Medical Radiology and Radiation Safety. 2026. Vol. 71. № 3

DOI:10.33266/1024-6177-2026-71-3-11-18

V.I. Arkhipova¹, A.M. Lyaginskaya¹, O.V. Parinov¹, R.M. Sarimov², S.A. Abdullaev¹,² 

Mitochondrial Dysfunction in the Ovaries and Blood Lymphocytes of Mice and their Offspring after Exposure to X-Ray Radiation

1 A.I. Burnazyan Federal Medical Biophysical Center, Moscow, Russia

² A.M. Prokhorov General Physics Institute, Moscow, Russia

Contact person: V.I. Arkhipova, e-mail: This email address is being protected from spambots. You need JavaScript enabled to view it.  

ABSTRACT 

Objective: To experimentally investigate the long-term effects of X-ray irradiation at a dose of 2 Gy in female mice and the transgenerational transmission of mitochondrial dysfunction to their offspring.

Materials and methods: In the blood lymphocytes and ovarian tissue of irradiated female mice (one month post-exposure) and their F1 offspring, we assessed damage to nuclear (nDNA) and mitochondrial (mtDNA) DNA using long-range quantitative PCR (Q-PCR); the total mtDNA copy number; the level of mutant mtDNA copies (D-loop 1 gene); and markers of oxidative stress, namely malondialdehyde (MDA) and reduced glutathione (GSH).

Results: A tissue-specific response was observed in irradiated females. Lymphocytes showed no gross nDNA damage (normal Q-PCR), alongside a moderate increase in mtDNA mutations (+8%) and a trend toward reduced mtDNA copy number. In the ovaries of irradiated females, we registered a persistent decrease in Q-PCR product yield, a significant reduction in mtDNA copy number, the highest level of mutations (+11%), and elevated MDA. Offspring of irradiated females exhibited an increased level of mutant mtDNA copies in both lymphocytes (+8%) and ovaries (+11%); however, a decrease in Q-PCR products and elevated MDA were observed only in the ovaries. GSH levels did not change significantly in any of the groups.

Conclusion: The obtained data indicate the inheritance not so much of fixed mtDNA mutations, but rather of a dysfunctional mitochondrial phenotype (characterized by elevated reactive oxygen species (ROS) generation). This phenotype is realized in the offspring in a tissue-specific manner, depending on the proliferative activity and metabolic load. These results substantiate the necessity of considering mitochondrial status when assessing long-term reproductive risks in women exposed to radiation.

Keywords: mitochondrial DNA, ionizing radiation, oxidative stress, ovaries, lymphocytes, transgenerational effects, long-range PCR, mtDNA, mitochondrial dysfunction, mice

For citation: Arkhipova VI, Lyaginskaya AM, Parinov OV, Sarimov RM, Abdullaev SA. Mitochondrial Dysfunction in the Ovaries and Blood Lymphocytes of Mice and their Offspring after Exposure to X-Ray Radiation Express diagnostics of the health condition of workers in hazardous industries. Medical Radiology and Radiation Safety. 2026;71(3):11–18. DOI:10.33266/1024-6177-2026-71-3-11-18

 

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Conflict of interest. The authors declare no conflict of interest.

Financing. The study had no sponsorship.

Contribution. Article was prepared with equal participation of the authors.

Article received: 20.02.2026. Accepted for publication: 25.03.2026.