Effect of gamma irradiation on the grain yield of Nigerian Zea mays and Arachis hypogaea.

As a follow-up to our earlier investigation on the effect of gamma radiation on the germination and growth of certain Nigerian agricultural crops, the present study sought to determine the effect of gamma radiation on the grain yield of Zea mays (maize) and Arachis hypogaea (groundnut). The seeds were planted after irradiation without the application of fertiliser. The results show that for maize, grain yield for irradiated samples is increased to levels above the unirradiated yield at doses up to about 250 Gy with the optimum yield occurring at 150 Gy. The corresponding increase for groundnut is observed at doses up to about 930 Gy with optimum yield at a dose of 300 Gy. Inhibition in yield was observed to set in at a dose greater than 250 Gy for maize and 930 Gy for groundnut. The actual relationship between mean yield of these crops and gamma radiation dose was obtained using sixth-degree polynomial equations.     

Dose-dependent analysis of acute medical effects of mixed neutron-gamma radiation from selected severe 235U or 239Pu criticality accidents in USSR, United States, and Argentina

Eight of the most severe cases of acute radiation disease (ARS) known to have occurred in humans (as the result of criticality accidents) had survival times less than 120 h (herein defined as "early death"). These accidents were analyzed and are discussed with respect to the specific accident scenarios and the resulting accident-specific, mixed neutron-gamma radiation clinical dose distributions. This analysis concludes that the cardiovascular system appears to be the most critical organ system failure for causing "early death" following approximate total body, mixed gamma-neutron radiation doses greater than 40-50 Gy. The clinical data also suggest that there was definite chest dose dependence in the resulting survival times for these eight workers, who unfortunately suffered profound radiation injury and unusual clinical effects from such high dose radiation exposures. In addition, "toxemic syndrome" is correlated with the irradiation of large volumes of soft tissues. Doses to the hands or legs greater than 80-100 Gy or radiation lung injury also play significant but secondary roles in causing "early death" in accidents delivering chest doses greater than 50 Gy.     

MicroRNA-21与乳腺癌细胞MDA-MB-231放射敏感性之间关系的研究

目的:研究MicroRNA-21与乳腺癌细胞MDA-MB-231放射敏感性之间关系及其表达规律。方法:①对乳腺癌细胞MDA-MB-231分别转染miR-21 mimics、miR-21 mimics Scramble(阴性对照)、miR-21 inhibitor、miR-21 inhibitorScramble(阴性对照),转染后进行集落形成实验,通过存活分数(Surviving Fraction SF)的变化检测其辐射敏感性是否发生变化;②时程实验:3Gy X-Ray照射后,分别于0、4、8、12、24 h后,实时荧光定量PCR检测miR-21的表达;③量效实验:0、1、2、4、6Gy X-Ray分别照射细胞24 h后,实时荧光定量PCR检测miR-21的表达。结果:MDA-MB-231细胞转染miR-21mimics后,SF明显升高,与正常对照组比较有显著性差异(P<0.05);MDA-MB-231细胞转染miR-21 inhibitor后,SF明显降低,与正常对照组比较有显著性差异(P<0.05);3GyX射线照射乳腺癌细胞株MDA-MB-231后,miR-21表达量上调,与对照组比较差异具有显著性(P<0.05),并在12 h时达到峰值,24 h时恢复到照前水平;miR-21的表达量随着照射剂量的增加而发生变化,2Gy时达到峰值,照射剂量进一步加大,miR-21表达量开始下调,与对照组比较具有显著性差异(P<0.05),6Gy时miR-21表达量明显低于未照射组。结论:miR-21对于增加乳腺癌细胞株MDA-MB-231的辐射抗性具有一定作用。     

Biological effects of intermittent radiation in cultured tumor cells: influence of fraction number and dose per fraction

In intensity-modulated radiation therapy (IMRT) and stereotactic irradiation using a linear accelerator, radiation is administered intermittently and one treatment session often requires 30 min or a longer time. The purpose of the present study was to investigate the effect of fractionation and dose per fraction on cell killing by irradiation in intermittent exposure. Murine EMT6 and SCCVII cells were used. The cells were irradiated to a total dose of 8 Gy in 2, 5, 10, 20 and 40 fractions over 15, 30 and 46 min. The cells were also given 8 Gy in a single fraction over 15, 30 and 46 min using lower dose rates (continuous prolonged radiation groups). As compared with the control group receiving a single dose of 8 Gy at 1.55 Gy/min, the cell surviving fraction generally increased in groups receiving fractionated or continuous prolonged radiation. There was a general trend for cell survival to increase with the fraction number up to 20 or 40 fractions in both cell lines. The effects of IMRT and linear accelerator radiosurgery given over 15 min or longer may be less than those of 1- or 2-fraction irradiation. There was a trend for radiation effect to decrease with fraction number.     

