It did not take long after the discovery of X-rays in the 1890s for scientists to begin exploring the harmful effects of radiation on living organisms. Yet even after more than a century of research, new insights continue to emerge about how radiation affects the body. In a recent study, researchers at Hokkaido University uncovered a previously unrecognized effect of radiation that leads to changes in the mitochondria of the offspring. The study was published in March 2026 in the journal Redox Biology.

“Our results show that exposing mice to ionizing radiation before conception can influence mitochondrial biology in the next generation, suggesting that mitochondria could represent an additional layer through which environmental stresses including ionizing radiation can be passed on to the offspring,” says Dr. Hisanori Fukunaga, corresponding author of the research article.

Mitochondria are structures within our cells that produce energy. They contain their own DNA, which encodes proteins that help them fulfill their function. Unlike nuclear DNA, which is inherited from both parents, mitochondrial DNA is inherited only from the mother and exists in many copies—hundreds to thousands per cell.

While radiation is well known to damage nuclear DNA, what effects it has on the mitochondrial DNA of parents and their offspring is not yet fully understood.

“Previous studies have mainly focused on radiation-induced mutations in the nuclear genome. However, mitochondria play a central role in cellular metabolism, oxidative stress, and development,” explains Fukunaga.

In this study, the researchers exposed adult male and female mice to a single dose of X-ray radiation before mating. This produced offspring from four groups: control parents, irradiated fathers, irradiated mothers, and both parents irradiated. When the researchers examined the parent mice, they found that radiation exposure increased the number of copies of the mitochondrial DNA in their blood.

Mitochondrial DNA copy number is often used as a sensitive indicator of cellular stress. This makes mtDNA copy number a useful marker for assessing radiation-induced cellular responses.

After the parent mice gave birth, the team checked the offspring and their mitochondria. They focused on three organs—the brain, heart, and liver. The effects varied depending on which parent had been exposed to radiation.

“We observed clear organ-specific changes, particularly in the brain and liver of the offspring,” says Fukunaga. When only the father mice were exposed, mitochondrial DNA copy number decreased in the brains of the offspring. When only the mothers were exposed, a decrease was observed in the liver. No significant changes were detected in the heart in any of the groups.

In addition, a lower mitochondrial DNA copy number in the liver was associated with increased liver weight, highlighting a potential role of mitochondrial regulation in neonatal organ growth.

“The resulting mitochondrial changes in the offspring were also linked to an increase in body weight and liver weight,” says Fukunaga.
Since this effect of radiation on mitochondrial DNA copy number in cells may represent a dynamic and potentially reversible response rather than a permanent genetic mutation, understanding it better could help us respond more effectively to such effects.