Embryonic exposure to diclofenac disturbs actin organization and leads to myofibril misalignment
Article first published online: 17 MAR 2011
© 2011 Wiley-Liss, Inc.
Birth Defects Research Part B: Developmental and Reproductive Toxicology
Volume 92, Issue 2, pages 139–147, April 2011
How to Cite
Chen, Y.-H., Chang, C.-Y., Wang, Y.-H., Wen, C.-C., Chen, Y.-C., Hu, S.-C., Yu, D.-S. and Chen, Y.-H. (2011), Embryonic exposure to diclofenac disturbs actin organization and leads to myofibril misalignment. Birth Defects Research Part B: Developmental and Reproductive Toxicology, 92: 139–147. doi: 10.1002/bdrb.20292
- Issue published online: 11 APR 2011
- Article first published online: 17 MAR 2011
- Manuscript Accepted: 14 FEB 2011
- Manuscript Received: 15 DEC 2010
- The Zebrafish International Resource Center. Grant Numbers: P40 RR012546, NIH-NCRR
- National Science Council, Republic of China. Grant Number: NSC 97-2313-B-032-001-MY3
The objective of this study was to investigate the embryotoxicity of diclofenac. Zebrafish (Danio rerio) embryos at 12 hpf were treated with different dosages of diclofenac (0–2,000 ppm) for different time courses (12–72 hr). Results showed no evident differences in survival rates or morphological changes between the mock-treated control (0 ppm) zebrafish embryos and those with 1-ppm diclofenac-exposure (12–24, 12–36 hpf). In contrast, after higher doses (5 and 10 ppm) of exposure, embryos displayed some defective phenotypes, including malformed somite boundary, a twisted body axis, and shorter body length. In addition, diclofenac-treated embryos exhibited significantly reduced frequencies of spontaneous in-chorion contractions in comparison with mock-control littermates (mock-control: 13.20±2.24 vs. 5–10 ppm diclofenac: 6.66±1.35–3.03±1.84). Subtle changes were easily observed by staining with specific monoclonal antibodies F59 and phalloidin to detect morphological changes in muscle fibers and formation of F-actin, respectively. Our data show that diclofenac treatment disturbs actin organization and muscle fiber alignment, thus causing malformed somite phenotypes. Birth Defects Res (Part B) 92:139–147, 2011. © 2011 Wiley-Liss, Inc.