不同剂量电离辐射对大肠癌HCT-8细胞P-gp表达的影响

目的 通过检测不同剂量电离辐射对大肠癌细胞多药耐药基因MDR1的蛋白表达产物P-糖蛋白(P-gp)的影响,探讨逆转肿瘤多药耐药的方法。方法 采用流式细胞术检测P-gp蛋白表达的变化。结果 与假照组相比,2Gy大剂量照射后P-gp阳性细胞百分率明显增加(P<0.01),先给予低剂量照射(0.05Gy,0.1Gy)后,再给予大剂量照射,P-gp阳性细胞百分率亦有明显增加(P<0.05),0.2Gy+2Gy组P-gp阳性细胞百分率明显增加(P<0.01)。与单纯2Gy大剂量照射组比较,0.1Gy+2Gy组P-gp阳性细胞百分率明显降低(P<0.05)。结论 低剂量辐射可以逆转大剂量辐射所致的多药耐药性。     

Similarity between the effects of carbon-ion irradiation and X-irradiation on the development of rat brain

The effects of carbon-ion irradiation and X-irradiation on the development of rat brain were compared. Twenty pregnant rats were injected with bromodeoxyuridine (BrdU) at 9 pm on day 18 of pregnancy and divided into five groups. Three hours after injection (day 19.0) one group was exposed to 290 MeV/u carbon-ion radiation by a single dose of 1.5 Gy. Other groups were exposed to X-radiation by 1.5, 2.0 or 2.5 Gy, or sham-treated, respectively. Fetuses were removed from one dam in each group 8 h after exposure and examined histologically. Extensive cell death was observed in the brain mantle from the irradiated groups. The cell death after 1.5 Gy carbon-ion irradiation was remarkably more extensive than that after 1.5 Gy X-irradiation, but comparable to that after 2.0 Gy or 2.5 Gy X-irradiation. The remaining rats were allowed to give birth and the offspring were sacrificed at 6 weeks of age. All of the irradiated offspring manifested microcephaly. The size of the brain mantle exposed to 1.5 Gy carbon-ion radiation was significantly smaller than that exposed to 1.5 Gy X-radiation and larger than that exposed to 2.5 Gy X-radiation. A histological examination of the cerebral cortex revealed that cortical layers II-IV were malformed. The defect by 1.5 Gy carbon-ion irradiation was more severe than that by the same dose of X-irradiation. Although the BrdU-incorporated neurons were greatly reduced in number in all irradiated groups, these cells reached the superficial area of the cortex. These findings indicated that the effects of both carbon-ion irradiation and X-irradiation on the development of rat brain are similar in character, and the effect of 1.5 Gy carbon-ion irradiation compares to that of 2.0-2.5 Gy X-irradiation.     

An Investigation of the Early Detection of Radiation Induced Apoptosis by ^99mTc-Annexin V and ²⁰¹Thallium-Chloride in a Lung Cancer Cell Line

This study aims to investigate the efficacy of in vitro Thallium-201 Chloride (Tl-201) and in vitro and in vivo Tc-99m HYNIC-coupled Annexin V (TAV) in the early detection of radiation induced apoptosis, a proxy indicator of radiation therapy (RT) efficacy. In vitro Tl-201 and TAV accumulation and efflux in non-small cell lung cancer were measured post irradiation at 5 different gamma ray doses. The replication rates (RR) of the cell lines were also measured. The same non-small cell lung cancer line was inoculated into the left femur. In vivo non-invasive Tl-201 and TAV tracer biodistribution studies were performed. Cell RR decrease with increased radiation dose was observed 48 hours after irradiation. Apoptotic cell number was found to have increased in response to 9 Gy and 12 Gy radiation dose. Tl-201 accumulation in the 9 Gy and 12 Gy irradiation groups was found to be higher than the lower irradiation groups. Quick Tl-201 efflux was observed in the 9 Gy and 12 Gy irradiated cells. At 48 hours after irradiation with 9 Gy and 12 Gy, Annexin V accumulation was found to be higher than in the control and 3-6 Gy groups. In vivo mouse model confirmed the increased TAV uptake in implanted tumors for relatively high 9 Gy irradiation as compared to non-irradiated controls. TAV may prove to be an effective radiotracer for early assessment of radiation therapy efficacy, via apoptosis, in human lung cancers.     

