RADIATION EFFECTS: CLASSIFICATION: Japan 
EFFECTS
R ADIACION: CLASSIFICATION:
The effects of radiation may be acute, appearing shortly after radiation exposure, or chronic, which often appear many years after receiving the exposure. They may be classified into somatic, genetic, if they affect the germ cells and lead to effects on the offspring of irradiated individuals, or teratogenic, they affect the fetus during pregnancy.
In general, be divided into stochastic effects, which occur at random, so no threshold and its effect can occur independently of the dose received. To be based on probabilities, the possibility of occurrence of the effect increases with increasing doses. One example is the increased incidence of cancer. The non-stochastic effects are directly related to the amount of radiation received, so the effect is more severe the higher the dose, for example, burns. They typically have a threshold dose, below which it is estimated that the adverse effect does not appear.
Doses and dose limits:
The time lag between exposure and onset of the effect of radiation is called the latency period. The threshold dose for each specific biological effect, is the minimum dose of radiation that produces the effect. The maximum dose is the maximum allowable dose in the current state of our knowledge, is not expected to cause any significant damage in the irradiated person at any time in its existence. The limits are usually expressed as annual maximum allowed, are reviewed from time to time, and are different when looking at a total exposure of the entire body individual, or when exposure is considered located in an area, and also for people at risk of occupational exposure, or the general public. As an example, we give in Table II
some of the dose limit of English law 1 : for occupationally exposed workers, in relation to any period of twelve consecutive months:
In the same legislation, is defined as workers occupationally exposed to those who, by the circumstances in which they work, are likely to receive higher doses than one tenth of any of the annual dose limits. By law, they must all necessarily use a dosimeter to be sent each month for reading the CentroNacional Dosimetry, located in Valencia. Returns the dosimeter Center, along with a reading of the dose received in the previous month. Any dose higher than 4 mSv received in one month, when it comes to total body exposure, or 40 mSv if it relates to surface dose in the hands or skin, is a warning that, if repeated in the months following, could eventually exceeded the maximum allowable total annual dose. These doses may be revised, since 1995, the International Commission of Radiation Protection (ICRP) recommended reducing the previous standards, especially because extrapolation the effects of high doses to low doses may not be suitable 2 Much of the data on the allowable radiation dose have been drawn from American sources, Australian or United Kingdom, from data collected in the different radioactive accidents, the data of the atomic bombs of Hiroshima and Nagasaki, and some experimental data. Most information is perfectly extrapolated to the English public In fact, the limits of the table presented above correspond exactly with those of U.S. law. For children, and fetuses, the maximum is 5 mSv / year, equivalent, respectively.
RADIATION AS A RISK FACTOR O:
On average, a person receives about 360 mrem each year, most of it, from natural radiation sources. According to 1992 data, the average dose received by workers of a Nuclear Power Plant in USA was 300 mrem, in addition to the basal radiation, called background radiation that any resident that receives on average, even without exposed to any radiation source.
The Table III shows the background radiation dose received by an average citizen of USA, according to different general sources of exposure: In the following table (Table IV ) are described in detail some of the doses received from specific sources is unlikely that an ordinary citizen can receive doses greater than 5 rem per year, so the risk estimates of radiation tend to be more increases in the frequency of malignancies in deaths due directly to radiation. However, exceptionally, and as a result of accidents in which radioactive material is involved, or due to defective control of the instruments that are used in the diagnosis medical imaging, or therapeutic radiation for treatment of cancer, some patients may receive much higher doses. Beyond the 100 rem, begin to develop the various aspects of radiation sickness.
