TCDD-induced chick cardiotoxicity is abolished by a selective cyclooxygenase-2 (COX-2) inhibitor NS398

Fujisawa, Nozomi; Nakayama, Shouta M.M.; Ikenaka, Yoshinori et al.

Archives of Toxicology, 2014, 88(9), 1739-1748

Permalink : https://hdl.handle.net/2115/59756

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アクセス権
open access
URI
https://hdl.handle.net/2115/59756
タイトル
TCDD-induced chick cardiotoxicity is abolished by a selective cyclooxygenase-2 (COX-2) inhibitor NS398
著者
Fujisawa, Nozomi ; Nakayama, Shouta M.M. ; Ikenaka, Yoshinori ; Ishizuka, Mayumi
著者名
Fujisawa, Nozomi
著者名
Nakayama, Shouta M.M.
e-Rad_Researcher
40543509
著者名
Ikenaka, Yoshinori
e-Rad_Researcher
50332474
著者名
Ishizuka, Mayumi
言語
英語
キーワード
Atrial natriuretic factor
Cardiac malformation
Chick embryo
Cyclooxygenase-2 inhibitor
Nongenomic pathway
TCDD
発行日
2014-09
出版者
Springer
収録物名
Archives of Toxicology
巻(号)
88(9)
ページ
1739-1748
抄録
Halogenated aromatic hydrocarbons, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), are known to cause severe heart defects in avian species. However, the mechanism of TCDD-induced chick cardiovascular toxicity is unclear. In this study, we investigated cyclooxygenase-2 (COX-2) as a possible mechanism of TCDD-induced cardiotoxicity. Fertile chicken eggs were injected with TCDD and a COX-2 selective inhibitor, NS398, and we investigated chick heart failure on day 10. We found that the chick heart to body weight ratio and atrial natriuretic factor mRNA expression were increased, but this increase was abolished with treatment of NS398. In addition, the morphological abnormality of an enlarged ventricle resulting from TCDD exposure was also abolished with co-treatment of TCDD and NS398. Our results suggested that TCDD-induced chick heart defects are mediated via the nongenomic pathway and that they do not require the genomic pathway.
資源タイプ
学術雑誌論文
出版タイプ
Accepted Manuscript
権利情報
The final publication is available at link.springer.com
PISSN
0340-5761
NCID
AA00548865
関連情報 (isVersionOf)
出版社版DOI
https://doi.org/10.1007/s00204-014-1225-7