Radiation hormesis: its expression in the immune system

The effects of low-dose single and continuous whole-body irradiation on immune functions were studied in C57BL/6 mice. Plaque-forming cell reaction of the spleen was found to be stimulated by single doses of x rays in the range of 0.025 to 0.075 Gy and by continuous exposure to gamma rays with a cumulative dose of 0.065 Gy. The reactivity of thymocytes to interleukin 1 showed a dose-dependent depression in the dose range of 0.025 to 0.25 Gy, but there was an increase in cell number in the thymus between doses of 0.025 and 0.10 Gy, resulting in enhancement of reaction of the whole organ. Unscheduled DNA synthesis of spleen cells was stimulated by single irradiation with 0.05 Gy and continuous irradiation with a cumulative dose of 0.13 Gy. The implications of these immunologic changes under low-dose radiation are discussed.     

电离辐射激活细胞膜受体凋亡信号通路

目的 探讨细胞膜死亡受体信号通路激活在电离辐射诱导细胞凋亡中的作用。方法 BET-2细胞经0、1、3、5、7、10 Gy不同剂量照射后分为对照组与caspase-8特异性抑制剂IETD-fmk-处理组,应用Annexin-V法观测照射后不同时间caspase-8、caspase-3的改变与细胞凋亡的变化。结果 电离辐射可引起BET-2细胞caspase-8、caspase-3增高,并诱导细胞凋亡,上述变化具有较好的照射剂量效应和时间效应;照射后加入caspase-8特异性抑制剂IETD-fmk,可在一定程度上减少电离辐射诱导的细胞凋亡。结论 电离辐射可直接激活细胞膜上死亡受体介导的细胞凋亡信号通路,诱导细胞凋亡。     

肿瘤放射治疗及造血干细胞移植预处理致放射性口腔炎的临床研究

目的探讨电离辐射所致急、慢性放射性口腔炎的诊断标准,为有效指导放射性口腔疾病的诊治提供科学依据。方法观察并分析了40例头颈部肿瘤放射治疗患者和40例造血干细胞移植预处理全身照射(TBI)患者,依据患者的症状和体征进行诊断。结果头颈部肿瘤放射治疗患者在累积剂量30Gy时出现急性口腔黏膜改变者28例,急性放射性口腔炎的发生率为70/。TBI患者在照射剂量7～8Gy时出现口腔溃疡者20例,放射性口腔炎的发生率为50/。结论急、慢性放射性口腔炎累积阈剂量分别为20～30Gy和50～60Gy,并根据患者情况决定继续或暂停放射治疗。     

Strain difference in the susceptibility of thymocytes to radiation-induced apoptosis: in vitro study.

The susceptibility of thymocytes from STS/A to radiation-induced cell death was compared with that of thymocytes from BALB/cHeA. After in vitro exposure to 12 Gy X-ray, thymocytes were incubated at 37 degrees C for 8 h and then cell mortality was assessed by 0.02% erythrosin B exclusion. Cell death took place from 2 h in the incubation period, reaching a maximum at 6 h for both strains. The dose-effect on cell death at 4 h of incubation was examined after 1-24 Gy of X-irradiation. An increase in cell death was detectable even at 1 Gy in both strains. The number of dead cells in BALB/cHeA gradually increased with doses of more than 1 Gy, finally to a maximum (approximately 60%) in the dose range of 8-12 Gy, whereas the maximum cell death in STS/A was approximately 40%. The difference between the strains at maximum cell death was significant (P less than 0.005). The difference in the radiosensitivity of thymocytes between the two strains could not be attributed to a difference in the composition of their subpopulations because flow cytometric analysis based on the expression of CD4 and CD8 showed no intrinsic difference in the thymocyte subpopulations of BALB/cHeA and STS/A.     

