-Hee Kim-
dc.contributor.googleauthorKi Taek Nam-
dc.contributor.googleauthorJayoung Jeong-
dc.contributor.googleauthorJong Kwon Lee-
dc.contributor.googleauthorJae-Ho Oh-
dc.identifier.doi10.3390/toxics8030054-
dc.contributor.localIdA06017-
dc.contributor.localIdA01243-
dc.contributor.localIdA01243-
dc.relation.journalcodeJ03975-
dc.identifier.eissn2305-6304-
dc.identifier.pmid32784452-
dc.subject.keywordF-53B-
dc.subject.keywordsubchronic oral toxicity-
dc.subject.keywordthyroid dysfunction-
dc.subject.keywordthyroid hormone-
dc.contributor.alternativeNameKim, Sung-Hee-
dc.contributor.affiliatedAuthor김성희-
dc.contributor.affiliatedAuthor남기택-
dc.contributor.affiliatedAuthor남기택-
dc.citation.volume8-
dc.citation.number3-
dc.citation.startPage54-
dc.identifier.bibliographicCitationTOXICS, Vol.8(3) : 54, 2020-09-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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