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International Journal of Cell Biology
Volume 2014 (2014), Article ID 850460, 8 pages
Research Article

Mitochondrial DNA and Functional Investigations into the Radiosensitivity of Four Mouse Strains

1Department of Radiation Oncology, University of Florida Shands Cancer Center, 2033 Mowry Road, P.O. Box 103633, Gainesville, FL 32610, USA
2Department of Immunology, Second Military Medical University, Shanghai 200433, China
3First Affiliated Hospital, Fujian Medical University, Fuzhou, Fujian 350108, China
4Institute of Digestive Diseases, Zhengzhou University, Henan 45001, China
5Department of Cardiovascular Diseases, Hospital of Fujian Province, Fuzhou 350004, China
6Department of Physiology, Shanghai University of Sport, Shanghai 100044, China
7Institute of Radiobiology, National Academy of Sciences of Belarus, 220072 Gomel, Belarus

Received 13 September 2013; Accepted 6 December 2013; Published 12 February 2014

Academic Editor: J. R. Davie

Copyright © 2014 Steven B. Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We investigated whether genetic radiosensitivity-related changes in mtDNA/nDNA ratios are significant to mitochondrial function and if a material effect on mtDNA content and function exists. BALB/c (radiosensitive), C57BL/6 (radioresistant), and F1 hybrid mouse strains were exposed to total body irradiation. Hepatic genomic DNA was extracted, and mitochondria were isolated. Mitochondrial oxygen consumption, ROS, and calcium-induced mitochondrial swelling were measured. Radiation influenced strain-specific survival in vivo. F1 hybrid survival was influenced by maternal input. Changes in mitochondrial content corresponded to survival in vivo among the 4 strains. Calcium-induced mitochondrial swelling was strain dependent. Isolated mitochondria from BALB/c mice were significantly more sensitive to calcium overload than mitochondria from C57BL/6 mice. Maternal input partially influenced the recovery effect of radiation on calcium-induced mitochondrial swelling in F1 hybrids; the hybrid with a radiosensitive maternal lineage exhibited a lower rate of recovery. Hybrids had a survival rate that was biased toward maternal input. mtDNA content and mitochondrial permeability transition pores (MPTP) measured in these strains before irradiation reflected a dominant input from the parent. After irradiation, the MPTP opened sooner in radiosensitive and hybrid strains, likely triggering intrinsic apoptotic pathways. These findings have important implications for translation into predictors of radiation sensitivity/resistance.