X射线对体外培养乳鼠心肌细胞损伤的实验研究

目的 研究X射线对体外培养的心肌细胞活性及凋亡的影响。方法 体外培养新生大鼠心肌细胞,分为对照组和放射组,放射组分别用X射线10Gy、20Gy、30Gy、40Gy单剂量照射心肌细胞,采用MTT法观察X射线对乳鼠心肌细胞活性的影响;血生化自动分析仪定量测定X射线作用后心肌细胞乳酸脱氢酶(LDH)的改变;吖啶橙/碘化丙啶(AO/PI)双染色法在激光扫描共聚焦显微镜下观察心肌细胞凋亡的形态学改变;流式细胞仪定量检测心肌细胞的凋亡率。结果 ①X射线剂量在10~40Gy均能抑制心肌细胞活性并成剂量依赖性;②细胞心肌酶谱检测到LDH释放量与X射线剂量相关;③流式细胞仪发现心肌细胞凋亡率与X射线照射剂量有相关性。结论 本研究结果显示X射线对心肌细胞有毒性作用,可致心肌细胞损伤,表现为心肌细胞坏死和凋亡发生率增加。     

Microbeam Studies of Soft X-ray Induced Bystander Cell Killing Using Microbeam X-ray Cell Irradiation System at CRIEPI

The radiation induced bystander response is defined as a response in cells which have not been directly targeted by radiation, but which are in the neighborhood of cells which have been directly exposed. In many cases, the bystander response is saturated with increasing dose and is observed when only one cell in a population is targeted by high-LET particle radiations or ultrasoft X-rays (278 eV). However, in our studies using synchrotron X-ray microbeams (5.35 keV), the bystander cell killing effect in normal human fibroblast WI-38 cells had a parabolic relationship to the irradiating dose and was detected if 5 or more cell nuclei were irradiated. To evaluate the feature of the X-ray-induced bystander cell killing effect at a wider dose range and the existence of photon energy dependence, the effects were assessed by irradiating cell nuclei in confluent WI-38 cells with AlK X-ray microbeams (1.49 keV). The surviving fraction decreased when only a single cell nucleus was irradiated, suggesting the minimal number of targeted cells to induce the effect may depend on the energy of photons used. In this study, we found that the bystander cell killing effect showed a biphasic relationship to the irradiating dose. The decrease in bystander cell survival at the doses higher than 0.23 Gy was partially suppressed between 2.3 and 7.0 Gy, followed by level-off around 90% above 14 Gy, suggesting that the X-ray-induced bystander response is dose dependent. In addition, NO is one of chief initiators/mediators of the effect at least 0.47 Gy.     

Circulatory disease mortality in the Massachusetts tuberculosis fluoroscopy cohort study

High-dose ionizing radiation is associated with circulatory disease. Risks from lower-dose fractionated exposures, such as from diagnostic radiation procedures, remain unclear. In this study we aimed to ascertain the relationship between fractionated low-to-medium dose radiation exposure and circulatory disease mortality in a cohort of 13,568 tuberculosis patients in Massachusetts, some with fluoroscopy screenings, between 1916 and 1961 and follow-up until the end of 2002. Analysis of mortality was in relation to cumulative thyroid (cerebrovascular) or lung (all other circulatory disease) radiation dose via Poisson regression. Over the full dose range, there was no overall radiation-related excess risk of death from circulatory disease (n = 3221; excess relative risk/Gy ?0.023; 95 % CI ?0.067, 0.028; p = 0.3574). Risk was somewhat elevated in hypertensive heart disease (n = 89; excess relative risk/Gy 0.357; 95 % CI ?0.043, 1.030, p = 0.0907) and slightly decreased in ischemic heart disease (n = 1950; excess relative risk/Gy ?0.077; 95 % CI ?0.130, ?0.012; p = 0.0211). However, under 0.5 Gy, there was a borderline significant increasing trend for all circulatory disease (excess relative risk/Gy 0.345; 95 % CI ?0.032, 0.764; p = 0.0743) and for ischemic heart disease (excess relative risk/Gy 0.465; 95 % CI, ?0.032, 1.034, p = 0.0682). Pneumolobectomy increased radiation–associated risk (excess relative risk/Gy 0.252; 95 % CI 0.024, 0.579). Fractionation of dose did not modify excess risk. In summary, we found no evidence of radiation-associated excess circulatory death risk overall, but there are indications of excess circulatory death risk at lower doses (<0.5 Gy). Although consistent with other radiation-exposed groups, the indications of higher risk at lower doses are unusual and should be confirmed against other data.     