doses of certain medical tests are shown in Table V . X-ray doses are from assessments conducted in 1908-1985, and the tube current can be somewhat lower. Since the human body is composed of chemicals that we take from our environment, that some fraction of these chemicals are formed by radioactive isotopes, and that the agency has not, to our knowledge, no ability to select isotopes of the same element, is not surprising that in our body there are radioactive substances, some with extremely long half-life. According to the Intern ational
Committee for Radiation Protection (ICRP), the concentrations of radioactive elements in a human weight of 70 K would be ( TablaVI ): Some areas of the globe have, by virtue of high concentrations accumulated radioactive minerals in its soil, a basal level of radiation that far exceeds the average radiation of the above tables. In most cases, is due to the monazite, a highly insoluble mineral that usually go together with ilmenite, which gives the sand of some beaches
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its characteristic black lor. The monazite is relatively rich in derivatives Series 232 Th, but also Series 226 Ra. In some Brazilian beaches, the radiation is up to 5 mrad / h (50 m Gy / h), almost 400 times the background radiation as described above. The use of this sand to pave the streets makes some of them have a radiation 10 times higher than normal background radiation. In the southwest of India, monazite deposits are even more abundant than in Brazil. The locals are on average 500-600 mrad / yr (5-6 mGy) per year. In these areas it has detected a high frequency of chromosomal aberrations similar to those of workers in radioactive areas or in those exposed to high levels of radiation, although the frequency of these aberrations is higher than predicted for doses received, the it may mean that the ion
asunc effects within these limits, is linear with dose, may not be completely true. If one takes into account the assessments scientific committees appointed for this purpose, whose work began in the fifties, shortly after the dramatic end of the Second World War, the risks of radiation are scarce for the average citizen. The most recent of these committees, the Biological Effects of Ionizing Radiation Committee Five (BEIR V) published its findings in 1990, and, unlike the previous one (BEIR IV), which had focused attention on the dangers of radiation-emitting agents alpha inside the body, mainly on the risks of radon, focused his attention precisely on continuous exposure to external radiation. The risk estimates from external radiation has encountered numerous difficulties because most
known cases of whole body irradiation in humans have been close to the dose received from background radiation. Fundamental data is still extracted from the survivors of the atomic bombings of Hiroshima and Nagasaki, which received fairly high doses, by extrapolation. Since radiation is not the sole cause of the occurrence of cancer, must be taken into account in each population studied this risk ethnic group, the usual frequency of cancers, the frequency of smoking habits or other that could influence the rate of cancer, etc. According to BEIR V, the risk of death from cancer is 0.08% per rem for doses received rapidly, and up to 2-4 times lower (0.04 to 0.02%) per rem if the doses received during an extended period. Since this is an overall estimate, regardless of sex, age groups or specific forms of cancer, there is a high level of uncertainty associated with these figures. Therefore, attempts have been made based on actuarial data, compare the radiation risks with other common hazards. So, if you consider that in the USA, the frequency and d
cancer deaths is approximately 20%, and as a conservative approach is estimated that low doses of radiation, the risk is linearly related to dose, exposure of a population of 1000 people, with the risks highlighted above, to 1 rem of radiation would mean the emergence of eight additional deaths, ie 2008 would die instead of 2000. The figure would be lower if the same dose had been received for an extended period. This risk has led to decline in life expectancy, measuring the days lost from a population due to a death by various ca
use divided by the total population, as a way of considering the relative risk (Table VII): And in terms of risks purely work ( TablaVIII ) 3 : Another way of expressing the problem is to consider the equivalence of relative risk of 1 chance in a million die of common activities in our society ( Table IX): Based on information that there is a death per 7.3 million cigarettes smoked, or what is, 1.37 * 10 -7 deaths per cigarette, 5.6 * 10 -8 deaths per mile driven, and 4% fatal cancers per Sv (100 rem) from exposure to low doses, some regular medical exams would have a similar risk ( TablaX ) 4 :
MECHANISM OF
radiation damage:
Radiation causes ionizations in the molecules that make up the cells, separating electrons those atoms. The ions formed can react with other chemical structures near the cell, causing damage. At low doses, as they are received daily from ambient background radiation, the cells repair the damage fairly quickly. At very high doses, cells may be unable to repair defect, and may suffer permanent damage or even death. Still, many cells may die without the organism itself suffers serious consequences, since they can be replaced. If the cells undergo changes
perm anent able to divide, may lead to abnormal daughter cells. In the worst case, if these cells are not eliminated by the mechanisms of recognition of foreign proteins, can lead to cancer. At higher doses, the damaged cells can not be replaced quickly enough to the tissues and organs carry out their tasks properly, appearing different degrees of radiation sickness to be described later. This is a broad spectrum of manifestations, depending mainly on the radiation dose received, but also the previous state of the individual, and care and attention this received.
