Estrogenic endocrine-disrupting chemicals modulate the production of inflammatory mediators and cell viability of lipopolysaccharide-stimulated macrophages

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dc.contributor.authorH G Kim-
dc.contributor.authorS M Yeon-
dc.contributor.authorK H Kim-
dc.contributor.authorH Kim-
dc.contributor.authorJ I Park-
dc.contributor.authorH J Kang-
dc.contributor.authorE J Cha-
dc.contributor.authorH D Park-
dc.contributor.authorH J Kang-
dc.contributor.authorT W Park-
dc.contributor.authorY H Jeon-
dc.contributor.authorY I Park-
dc.contributor.authorKyu Tae Chang-
dc.contributor.authorY W Jung-
dc.date.accessioned2017-04-19T10:10:46Z-
dc.date.available2017-04-19T10:10:46Z-
dc.date.issued2015-
dc.identifier.issn03603997-
dc.identifier.uri10.1007/s10753-014-9966-2ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/12823-
dc.description.abstractEstrogenic endocrine-disrupting chemicals (EDCs) are exogenous substances that act as competitive inhibitors of estrogen in the endocrine system. By disrupting the endocrine system, EDCs can cause severe disabilities and diseases, including cancers and altered sexual development. Although the influence of these molecules in the endocrine system is evident, the effects of EDCs on the immune system as well as their cytotoxicity have been poorly examined. Therefore, we selected 21 EDCs that are commonly found in Korean ecosystems, such as surface waters and effluents, and studied their immunologic effects by comparing nitric oxide (NO) production and cytotoxicity in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells (RAW cells), a macrophage cell line. Among the EDCs tested, fenitrothion (FTH) inhibited the messenger RNA (mRNA) expression of inducible NO synthase (iNOS), resulting in reduced NO production, while treatment with andostenedione (AD), diethyl phthalate, di-n-butyl phthalate (DBP), estriol, or molinate decreased production of NO in an iNOS-independent fashion. In contrast, benzo(a)pyrene (B(a)P) increased the production of NO in RAW cells. In addition, AD, DBP, or FTH inhibited the mRNA expression of tumor necrosis factor alpha or interleukin-1 beta. Treatment with 17-α-ethynylestradiol, 17-β-estradiol, 4-n-butyl phenol, or alachlor induced apoptosis of RAW cells, while dicyclohexyl phthalate and B(a)P caused cell death in an apoptosis-independent manner. These data suggest that EDCs can influence the immune response to pathogens by modulating the functions of macrophages.-
dc.publisherSpringer-
dc.titleEstrogenic endocrine-disrupting chemicals modulate the production of inflammatory mediators and cell viability of lipopolysaccharide-stimulated macrophages-
dc.title.alternativeEstrogenic endocrine-disrupting chemicals modulate the production of inflammatory mediators and cell viability of lipopolysaccharide-stimulated macrophages-
dc.typeArticle-
dc.citation.titleInflammation-
dc.citation.number2-
dc.citation.endPage605-
dc.citation.startPage595-
dc.citation.volume38-
dc.contributor.alternativeName김현경-
dc.contributor.alternativeName연승민-
dc.contributor.alternativeName김경훈-
dc.contributor.alternativeName김희중-
dc.contributor.alternativeName박종일-
dc.contributor.alternativeName강현진-
dc.contributor.alternativeName차은지-
dc.contributor.alternativeName박희등-
dc.contributor.alternativeName강효정-
dc.contributor.alternativeName박태원-
dc.contributor.alternativeName전영호-
dc.contributor.alternativeName박영인-
dc.contributor.alternativeName장규태-
dc.contributor.alternativeName정용우-
dc.identifier.bibliographicCitationInflammation, vol. 38, no. 2, pp. 595-605-
dc.identifier.doi10.1007/s10753-014-9966-2-
dc.subject.keywordcell death-
dc.subject.keywordestrogenic endocrine-disrupting chemical-
dc.subject.keywordmacrophage-
dc.subject.keywordnitric oxide-
dc.subject.keywordproinflammatory cytokine-
dc.subject.localcell death-
dc.subject.localCell death-
dc.subject.localestrogenic endocrine-disrupting chemical-
dc.subject.localmacrophage-
dc.subject.localMacrophage-
dc.subject.localnitric oxide-
dc.subject.localNitric oxide (NO)-
dc.subject.localproinflammatory cytokine-
dc.subject.localPro-inflammatory cytokine-
dc.description.journalClassY-
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