Ionizing radiation has a direct effect on the structure of DNA, inducing DNA breaks, particularly double-stranded breaks (DSB). This can lead to the generation of reactive oxygen species (ROS) that oxidize proteins and lipids, as well as various types of DNA damage, such as the creation of abasic sites and single-stranded breaks (SSB). Scientific experiments have shown that genetic mutations can occur in many organisms due to radiation-induced DNA damage. Generally, the frequency of a given mutation increases in proportion to the radiation dose in the low to intermediate dose range.
However, at higher doses, the frequency of mutations induced by a given dose may depend on the rate at which the dose accumulates, tending to be lower if the dose accumulates over a long period of time. This means that ionizing radiation can cause mutations in cells deep within us, not just cells on the surface of our body. Over time, these mutations can cause cancer; ionizing radiation is known to cause leukemia and thyroid cancer, just to name a few. The energy of ionizing radiation breaks chemical bonds in DNA, resulting in several different types of damage.
A recent study has highlighted the importance of a particular type of DNA damage involving breaks in both strands of DNA in thyroid tumors. The relationship between DNA double-stranded breaks and radiation exposure was strongest in children exposed to older ages. Ionizing radiation can also affect important molecules other than DNA. For example, it can break the bonds that hold water molecules together.
This creates hydrogen (H+) and hydroxyl (OH-) ions. With densely ionizing radiation, in comparison, the performance of double-break aberrations for a given dose is greater than with sparsely ionizing radiation and is proportional to dose regardless of dose rate. It is well established that DNA damage is the primary mechanism associated with the tumorigenicity of ionizing radiation; however, ionizing radiation also causes significant aberrations in the cellular epigenome, including alterations in DNA methylation, histone modifications, and chromatin accessibility.