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2019/10/15
C3orf70 Is Involved in Neural and Neurobehavioral Development

2019/09/22
Generation of a Triple-Transgenic Zebrafish Line for Assessment of Developmental Neurotoxicity during Neuronal Differentiation

2019/07/17
Aging-associated microstructural deterioration of vertebra in zebrafish

2019/03/18
Zebrafish yolk sac microinjection of thalidomide for assessment of developmental toxicology

2019/02/18
Toxicological Evaluation of SiO2 Nanoparticles by Zebrafish Embryo Toxicity Test

tDNA Damage Response Is Involved in the Developmental Toxicity of Mebendazole in Zebrafish Retina

                     
2016/03/14

Front Pharmacol. 2016 Mar 14;7:57. doi: 10.3389/fphar.2016.00057. eCollection 2016.
DNA Damage Response Is Involved in the Developmental Toxicity of Mebendazole in Zebrafish Retina.
Sasagawa S, Nishimura Y, Kon T, Yamanaka Y, Murakami S, Ashikawa Y, Yuge M, Okabe S, Kawaguchi K, Kawase R, Tanaka T.

Abstract
Intestinal helminths cause iron-deficiency anemia in pregnant women, associated with premature delivery, low birth weight, maternal ill health, and maternal death. Although benzimidazole compounds such as mebendazole (MBZ) are highly efficacious against helminths, there are limited data on its use during pregnancy. In this study, we performed in vivo imaging of the retinas of zebrafish larvae exposed to MBZ, and found that exposure to MBZ during 2 and 3 days post-fertilization caused malformation of the retinal layers. To identify the molecular mechanism underlying the developmental toxicity of MBZ, we performed transcriptome analysis of zebrafish eyes. The analysis revealed that the DNA damage response was involved in the developmental toxicity of MBZ. We were also able to demonstrate that inhibition of ATM significantly attenuated the apoptosis induced by MBZ in the zebrafish retina. These results suggest that MBZ causes developmental toxicity in the zebrafish retina at least partly by activating the DNA damage response, including ATM signaling, providing a potential adverse outcome pathway in the developmental toxicity of MBZ in mammals.

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Frontiers

PubMed