Recent progress especially in the field of gene identification and expression has attracted greater attention to the genetic and epigenetic susceptibility to cancer, possibly enhanced by ionising radiation. This issue is especially important for radiation therapists since hypersensitive patients may suffer from adverse effects in normal tissues following standard radiation therapy, while normally sensitive patients could receive higher doses of radiation, offering a better likelihood of cure for malignant tumours. Although only a small percentage of individuals are "hypersensitive" to radiation effects, all medical specialists using ionising radiation should be aware of the aforementioned progress in medical knowledge. The present paper, the second of two parts, reviews human disorders known or strongly suspected to be associated with hypersensitivity to ionising radiation. The main tests capable of detecting such pathologies in advance are analysed, and ethical issues regarding genetic testing are considered. The implications for radiation protection of possible hypersensitivity to radiation in a part of the population are discussed, and some guidelines for nuclear medicine professionals are proposed.
The effectiveness of chemiluminescence (ChL) in vitro to measure free radicals generated as a result of metabolic disorganization caused by radiation sickness is evaluated. The results are correlated with those obtained by measuring superoxide dismutase (SOD) activity and lipid peroxide as levels of thiobarbituric acid reacting substances (TBARS). To this aim, livers from irradiated Wistar rats were removed immediately (day 0) after irradiation and also 7 and 14 d later. ChL results, expressed in arbitrary units (AU)/min/mg protein, were analyzed for irradiated samples and controls, for different doses at different times. Increased levels of ChL emission were observed not only on day 0, but also on days 7 and 14. On the other hand, SOD activity showed a decrease on the 7th d, and significantly higher lipid peroxide levels were observed in the assays performed on the 14th d, at all exposure doses. The correlation between temporal changes in the SOD activity, ChL emission, and higher TBARS levels a week later were evident from the data. These results indicate that the ChL technique proved to be useful in combination with other techniques currently used for evaluating radiation oxidative injury.
Recent progress especially in the field of gene identification and expression has attracted greater attention to genetic and epigenetic susceptibility to cancer, possibly enhanced by ionising radiation. It has been proposed that the occurrence and severity of the adverse reactions to radiation therapy are also influenced by such genetic susceptibility. This issue is especially important for radiation therapists since hypersensitive patients may suffer from adverse effects in normal tissues following standard radiation therapy, while normally sensitive patients could receive higher doses of radiation offering a better likelihood of cure for malignant tumours. This paper, the first of two parts, reviews the main mechanisms involved in cell response to ionising radiation. DNA repair machinery and cell signalling pathways are considered and their role in radiosensitivity is analysed. The implication of non-targeted and delayed effects in radiosensitivity is also discussed.
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