Institute of Clinical Research West Medical Center

Hiroshima-shi, Japan

Institute of Clinical Research West Medical Center

Hiroshima-shi, Japan
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Fukumoto W.,Hiroshima University | Ishida M.,Hiroshima University | Sakai C.,Hiroshima University | Tashiro S.,Hiroshima University | And 4 more authors.
European Radiology | Year: 2016

Objectives: To investigate whether physical exposure parameters such as the dose index (CTDI), dose length product (DLP), and size-specific dose estimate (SSDE) are predictive of DNA damage. Methods: In vitro, we scanned a phantom containing blood samples from five volunteers at CTDI 50, 100, and 150 mGy. One sample was not scanned. We also scanned samples in three different-size phantoms at CTDI 100 mGy. In vivo, we enrolled 45 patients and obtained blood samples before and after cardiac CT. The γ-H2AX foci were counted. Results: In vitro, in the control and at CTDI 50, 100, and 150 mGy, the number of γ-H2AX was 0.94 ± 0.24 (standard error, SE), 1.28 ± 0.30, 1.91 ± 0.47, and 2.16 ± 0.20. At SSDE 180, 156, and 135 mGy, it was 2.41 ± 0.20, 1.91 ± 0.47, and 1.42 ± 0.20 foci/cell. The γ-H2AX foci were positively correlated with the radiation dose and negatively correlated with the body size. In vivo, the γ-H2AX foci were significantly increased after CT (from 1.21 ± 0.19 to 1.92 ± 0.22 foci/cell) and correlated with CTDI, DLP, and SSDE. Conclusions: DNA damage was induced by cardiac CT. There was a correlation between the physical exposure parameters and γ-H2AX. Key Points: • DNA damage was induced by radiation exposure from cardiac CT. • The γ-H2AX foci number was correlated with the CT radiation dose. • Physical exposure parameters reflect the DNA damage by CT radiation exposure. © 2016 European Society of Radiology


PubMed | Hiroshima University and Institute of Clinical Research West Medical Center
Type: | Journal: European radiology | Year: 2016

To investigate whether physical exposure parameters such as the dose index (CTDI), dose length product (DLP), and size-specific dose estimate (SSDE) are predictive of DNA damage.In vitro, we scanned a phantom containing blood samples from five volunteers at CTDI 50, 100, and 150 mGy. One sample was not scanned. We also scanned samples in three different-size phantoms at CTDI 100 mGy. In vivo, we enrolled 45 patients and obtained blood samples before and after cardiac CT. The -H2AX foci were counted.In vitro, in the control and at CTDI 50, 100, and 150 mGy, the number of -H2AX was 0.94 0.24 (standard error, SE), 1.28 0.30, 1.91 0.47, and 2.16 0.20. At SSDE 180, 156, and 135 mGy, it was 2.41 0.20, 1.91 0.47, and 1.42 0.20 foci/cell. The -H2AX foci were positively correlated with the radiation dose and negatively correlated with the body size. In vivo, the -H2AX foci were significantly increased after CT (from 1.21 0.19 to 1.92 0.22 foci/cell) and correlated with CTDI, DLP, and SSDE.DNA damage was induced by cardiac CT. There was a correlation between the physical exposure parameters and -H2AX. DNA damage was induced by radiation exposure from cardiac CT. The -H2AX foci number was correlated with the CT radiation dose. Physical exposure parameters reflect the DNA damage by CT radiation exposure.

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