Search Results (5)

Ionizing radiation is a well-known carcinogen that causes genomic instability. However, the biological and carcinogenetic effects of occupational radiation exposure at low doses have not been extensively studied. The aim of this study was to assess chromosomal instability in power plant workers exposed to occupational radiation at low doses in South Korea. Chromosomal aberrations in the lymphocytes of 201 nuclear power plant workers and 59 sex-matched controls were measured. Chromosomal aberrations in the lymphocytes of 201 nuclear power plant workers (mean age: 41.4 ± 10.0 years) and 59 sex-matched controls (mean age: 47.2 ± 6.0 years) were measured. A total of 500 metaphases for each subject were scored randomly. The means of recent 1.5-year, recent 5.5-year, and cumulative exposed radiation doses among workers were 8.22 ± 7.0 mSv, 30.7 ± 22.0 mSv, and 158.8 ± 86.1 mSv, respectively. The frequency of chromosome-type and chromatid-type aberrations was significantly higher in workers than that in the control group (p < 0.001), and the frequency of chromosome-type aberrations among workers increased in a radiation dose-dependent manner (τ = 0.16, p = 0.005). Poisson regression analyses revealed that chromosome-type aberrations were significantly associated with recent 1.5-year dose after adjusting for confounding variables such as age, smoking, and alcohol intake, even when only the exposed worker was considered. Frequency of multi-aberrant cells (two or more chromosome aberrations within a cell) increased according to cumulative neutron exposure. Our study demonstrates that chromosome damage can be induced in nuclear power plant workers occupationally exposed to ionizing radiation at low doses below the occupational permissible dose limit. Furthermore, an increase in multi-aberrant cells may provide evidence for chronic neutron exposure in nuclear power plant workers. This study was performed to obtain baseline data for a surveillance program of workers occupationally exposed to ionizing radiation long-term. Full article

A recognized risk of long-duration space travel arises from the elevated exposure astronauts face from galactic cosmic radiation (GCR), which is composed of a diverse array of energetic particles. There is now abundant evidence that exposures to many different charged particle GCR components within acute time frames are sufficient to induce central nervous system deficits that span from the molecular to the whole animal behavioral scale. Enhanced spacecraft shielding can lessen exposures to charged particle GCR components, but may conversely elevate neutron radiation levels. We previously observed that space-relevant neutron radiation doses, chronically delivered at dose-rates expected during planned human exploratory missions, can disrupt hippocampal neuronal excitability, perturb network long-term potentiation and negatively impact cognitive behavior. We have now determined that acute exposures to similar low doses (18 cGy) of neutron radiation can also lead to suppressed hippocampal synaptic signaling, as well as decreased learning and memory performance in male mice. Our results demonstrate that similar nervous system hazards arise from neutron irradiation regardless of the exposure time course. While not always in an identical manner, neutron irradiation disrupts many of the same central nervous system elements as acute charged particle GCR exposures. The risks arising from neutron irradiation are therefore important to consider when determining the overall hazards astronauts will face from the space radiation environment. Full article

The proposed deep space exploration to the moon and later to Mars will result in astronauts receiving significant chronic exposures to space radiation (SR). SR exposure results in multiple neurocognitive impairments. Recently, our cross-species (mouse/rat) studies reported impaired associative memory formation in both species following a chronic 6-month low dose exposure to a mixed field of neutrons (1 mGy/day for a total dose pf 18 cGy). In the present study, we report neutron exposure induced synaptic plasticity in the medial prefrontal cortex, accompanied by microglial activation and significant synaptic loss in the hippocampus. In a parallel study, neutron exposure was also found to alter fluorescence assisted single synaptosome LTP (FASS-LTP) in the hippocampus of rats, that may be related to a reduced ability to insert AMPAR into the post-synaptic membrane, which may arise from increased phosphorylation of the serine 845 residue of the GluA1 subunit. Thus, we demonstrate for the first time, that low dose chronic neutron irradiation impacts homeostatic synaptic plasticity in the hippocampal-cortical circuit in two rodent species, and that the ability to successfully encode associative recognition memory is a dynamic, multicircuit process, possibly involving compensatory changes in AMPAR density on the synaptic surface. Full article

Although in vivo and in vitro studies have shown that chromium has protective effects against metabolic diseases, few studies have examined this association in humans. The present study examined chronic chromium (Cr) exposure among Koreans based on the measurement of toenail Cr concentrations, and analyzed the associations between toenail Cr concentrations and metabolic syndrome (MetS) and its components. We conducted a cross-sectional analysis using baseline data from the prospective cohort study in the Yeungnam area of South Korea that included 232 men and 268 women. Toenail Cr concentration was quantified by neutron activation analysis, and metabolic biomarker levels were obtained through medical examinations. The odd ratios (OR) of prevalent MetS and its components in correlation with Cr concentrations were calculated using multivariable logistic regression. After multiple confounding variables were adjusted for, participants with higher concentrations of Cr had a prevalence rate of MetS similar to those with lower concentrations (OR, 1.84; 95% confidence interval, 0.65–5.23). Our results do not support an association between long-term exposure to Cr and a lower prevalence of MetS in Koreans, whose Cr concentrations are relatively low compared to those of populations in Europe and the United States. Full article

Background: Although Asian populations consume relatively large amounts of fish and seafood and have a high prevalence of metabolic diseases, few studies have investigated the association between chronic mercury exposure and metabolic syndrome and its effect modification by selenium. Methods: We analyzed baseline data from the Trace Element Study of Korean Adults in the Yeungnam area. Participants included 232 men and 269 women, aged 35 years or older, who had complete data regarding demographic, lifestyle, diet, toenail mercury and selenium levels, and health. Toenail mercury and selenium concentrations were measured using instrumental neutron-activation analysis. The metabolic biomarker levels were obtained through biannual medical checkups. Results: Higher toenail mercury levels were associated with habitual consumption of whale and shark meats, older age, obesity, smoking, alcohol drinking, and higher household income. Multivariable analysis showed a positive association between toenail mercury exposure and metabolic syndrome. In addition, this association was significantly stronger at lower selenium levels and was weaker at higher selenium levels. Conclusion: The possible harmful effects of mercury on metabolic syndrome may be attenuated by high levels of selenium. Future studies are needed to suggest optimal dietary guidelines regarding fish and selenium intakes, particularly for Asians with high levels of fish intake. Full article