|
Up to 10% of invasive cancers are related to radiation exposure, including both ionizing radiation and non-ionizing radiation. Additionally, the vast majority of non-invasive cancers are non-melanoma skin cancers caused by non-ionizing ultraviolet radiation. Ultraviolet's position on the electromagnetic spectrum is on the boundary between ionizing and non-ionizing radiation. Non-ionizing radio frequency radiation from mobile phones, electric power transmission, and other similar sources have been described as a possible carcinogen by the World Health Organization's International Agency for Research on Cancer, but the link remains unproven.〔(【引用サイトリンク】url=http://www.iarc.fr/en/media-centre/pr/2011/pdfs/pr208_E.pdf )〕 Exposure to ionizing radiation is known to increase the future incidence of cancer, particularly leukemia. The mechanism by which this occurs is well understood, but quantitative models predicting the level of risk remain controversial. The most widely accepted model posits that the incidence of cancers due to ionizing radiation increases linearly with effective radiation dose at a rate of 5.5% per sievert.〔 If the linear model is correct, then natural background radiation is the most hazardous source of radiation to general public health, followed by medical imaging as a close second. ==Mechanism== Cancer is a stochastic effect of radiation, meaning that the probability of occurrence increases with effective radiation dose, but the severity of the cancer is independent of dose. The speed at which cancer advances, the prognosis, the degree of pain, and every other feature of the disease are not functions of the radiation dose to which the person is exposed. This contrasts with the deterministic effects of acute radiation syndrome which increase in severity with dose above a threshold. Cancer starts with a single cell whose operation is disrupted. Normal cell operation is controlled by the chemical structure of DNA molecules, also called chromosomes. When radiation deposits enough energy in organic tissue to cause ionization, this tends to break molecular bonds, and thus alter the molecular structure of the irradiated molecules. Less energetic radiation, such as visible light, only causes excitation, not ionization, which is usually dissipated as heat with relatively little chemical damage. Ultraviolet light is usually categorized as non-ionizing, but it is actually in an intermediate range that produces some ionization and chemical damage. Hence the carcinogenic mechanism of ultraviolet radiation is similar to that of ionizing radiation. Unlike chemical or physical triggers for cancer, penetrating radiation hits molecules within cells randomly.〔In the case of internal contamination with alpha emitters, the distribution may not be so random. Transuranic elements are believed to have a chemical affinity for DNA, and any radioactive element could be part of a chemical compound that targets certain molecules.〕 Molecules broken by radiation can become highly reactive free radicals that cause further chemical damage. Some of this direct and indirect damage will eventually impact chromosomes and epigenetic factors that control the expression of genes. Cellular mechanisms will repair some of this damage, but some repairs will be incorrect and some chromosome abnormalities will turn out to be irreversible. DNA double-strand breaks (DSBs) are generally accepted to be the most biologically significant lesion by which ionizing radiation causes cancer.〔 In vitro experiments show that ionizing radiation cause DSBs at a rate of 35 DSBs per cell per Gray,〔( Evidence for a lack of DNA double-strand break repair in human cells exposed to very low x ) "The line is a linear fit to the data points with a slope of 35 DSBs per cell per Gy." e.g. 35() *65()=2.27()〕 and removes a portion of the epigenetic markers of the DNA,〔( Fractionated Low-Dose Radiation Exposure Leads to Accumulation of DNA Damage and Profound Alterations in DNA and Histone Methylation in the Murine Thymus ) "fractionated low-dose radiation exposure resulted in even more substantial decrease in global DNA methylation than acute irradiation, causing 2.5- and 6.1-fold (P < 0.05) reduction in global DNA methylation〕 which regulate the gene expression. Most of the induced DSBs are repaired within 24h after exposure, however, 25% of the repaired strands are repaired incorrectly and about 20% of fibroblast cells that were exposed to 200mGy died within 4 days after exposure.〔http://www.pnas.org/content/100/9/5057.full.pdf〕〔(DNA double strand break repair in brain: Reduced NHEJ activity in aging rat neurons ) "blunt and non-matching ends were very poorly repaired at all ages. Further, the end joining activity in neurons is not faithful"〕 A portion of the population possess a flawed DNA repair mechanism, and thus suffer a greater insult due to exposure to radiation.〔 Major damage normally results in the cell dying or being unable to reproduce. This effect is responsible for acute radiation syndrome, but these heavily damaged cells cannot become cancerous. Lighter damage may leave a stable, partly functional cell that may be capable of proliferating and eventually developing into cancer, especially if tumor suppressor genes are damaged.〔Acharya, PVN; The Effect of Ionizing Radiation on the Formation of Age-Correlated Oligo Deoxyribo Nucleo Phospheryl Peptides in Mammalian Cells; 10th International Congress of Gerontology, Jerusalem. Abstract No. 1; January 1975. Work done while employed by Dept. of Pathology, University of Wisconsin, Madison.〕〔Acharya, PVN; Implicatons of The Action of Low Level Ionizing Radiation on the Inducement of Irreparable DNA Damage Leading to Mammalian Aging and Chemical Carcinogenesis.; 10th International Congress of Biochemistry, Hamburg, Germany. Abstract No. 01-1-079; July 1976. Work done while employed by Dept. of Pathology, University of Wisconsin, Madison.〕〔Acharya, PV Narasimh; Irreparable DNA-Damage by Industrial Pollutants in Pre-mature Aging, Chemical Carcinogenesis and Cardiac Hypertrophy: Experiments and Theory; 1st International Meeting of Heads of Clinical Biochemistry Laboratories, Jerusalem, Israel. April 1977. Work conducted at Industrial Safety Institute and Behavioral Cybernetics Laboratory, University of Wisconsin, Madison.〕 The latest research suggests that mutagenic events do not occur immediately after irradiation. Instead, surviving cells appear to have acquired a genomic instability which causes an increased rate of mutations in future generations. The cell will then progress through multiple stages of neoplastic transformation that may culminate into a tumor after years of incubation. The neoplastic transformation can be divided into three major independent stages: morphological changes to the cell, acquisition of cellular immortality (losing normal, life-limiting cell regulatory processes), and adaptations that favor formation of a tumor.〔 In some cases, a small radiation dose reduces the impact of a subsequent, larger radiation dose. This has been termed an 'adaptive response' and is related to hypothetical mechanisms of hormesis. A latent period of decades may elapse between radiation exposure and the detection of cancer. Those cancers that may develop as a result of radiation exposure are indistinguishable from those that occur naturally or as a result of exposure to other carcinogens. Furthermore, National Cancer Institute literature indicates that chemical and physical hazards and lifestyle factors, such as smoking, alcohol consumption, and diet, significantly contribute to many of these same diseases. Evidence from uranium miners suggests that smoking may have a multiplicative, rather than additive, interaction with radiation.〔 Evaluations of radiation's contribution to cancer incidence can only be done through large epidemiological studies with thorough data about all other confounding risk factors. 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Radiation-induced cancer」の詳細全文を読む スポンサード リンク
|