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Early embryonic exposure of ionizing radiations disrupts zebrafish pigmentation
Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk kemi och biofysik.
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2019 (Engelska)Ingår i: Journal of Cellular Physiology, ISSN 0021-9541, E-ISSN 1097-4652, Vol. 234, nr 1, s. 940-949Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Studies have demonstrated that zebrafish are powerful tools for monitoring environmental toxicity, including radiation hazard. Here we investigated the developmental toxicity of ionizing radiation (IR) in an in vivo embryonic zebrafish model. The effects of heavy ion (C-12(6+)), proton, and X-ray radiation on early zebrafish embryos were determined. A similar dose-dependent decrease in the hatch and survival rate of zebrafish embryos was observed after exposure to these irradiations. Exposure of zebrafish embryos to 1-4 Gy IR caused significant loss of pigmentation. Quantitative real-time reverse transcription polymerase chain reaction, western blot analysis, and in situ hybridization (ISH) experiment revealed that atp5 alpha 1 was markedly upregulated in irradiated zebrafish embryos. In addition, IR resulted in a rapid decrease in total adenosine triphosphate (ATP) generation. With dual functions of synthesizing or hydrolyzing ATP, ATP synthase regulated H+ transport crossing the mitochondrial inner. Administration of the mitochondrial ATP synthase inhibitor, oligomycin, partially restored pigmentation in irradiated zebrafish embryos, but the ATPase inhibitor, BTB06584, had no effect. Taken together, these results showed that IR exposure downregulated zebrafish pigmentation through regulation of H+ ion transport in mitochondria.

Ort, förlag, år, upplaga, sidor
WILEY , 2019. Vol. 234, nr 1, s. 940-949
Nyckelord [en]
ATP synthase, ionizing radiation, pigmentation, zebrafish
Nationell ämneskategori
Utvecklingsbiologi
Identifikatorer
URN: urn:nbn:se:umu:diva-154330DOI: 10.1002/jcp.26922ISI: 000451533300079PubMedID: 30144054OAI: oai:DiVA.org:umu-154330DiVA, id: diva2:1271899
Tillgänglig från: 2018-12-18 Skapad: 2018-12-18 Senast uppdaterad: 2018-12-18Bibliografiskt granskad

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Zhou, Xin

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