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Antiestrogenic potentials of ortho-PCB congeners by single or complex exposure

Authors
Oh, SM[Oh, Seung Min]Ryu, BT[Ryu, Byung Taek]Lee, SK[Lee, Sang Ki]Chung, KH[Chung, Kyu Hyuck]
Issue Date
Feb-2007
Publisher
PHARMACEUTICAL SOCIETY KOREA
Keywords
ortho-PCB congeners; complex mixture; antiestrogenic activity; E-screen assay; EROD activity; aromatase activity
Citation
ARCHIVES OF PHARMACAL RESEARCH, v.30, no.2, pp.199 - 209
Indexed
SCIE
SCOPUS
KCI
Journal Title
ARCHIVES OF PHARMACAL RESEARCH
Volume
30
Number
2
Start Page
199
End Page
209
URI
https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/85031
DOI
10.1007/BF02977695
ISSN
0253-6269
Abstract
Di-ortho PCB congeners 52, 138, 153 and 180, and the mono-ortho coplanar congener 118 have been detected as a complex mixture in human tissue in Korea. This study examined the antiestrogenic effects of samples exposed to single or combination treatment of the ortho-PCB congeners. In order to determined the combined toxicity, a sample mixture (M1, M2, M3, M4, and M5) was designed based on the ortho-PCB congeners found in Korean human tissue. With the exception of PCB 52, the ortho-PCB congeners (PCB 118, 138, 153, and 180) showed weak antiestrogenic activity. The antiestrogenic activity of di-ortho PCB congeners (PCB 138, 153, and 180) was induced by the depletion of endogenous E-2 as well as through the ER-dependent pathway, whereas the antiestrogenic activity of mono-ortho PCB 118 was only induced through the depletion of endogenous E-2. When the MCF7-BUS cells were treated with mixtures containing the no effective concentration (10(-6) M) of the PCB congeners, M3 (PCB 118 + PCB 138 + PCB 180) and M4 (PCB 118 + PCB 138) had an antiestrogenic effect but the other mixtures (M 1; PCB 52 + PCB 118 + PCB 138 + PCB 180, M2; PCB 118 + PCB 138 + PCB 153 + PCB 180, M5; PCB 118 + PCB 180) did not. Although the mechanism for the interaction between the PCB congeners is not completely understood, it was presumed that exposure to a mixture of the PCB congeners might have synergistic effects on their antiestrogenicity through the ER-independent pathway.
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