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Zhou, Xin
Alternative names
Publications (2 of 2) Show all publications
Wang, Y., Zhou, X., Zhao, B., Ren, X., Chen, Y., Si, J., . . . Zhang, H. (2019). Early embryonic exposure of ionizing radiations disrupts zebrafish pigmentation. Journal of Cellular Physiology, 234(1), 940-949
Open this publication in new window or tab >>Early embryonic exposure of ionizing radiations disrupts zebrafish pigmentation
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2019 (English)In: Journal of Cellular Physiology, ISSN 0021-9541, E-ISSN 1097-4652, Vol. 234, no 1, p. 940-949Article in journal (Refereed) 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.

Place, publisher, year, edition, pages
WILEY, 2019
ATP synthase, ionizing radiation, pigmentation, zebrafish
National Category
Developmental Biology
urn:nbn:se:umu:diva-154330 (URN)10.1002/jcp.26922 (DOI)000451533300079 ()30144054 (PubMedID)
Available from: 2018-12-18 Created: 2018-12-18 Last updated: 2018-12-18Bibliographically approved
Moodie, L. W. K., Hubert, M., Zhou, X., Albers, M. F., Lundmark, R., Wanrooij, S. & Hedberg, C. (2019). Photoactivated Colibactin Probes Induce Cellular DNA Damage. Angewandte Chemie International Edition, 58(5), 1417-1421
Open this publication in new window or tab >>Photoactivated Colibactin Probes Induce Cellular DNA Damage
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2019 (English)In: Angewandte Chemie International Edition, ISSN 1433-7851, E-ISSN 1521-3773, Vol. 58, no 5, p. 1417-1421Article in journal (Refereed) Published
Abstract [en]

Colibactin is a small molecule produced by certain bacterial species of the human microbiota that harbour the pks genomic island. Pks(+) bacteria induce a genotoxic phenotype in eukaryotic cells and have been linked with colorectal cancer progression. Colibactin is produced in a benign, prodrug form which, prior to export, is enzymatically matured by the producing bacteria to its active form. Although the complete structure of colibactin has not been determined, key structural features have been described including an electrophilic cyclopropane motif, which is believed to alkylate DNA. To investigate the influence of the putative "warhead" and the prodrug strategy on genotoxicity, a series of photolabile colibactin probes were prepared that upon irradiation induced a pks(+) like phenotype in HeLa cells. Furthermore, results from DNA cross-linking and imaging studies of clickable analogues enforce the hypothesis that colibactin effects its genotoxicity by directly targeting DNA.

click chemistry, colibactin, DNA damage, microbiome, photochemistry
National Category
Biochemistry and Molecular Biology
urn:nbn:se:umu:diva-156892 (URN)10.1002/anie.201812326 (DOI)000458826100026 ()30506956 (PubMedID)
Available from: 2019-03-11 Created: 2019-03-11 Last updated: 2019-03-11Bibliographically approved

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