Free Radicals:
Radiation sickness is as a disease caused by free radicals 5, 6 , 7, 8 , 9, 10 , 11 , 12 , 13 as well as ischemia-reperfusion syndrome, which some poisoning, and many other pathological conditions. Most of the ions formed by the effect of radiation, are from well water molecules, not in vain because the water is the most abundant molecule in the body. A free radical is any atom or molecule capable of independent existence, which has in its outer electron shell an unpaired electron. Under this, it is substances with a high capacity to react with nearby molecules, which can cause chemical and structural changes coming to result in the loss of its function. Although not far from the only, the most abundant free radical in nature are free radicals oxygen, it is largely produced in the course of normal cellular respiration
14, 15 have, in addition to many pathological processes, primarily in some poisoning, paraquat, diquat 16, 17 , 18 , paracetamol 19 -, under the action of certain chemicals used as antineoplastic anthracyclines- 20, 21 - in the ischemia and subsequent reperfusion of the organs 22 , 23, 24 in polymorphonuclear leukocytes that have been activated by substances foreign to the body 25, 26 , 27 and, of course, under the action of radiation 28.
When the oxygen molecule acquires an electron, there is a radical called superoxide represented by O 2 .- . It is probably the most abundant of oxygen free radicals, though not the most reactive. However, spontaneously, with
course with some transition metals such as copper or iron, or through specific enzymes such as superoxide, can be transformed for the purchase of a new electron and two protons, hydrogen peroxide or hydrogen peroxide, which, although able to intervene in almost all reactions radicalares is not technically a free radical, it has no unpaired electrons. The hydroxyl radical is the result of the acquisition, by the oxygen molecule, three electrons, molecular breakage and addition of a proton. The hydroxyl free radical is one of the most reactive chemicals. Under precisely this reactivity, the hydroxyl radical, represented by HO . is the most harmful forms of oxygen radicalares. The hydroxyl radical is responsible for most of DNA damage to cell membranes and initially caused by ionizing radiation. HO reactions. can be of three types: H abstraction, addition, and electronic transfer. Regarding the latter, following a classical principle of the chemistry of free radicals, the reaction of a free radical with or
na no radical chemical species produces a different free radical, which may be more or less active than the free radical original. The most typical example of the hydrogen abstraction reaction is the reaction of hydroxyl radical with the fatty acids of cell membranes to produce, after some transformations complex fatty acid molecules, a chain reaction called lipid peroxidation, which will increasingly producing free radicals, and that if not stopped by antioxidants in the membrane itself or by external agents, can reach membrane injury, as well as degradation products such as hydroxynonenal or malondialdehyde which themselves have carcinogenic properties. When the production of hydroxyl radical is given by a chain of DNA, the radical can react with deoxyribose, transform
Andolan in a lot of different products, some of which have shown mutagenic properties in some bacteria. In addition, it can act directly on the purine and pyrimidine bases, usually by ADICI
ng, for example, in the double bond of thymine to thymine glycol convert, which gives the free radical character. This can then react with oxygen to form peroxitimina frankly reactive molecules that can bind to adjacent, modifying the structure of the DNA chain Some of the products of oxidative radical attack suffer
hidroxilono
further processing, and are excreted in the urine, which can be quantified. For example, it is estimated that timinaglicol and the timidinaglicol - timinaglicol is still attached deoxyribose-and 5-hidroximetiluracilo are excreted in the approximate amount of 100nmol (10 -9 mol) each, every day, in a normal human being. If all of these molecules came from the result of the repair of DNA chains (any amount is produced by intestinal bacteria, and another comes from the present in food), would correspond to an average of 1000 bases of DNA damage in each of the cells that make up the body. Since these are only some of the degradation products of radical attack to DNA damage that needed to be repaired every day can be much more numerous.