Detection of endonuclease III- and 8-oxoguanine glycosylase-sensitive base modifications in gamma-irradiated DNA and cells by the aldehyde reactive probe (ARP) assay

Ionizing radiation generates diverse DNA lesions that differentially induce cell death and mutations. In the present study, calf thymus DNA (400 microg/ml) and HeLa cells were irradiated by (60)Co gamma-rays, and abasic (AP) sites and endonuclease (Endo)III- and 8-oxoguanine glycosylase (hOGG1)-sensitive base modifications in DNA were quantitated by the aldehyde reactive probe (ARP) assay. The irradiation of calf thymus DNA in phosphate buffer generated 91 Endo III- and 100 hOGG1-sensitive base modifications and 110 AP sites per 10(6) base pairs (bp) per Gy. The yield of the lesions in Tris buffer was 41- to 91-fold lower than that in phosphate, demonstrating a radioprotective effect of Tris. The HeLa cell chromosomal DNA contained 12 Endo III- and 3.8 hOGG1-sensitive base modifications and less than 1 AP sites per 10(6) bp as endogenous damage, and their level was increased by irradiation. The yields of the damage at 1 Gy (roughly equivalent to the lethal dose of HeLa cells [1.6-1.8 Gy]) were 0.13 Endo III, 0.091 hOGG1, and 0.065 AP sites per 10(6) bp, showing that irradiation with a lethal dose brought about only a marginal increase in base damage relative to an endogenous one. A comparison of the present data with those reported for DNA strand breaks supports the primary importance of double-strand breaks and clustered lesions as lethal damages formed by ionizing radiation.     

Rapid and simple method for quantitative evaluation of neurocytotoxic effects of radiation on developing medaka brain

We describe a novel method for rapid and quantitative evaluation of the degree of radiation-induced apoptosis in the developing brain of medaka (Oryzias latipes). Embryos at stage 28 were irradiated with 1, 2, 3.5, and 5 Gy x-ray. Living embryos were stained with a vital dye, acridine orange (AO), for 1-2 h, and whole-mount brains were examined under an epifluorescence microscope. From 7 to 10 h after irradiation with 5 Gy x-ray, we found two morphologically different types of AO-stained structures, namely, small single nuclei and rosette-shaped nuclear clusters. Electron microscopy revealed that these two distinct types of structures were single apoptotic cells with condensed nuclei and aggregates of apoptotic cells, respectively. From 10 to 30 h after irradiation, a similar AO-staining pattern was observed. The numbers of AO-stained rosette-shaped nuclear clusters and AO-stained single nuclei increased in a dose-dependent manner in the optic tectum. We used the number of AO-stained rosette-shaped nuclear clusters/optic tectum as an index of the degree of radiation-induced brain cell death at 20-24 h after irradiation. The results showed that the number of rosette-shaped nuclear clusters/optic tectum in irradiated embryos exposed to 2 Gy or higher doses was highly significant compared to the number in nonirradiated control embryos, whereas no difference was detected at 1 Gy. Thus, the threshold dose for brain cell death in medaka embryos was taken as being between 1-2 Gy, which may not be so extraordinarily large compared to those for rodents and humans. The results show that medaka embryos are useful for quantitative evaluation of developmental neurocytotoxic effects of radiation.     

Endothelial cell migration was impaired by irradiation-induced inhibition of SHP-2 in radiotherapy: an in vitro study

The response of endothelial cells to radiation in the context of wound healing is not yet completely understood. In this study we investigated the mechanism involved in the wound healing process after low linear energy transfer (LET) radiation exposure. A scratch wound model on primary vascular endothelial cell monolayer was exposed to acute dose of 0.1, 2 or 10 Gy. The number of cells crossing the wound border and the wound closure percentage was measured. The expression of α(v)β? integrins, focal adhesion kinase (FAK) and phosphorylated FAK (tyr397) as well as SHP-2 phosphatase were assayed through immunoblotting, immunoprecipitation and optical imaging. Compared to the low dose irradiation, 2 and 10 Gy had remarkably inhibitory effects on cell motility and consequently the wound closure. Integrins α(v) and β? showed no irradiation-dose dependent variation. Contrast to the relatively constant level of FAK in all groups, the amount of phosphor-FAK tyr397 was higher with dose increasing. The protein and PCR analysis of SHP-2 revealed an opposite expression pattern to FAK tyr397. In conclusion, radiation-induced inhibition of cell migration could be attributed to the irradiative inhibition to SHP-2 phosphatase, and the subsequent accumulated phosphorylated FAK abrogated the contraction-extension cycle of cytoskeletons.     

