Radiation, a form of energy traveling through space, can impact cells. When this energy, particularly ionizing radiation, encounters cells, it can alter their function and structure. This interaction can affect a cell’s ability to survive and perform its roles.
How Radiation Interacts with Cells
Radiation interacts with cells through two mechanisms: direct action and indirect action. Direct action occurs when radiation directly strikes and transfers its energy to critical molecules within the cell, such as DNA. This collision can disrupt the molecular structure of these components, leading to damage.
Indirect action is more prevalent for certain radiation types. This mechanism involves radiation interacting with water molecules, a large part of a cell. This interaction causes water molecules to break apart and form free radicals, such as hydroxyl radicals. These free radicals react with cellular components, including DNA, proteins, and lipids, causing damage. Indirect action, through free radical generation, accounts for 60% of DNA damage from low linear energy transfer radiation.
The Primary Target: Cellular DNA
Cellular DNA is the primary target for radiation damage due to its role in cell function and heredity. DNA contains the genetic instructions for a cell’s survival, growth, and reproduction. Damage to DNA can affect these processes.
Radiation can induce several types of damage to the DNA molecule. One common form is a single-strand break (SSB), where only one DNA strand is broken. More severe are double-strand breaks (DSBs), involving breaks in both DNA strands. DSBs can lead to genetic instability if not properly repaired. Radiation can also cause base damage, altering the chemical bases, and cross-linking, forming abnormal bonds between DNA strands or with proteins.
Cellular Responses to Damage
Cells possess mechanisms to detect and respond to radiation-induced damage. A primary defense involves DNA repair pathways. These systems work to mend damaged DNA, aiming to restore the molecule’s original structure and function. Mechanisms like base excision repair and nucleotide excision repair address DNA alterations, while homologous recombination and non-homologous end joining are important for repairing double-strand breaks.
Beyond repair, cells can temporarily halt their division through a process called cell cycle arrest. This pause provides additional time for DNA repair mechanisms to operate effectively before the cell attempts to replicate its potentially damaged genetic material. If the damage is too extensive or irreparable, cells can initiate apoptosis, a process of programmed cell death. This self-destruct sequence prevents the proliferation of severely damaged cells. In some cases, severely damaged cells may also enter a state of cellular senescence, characterized by permanent growth arrest without dying, effectively removing them from the dividing cell population.
Potential Outcomes of Radiation Exposure
The outcome of cells exposed to radiation depends on the damage and the effectiveness of the cellular response mechanisms. If the damage is too severe, or if repair mechanisms are overwhelmed, the cell may die. This can occur immediately (interphase death) or after attempting to divide (mitotic death).
Alternatively, if DNA is incorrectly repaired, it can lead to mutations, which are permanent changes in the genetic code. These mutations can alter cell function, potentially affecting how the cell behaves or responds to its environment. Accumulated mutations and unrepaired DNA damage, particularly in genes that control cell growth and division, can contribute to cellular transformation. This transformation can lead to uncontrolled cell proliferation and, over time, the development of cancer. Some cells may also survive radiation exposure but with impaired or reduced functionality, impacting the overall health and performance of tissues and organs.