Apoptosis:
Another mechanism by which radiation can cause tissue damage is the induction of apoptosis. This mechanism does not exclude the previous one, and there is evidence that can be triggered by the prior formation of free radicals that damage the genetic material 29. The term apoptosis (from Greek apo apart, and ptosis, drooping - as rain falls ) was coined in 1972 by Kerr et al. 30 to describe a type of cell death that differs from necrosis, both biochemically morphologically. Other authors had already described morphological and functional aspects before, highlighting the potential importance for the phenomena of growth, senescence and normal cell proliferation or tumor. Some authors have also called "programmed cell death" 31, 32 . Apoptosis seems to be a necessary phenomenon in embryogenesis, in the involution of endocrine tissues after the secretory stimulus disappears, the elimination of ectopic cells, and in general, in the maintenance of the cellular composition of any organ system in which cells proliferate throughout the individual's life.
Unlike death by necrosis, where cell membranes are broken and the cell content is spread around, attracting inflammatory cells designed to engulf the fragments, in apoptosis, the membrane is also affected, losing its flexibility and appearing in it as a bulla or bubbles. The core shows a progressive condensation of chromatin and in the analysis, a fragmentation of the DNA strands. The cell appears to sink in on itself, probably by destruction of the cytoskeleton. The nucleus becomes pyknotic. Finally the cell is fragmented, always keeping a membrane and forming the so-called apoptotic bodies, which are finally phagocytosed not only by macrophages and neutrophils, as in the case of necrosis, but above all by the adjacent cells of the same type as that which has undergone apoptosis, in a way of "cannibalism", so that inflammatory changes are practically nil. Trowell and nuclear pyknosis in 1952 observed at doses as low as 0.5 Gy 33, with a dose-response relationship was linear up to 8 Gy, which has been confirmed by other authors in lymphocytes in the bone marrow in the cells of the crypts of the intestinal mucosa, in the cerebellum, etc. Some cells are more resistant than others the onset of apoptosis after irradiation. Even some radioresistant tumors showed no apoptosis or it appears only after a considerable delay after irradiation. The sensitivity to apoptosis is also determined by the maturity of the cell and their functional status. The process of apoptosis is far from being fully clarified, and even fewer reasons to put it up. In many cells, radiation damages DNA directly to communicate their energy to the nucleic acid chain, or the pre-production of free radicals, as described above, and this is the initial mechanism that triggers apoptosis. The presence of radical Free damaged cell membranes and activates among others the phospholipase C-g 34 that, by mobilizing Ca + + intracellular stores, and also allowing the entry of this from outside the cell activates a DNA endonuclease dependent Ca + + and Mg + +, and Zn-sensitive + +, which breaks the DNA into fragments of approximately 180 bp. Endonuclease activity increases up to seven times within three hours of irradiation, probably by de novo synthesis , as this post-irradiation chromosomal fragmentation can be inhibited by cycloheximide, an inhibitor of protein synthesis by actinomycin D, an inhibitor of RNA synthesis by Zn ions + + that inhibit the endonuclease directly, or by chelation of intracellular calcium. Has recently been recognized that there are genes whose activation triggers the apoptosis, genes whose activation is supported, and others whose activation is inhibited. In mammalian cells, the gene essential for apoptosis seems to be encoding the enzyme interleukin-1-convertase b . Parts of this enzyme are protein-like substances produced by genes from other species that also regulate them this form of cellular death TNF tabi seems to be an area of \u200b\u200b80 amino acids can trigger this cell death. In some cells the IL-4 appears to induce apoptosis, although other is protective. Besides the activator gene, the p53 gene seems to be indispensable to initiate apoptosis in some cellular systems. Its deletion causes the cells are much more resistant to radiation, while remaining sensitive to apoptosis induced by corticosteroids or calcium. We have found that gamma radiation induces the expression of this gene in several cell types in animals, and the extent of apoptosis coincides with p53 expression. By contrast, the bcl-2 and its related seem to inhibit apoptosis and prolong the survival of the cell lines. The protein produced by this gene has a 25% homology with the Epstein-Barr virusde, which also has been shown to protect B cells from programmed cell death. This protein appears to have antioxidant and blocks apoptosis induced by radiation, glucocorticoids, or by other mechanisms. The acid 9 - cis-retinoic is a potent inhibitor of activation of apoptosis, at least in T cells The difference in activity as trans , more than ten times higher, suggesting that the action depends to retinoic X receptor, which is much more affinity for a cis .
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From fiction to reality 
