The cells in the vicinity of irradiated cells show effects that cannot be attributed to targeting by ionizing radiation tracks. Additionally, when cells are irradiated and later transferred to another medium, the cells in proximity in the new medium exhibit DNA damage, mutation, and carcinogenesis. Through cell-to-cell interaction, the directly irradiated cells communicate with adjacent cells and spread the effect of radiation to a larger number of cells. The mechanism is not clearly understood; however, gap junctional intercellular communication [4] or release of soluble factors (such as cytokines) from irradiated cells is proposed. The bystander effect has been mainly described for densely ionizing radiation (such as alpha particles) but also is seen in low LET radiation (such as gamma or X-rays).

Maximal radiation-induced genetic damage is formed shortly (minutes to hours) after radiation exposure. Nevertheless, it has been observed that not only the irradiated cells but also descendents may show delayed effects. Cells that sustain nonlethal DNA damage show increased mutation rate in descendent cells several generations after the initial exposure. Delayed effects include delayed reproductive death up to six generations following the primary insult.

Various types of radiation differ in penetrability based on LET, which expresses energy loss per unit distance traveled (kiloelectron volts per micrometer). This value is high for alpha particles, lower for beta particles, and even less for gamma rays and X-rays. Thus, alpha particles penetrate a short distance but induce heavy damage, and beta particles travel a longer distance but much shorter than gamma rays.

The radiation dose is obviously an important factor. In addition, a single dose of radiation causes more damage than the same dose being divided (fractionated). Collectively these two factors are expressed as dose per fraction.

Dose rate expresses the time for which dose is administered. The longer the duration for the same total dose, the better the chance of cellular repair and the smaller the damage.

Although all cells can be affected by ionizing radiation, normal cells and their tumors vary in their sensitivity to radiation. Slowly and rapidly growing cells have different radiosensitivity in relation to their movement through the cell cycle. Radiosensitivity varies with the rate of mitosis and cellular maturity. Blood-forming cells are very sensitive to radiation, while neurons, muscle, and parathyroid cells are highly radioresistant. Within a given cell, the nucleus in general is relatively more radiosensitive than the cytoplasm.

Some cells are known to have a higher capacity than others to repair the damage caused by ionizing radiation; consequently, the biological effects of the same radiation dose are different. Significant repair is known to occur quickly, within 3 h.

All phases of the cell cycle can be affected by ionizing radiation. The radiosensitivity of a given cell varies from one cell cycle phase to another. Overall, sensitivity appears to be greatest in G₂ phase; irradiation during this phase retards the onset of cell division. Irradiation during mitosis induces chromosomal aberrations, i.e., breaks, deletions, translocations, and others. The sensitivity of a given cell cycle phase also differs from one cell type to another and by alteration of radiation injury [3]. For example, the reproductive cells are most sensitive during the M phase, while damage to DNA synthesis and chromosomes occurs mostly when the cell is in the G₂ phase. Recovery from sublethal damage occurs in all phases of the cell cycle. However, this is most pronounced in the S phase, which is also the most radioresistant phase [3].

Molecular oxygen is known to have the ability to potentiate the response to radiation; this is known as the oxygen effect. The amount of molecular oxygen rather than the rate of oxygen utilization by the cells is the most important factor for increasing the sensitivity of cells to radiation. The probable mechanism is the allowance of additional free radicals, which enhance the damage of cells [5].