When cells in the body are exposed to certain types of energy, they become irradiated. This exposure can happen from medical procedures like X-rays and cancer therapy, or environmental sources such as radon gas and cosmic rays. The effects of radiation on the body can range from harmless to beneficial to damaging. The outcome for an irradiated cell depends on the type and amount of radiation received and the cell’s internal machinery, which provides insight into how radiation is used for medical treatment.
The Cellular Encounter with Radiation
Radiation relevant to biological effects is known as ionizing radiation, which includes X-rays, gamma rays, and particle radiation. When this radiation passes through the body, it deposits energy into cells. This happens through direct action, where radiation strikes a molecule, or through the more common indirect action.
Since cells are about 80% water, radiation most often interacts with a water molecule, splitting it to create highly reactive molecules called free radicals. These free radicals travel within the cell and damage other molecules, with the most important target being the cell’s deoxyribonucleic acid, or DNA. Damage to DNA is the primary cause of the biological effects seen after radiation exposure.
The way different types of radiation deposit their energy influences the extent of the damage. Some particles deposit a large amount of energy in a short distance, while others deposit their energy more sparsely. This difference in energy deposition patterns determines the biological outcome for the cell, tissue, and organism.
DNA Under Siege: Radiation’s Primary Target
The DNA inside every cell contains the genetic blueprint for all cellular activities, making its integrity important for normal function and reproduction. When radiation strikes the DNA, it can cause several types of damage. These injuries range from single-strand breaks (SSBs), where one of the two DNA strands is cut, to double-strand breaks (DSBs), where both strands are severed. DSBs are considered the most serious type of DNA lesion because they can lead to the loss of genetic information if not repaired correctly.
Radiation can also damage the individual chemical bases that make up the DNA sequence or cause DNA-protein crosslinks, which interfere with normal cellular processes. Ionizing radiation has the ability to create clustered DNA damage. This involves multiple lesions, such as a combination of SSBs, DSBs, and base damages, occurring in close proximity on the DNA helix.
This complexity makes the damage difficult for the cell’s repair systems to handle. While the cell is proficient at fixing isolated lesions, a dense cluster of damage presents a challenge. The repair of such complex breaks is often slow and prone to errors, increasing the likelihood of mutations or cell death.
Cellular Emergency Response to Radiation
Upon detecting DNA damage, a cell initiates an emergency response. Sensor proteins recognize the DNA breaks and trigger signaling cascades that activate a network of proteins. A primary action of this response is the activation of cell cycle checkpoints, which are control points that temporarily halt cell division. This pause provides a window of time for repairs to be made before the cell attempts to replicate its damaged DNA or divide.
The cell employs different DNA repair pathways for certain types of damage. For the dangerous double-strand breaks, cells use two main mechanisms. One is a fast process that pastes the broken ends of the DNA back together but is more prone to errors. The other is a more accurate method that uses an undamaged copy of the DNA sequence as a template for a perfect repair, but it is only available in certain phases of the cell cycle.
If the DNA damage is too widespread to be repaired, the cell may initiate a self-destructive program. One is apoptosis, or programmed cell death, which eliminates the damaged cell to prevent it from passing on flawed genetic information. Another outcome is cellular senescence, where the cell enters a state of permanent growth arrest.
Fates of Irradiated Cells: Survival, Change, or Demise
The fate of an irradiated cell depends on the balance between the initial damage and the success of its repair. If the cellular repair machinery correctly fixes all DNA lesions, the cell can return to its normal function. This outcome is common after exposure to low doses of radiation.
When repair attempts fail or are inaccurate, the cell may survive but with permanent alterations to its DNA. This can result in mutations, which are changes to the genetic code. An accumulation of such errors can lead to genomic instability, where the cell has an increased tendency to acquire more genetic changes over time. This instability is a driving force in the development of cancer, as it can lead to the activation of cancer-promoting genes or the inactivation of tumor-suppressing ones.
In cases of severe damage, the cell may die. This can happen through mitotic death, where the cell fails during division due to damaged chromosomes, or through apoptosis. Widespread cell death caused by high radiation doses can impair the function of tissues and organs, leading to acute effects like radiation sickness or long-term organ damage.
Understanding and Utilizing Radiation’s Power
The biological impact of radiation is influenced by several factors. The total energy absorbed (dose) and the speed of delivery (dose rate) are primary considerations. A dose delivered over a long period is less damaging than the same dose delivered at once, as it allows more time for cellular repair.
The type of radiation also matters. Linear Energy Transfer (LET) describes how densely radiation deposits energy in tissue. High-LET radiation is more biologically destructive because it causes more complex, clustered DNA damage. The Relative Biological Effectiveness (RBE) is a value used to compare the damage from different radiation types.
The presence of oxygen is another factor, as it makes cells more sensitive to radiation by making free-radical damage harder to repair. These principles are applied in radiation therapy for cancer, allowing clinicians to maximize damage to tumors while minimizing harm to healthy tissues.