Sievert (Sv) is a unit of equivalent dose that depends on the biologic rather than the physical effects of radiation (it replaced a unit called the rem). For the same absorbed dose, various types of radiation differ in the extent of damage they produce. The equivalent dose controls for this variation and provides a uniform measuring unit. The equivalent dose (expressed in sieverts) corresponds to the absorbed dose (expressed in grays) multiplied by the relative biologic effectiveness of the radiation. The relative biologic effectiveness depends on the type of radiation, the type and volume of the exposed tissue, and the duration of the exposure, as well as other biologic factors (discussed next). The effective dose of x-rays, computed tomography (CT), and other imaging and nuclear medicine procedures are commonly expressed in millisieverts (mSv). For x-radiation, 1 mSv = 1 mGy.
Main Determinants of the Biologic Effects of Ionizing Radiation
In addition to the physical properties of the radiation, its biologic effects depend heavily on the following variables:
Rate of delivery. The rate of delivery significantly modifies the biologic effect. Although the effect of radiant energy is cumulative, delivery in divided doses may allow cells to repair some of the damage in the intervals. Thus, fractional doses of radiant energy have a cumulative effect only to the extent that repair during the intervals is incomplete. Radiotherapy of tumors exploits the capability of normal cells to repair themselves and to recover more rapidly than tumor cells.
Field size. The size of the field exposed to radiation has a great influence on its consequences. The body can sustain relatively high doses of radiation when they are delivered to small, carefully shielded fields, whereas smaller doses delivered to larger fields may be lethal.
Cell proliferation. Because ionizing radiation damages DNA, rapidly dividing cells are more vulnerable to injury than are quiescent cells. Except at extremely high doses that impair DNA transcription, DNA damage is compatible with survival in nondividing cells, such as neurons and muscle cells. However, as discussed in Chapter 6, in dividing cells DNA damage is detected by sensors that produce signals leading to the upregulation of p53, the “guardian of the genome.” p53 in turn upregulates the expression of genes that initially lead to cell-cycle arrest and, if the DNA damage is too great to repair, genes that cause cell death through apoptosis. Understandably, therefore, tissues with a high rate of cell turnover, such as gonads, bone marrow, lymphoid tissue, and the mucosa of the GI tract, are extremely vulnerable to radiation, and the injury is manifested early after exposure.
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Hypoxia. The production of ROS by the radiolysis of water is the most important mechanism of DNA damage by ionizing radiation. Tissue hypoxia, such as may exist in the center of rapidly growing, poorly vascularized tumors, may thus reduce the extent of damage and the effectiveness of radiotherapy directed against tumors.
Vascular damage. Damage to endothelial cells, which are moderately sensitive to radiation, may cause narrowing or occlusion of blood vessels, leading to impaired healing, fibrosis, and chronic ischemic atrophy. These changes may appear months or years after exposure. Despite the low sensitivity of brain cells to radiation, vascular damage after irradiation can lead to late manifestations of radiation injury in this tissue.
The most important cellular target of ionizing radiation is DNA (