Radiation kills cancer cells primarily by damaging their DNA, which disrupts their ability to grow and divide, eventually leading to cell death. When ionizing radiation—such as X-rays, gamma rays, or particle beams—hits a cancer cell, it causes breaks in the double-stranded DNA. This damage triggers a process called mitotic catastrophe where the cell can no longer successfully complete division and dies. Cancer cells are especially vulnerable because they divide rapidly and have less efficient DNA repair mechanisms compared to normal cells. Radiation also generates reactive oxygen species (ROS), highly reactive molecules that further damage cellular components including DNA, proteins, and membranes. The accumulation of such damage overwhelms the cancer cells’ survival pathways and leads to apoptosis (programmed cell death) or other forms of lethal injury.
However, radiation can also cause cancer because it damages normal healthy cells’ DNA as well. If this damage is not sufficient to kill the cell but instead causes mutations in critical genes controlling growth or repair processes—such as tumor suppressor genes or oncogenes—it can initiate carcinogenesis (the formation of new cancers). These mutations may accumulate over time if the damaged cells survive and proliferate abnormally. Radiation-induced reactive oxygen species contribute here too by causing oxidative stress that alters cellular structures beyond repairable limits.
The paradox arises from this dual nature: radiation’s power lies in its ability to break down genetic material irreparably in targeted tumor tissue but inevitably some collateral harm occurs in surrounding healthy tissues exposed during treatment or environmental exposure. Advances like FLASH radiotherapy deliver ultra-high dose rates extremely quickly; this approach appears promising because it kills tumor cells effectively while sparing normal tissues more than conventional radiation does—a phenomenon partly linked to differences in iron metabolism between tumors and healthy tissue that influence how ROS cause lethal damage selectively.
At a molecular level:
– **DNA double-strand breaks** caused by ionizing radiation are critical lesions leading directly to loss of genomic integrity.
– **Reactive oxygen species** generated during irradiation attack lipids forming plasma membranes as well as proteins involved in signaling pathways.
– Normal tissues have better antioxidant defenses and slower proliferation rates allowing them some recovery capacity after sub-lethal doses.
– Cancerous tissues often have higher iron levels promoting iron-dependent oxidative reactions that amplify ROS-mediated killing under FLASH conditions.
In summary, radiation therapy exploits vulnerabilities unique to cancer biology—rapid division rate combined with impaired repair—to induce fatal genetic injury selectively within tumors while risking mutagenic effects on normal tissue due mainly to off-target DNA damage from ionizing particles and free radicals formed during treatment exposure. This delicate balance explains why radiation both cures many cancers yet remains a risk factor for developing others later on through mutation accumulation triggered by its inherent destructive mechanism on cellular genomes.