Exploration of "over kill effect" of high-LET Ar- and Fe-ions by evaluating the fraction of non-hit cell and interphase death

The reason why RBE for cell killing fell to less than unity (1.0) with very high-LET heavy-ions ((40)Ar: 1,640 keV/microm; (56)Fe: 780, 1,200, 2,000 keV/microm) was explored by evaluating the fraction of non-hit cell (time-lapse observation) and cells undergoing interphase death (calculation based on our previous data). CHO cells were exposed to 4 Gy (30% survival dose) of Ar (1,640 keV/microm) or Fe-ions (2,000 keV/microm). About 20% of all cells were judged to be non-hit, and about 10% cells survived radiation damage. About 70% cells died after dividing at least once (reproductive death) or without dividing (interphase death). RBE for reproductive (RBE[R]) and interphase (RBE[I]) death showed a similar LET dependence with maximum around 200 keV/microm. In this LET region, at 30% survival level, about 10% non-survivors underwent interphase death. The corresponding value for very high-LET Fe-ions (2,000 keV/microm) was not particularly high (approximately 15%), whereas that for X-rays was less than 3%. However, reproductive death (67%) predominated over interphase death (33%) even in regard to rather severely damaged cells (1% survival level) after exposure to Fe-ions (2,000 keV/microm). These indicate that interphase death is a type of cell death characteristic for the cells exposed to high-LET radiation and is not caused by "cellular over kill effect". Both NHF37 (non-hit fraction at 37% survival) and inactivation cross-section for reproductive death (sigma[R]) began to increase when LET exceeded 100 keV/microm. The exclusion of non-hit fraction in the calculation of surviving fraction partially prevented the fall of RBE[R] when LET exceeded 200 keV/microm. On the other hand, the mean number of lethal damage per unit dose (NLD/Gy) showed the same LET-dependent pattern as RBE[R]. These suggest that the increase in non-hit fraction and sigma[R] with an increasing LET is caused by enhanced clustering of ionization and DNA damage which lowers the energy efficiency for producing damage and RBE.     

Prematurely condensed chromosome rings after neutron irradiation of human lymphocytes

Calibration curves for fission spectrum neutrons and other high LET radiations are scarce in cytogenetic dosimetry and particularly for Prematurely Condensed Chromosome Rings (PCC-ring). Here we analyzed the behavior of the PCC-ring frequency and PCC index after neutron irradiation in a broad dose interval from 1 to 26 Gy. PCC-rings were induced in lymphocytes with Calyculin A. 6455 PCC cells in G1, G2/M and M/A stages were analyzed. The best fitting between the frequency of PCC ring (Y) and the Dose (D) was obtained with the equation Y = (0.059 ± 0.003) D. The saturation of the PCC-ring was observed after around 4 Gy, but it was still possible to analyze cells exposed up to 26 Gy. The distribution of rings by cell follows Poisson or Neyman type distribution for all doses. This PCC-ring dose effect curve can be used in case of accidental overexposure to neutron radiation, allowing a dose assessment in a reliable way. Additionally, the PCC index seems to be well correlated with radiation dose and decrease in a dose dependent manner from 13% in non exposed sample down to 0.2%. This observation allows the possibility to perform a quick classification of victims exposed to high doses of both gamma and neutron radiations. The PCC assay can then be used for both neutron dose estimation up to 4 Gy and for the rapid classification of victims exposed to higher doses. This assay could be included in the multiparametric approach developed to optimize the medical treatment of radiation victims.     

Dosimetry by ESR spectroscopy following a radiation accident

On 2 September, 1982, one of the employees of the gamma-irradiation facility at The Institute for Energy and Technology (Kjeller, Norway) entered the irradiation cell with a 65.7-kCi 60Co source in unshielded position. The victim received an unknown radiation dose and died after 13 days. Using electron-spin resonance spectroscopy (ESR), the radiation dose in this accident was subsequently determined based on the production of long-lived free radicals in nitroglycerol tablets carried by the operator during accident. He used nitroglycerol for heart problems and free radicals are easily formed and trapped in sugar which is the main component of the tablets. Calibration experiments were carried out and the dose given to the tablets during the accident was determined to be 39 Gy. Phantom experiments based on this result indicate an average whole-body dose in the accident of 22.5 Gy.