Estrogenic Endocrine-Disrupting Chemicals Modulate the Production of Inflammatory Mediators and Cell Viability of Lipopolysaccharide-Stimulated Macrophages
- Authors
- Kim, Hyun Gyung; Yeon, Seung-min; Kim, Kyong Hoon; Kim, Heejoong; Park, Jong-Il; Kang, Hyun-Jin; Cha, Eun Ji; Park, Hee-Deung; Kang, Hyo Jung; Park, Tae Won; Jeon, Young-Ho; Park, Young In; Chang, Kyu-Tae; Jung, Yong Woo
- Issue Date
- Apr-2015
- Publisher
- SPRINGER/PLENUM PUBLISHERS
- Keywords
- estrogenic endocrine-disrupting chemical; macrophage; nitric oxide; proinflammatory cytokine; cell death
- Citation
- INFLAMMATION, v.38, no.2, pp 595 - 605
- Pages
- 11
- Journal Title
- INFLAMMATION
- Volume
- 38
- Number
- 2
- Start Page
- 595
- End Page
- 605
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/9670
- DOI
- 10.1007/s10753-014-9966-2
- ISSN
- 0360-3997
1573-2576
- Abstract
- Estrogenic 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-alpha-ethynylestradiol, 17-beta-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.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - College of Natural Sciences > Department of Life Science > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/9670)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.