Key Dates
- March 6, 2012 – Online Registration Opens
- March 12, 2012 – Abstract submission Closes (all abstracts due at this time)
- March 12, 2012 - New Investigator Award Applications Due
- April 16, 2012 - Accepted abstracts for Poster Session, New Investigators Announced
- May 4, 2012 - Hotel Reservations Close
- May 21, 2012 - Online Registration Closes
Long-term effects of chronic exposure to ionizing radiation on the hematopoietic system in man
Alexander Akleyev, Urals Research Center for Radiation Medicine Keywords: cellular effects, chronic radiation exposure, late effects, genomic instability, intracellular barrier mechanisms The Techa River Cohort includes about 30,000 individuals exposed to protracted IR resulting from releases of radioactive waste into the Techa River during the initial years (1949-1956) of operation of the Mayak nuclear facility (weapon-grade plutonium production) in the Southern Urals region of Russia. The exposure was of a two-component type: external ?-(contributed by 137Cs) and internal radiation (mostly due to 90Sr). The aim of this study was to assess the spectrum of intracellular markers to evaluate the adverse long-term health effects in hematopoietic system at late time after onset of exposure. The study group comprised of 1,117 exposed individuals (the mean cumulative dose to red bone marrow was 1.13 Gy) and 484 unexposed individuals. An increased rates of genetic disorders (CD3-CD4+ lymphocytes, mutations in the Tp53 gene, dicentrics, and micronucleus) and of DNA single- and double-stranded breaks frequency and repair ineffectiveness were detected among residents of the Techa riverside villages at late time after the onset of chronic radiation exposure. Cell Parameters of the cell’s functional status parameters (apoptosis, and cell cycle control) had a peak at small doses (about 0.3 Gy), and a decline at higher doses. Trade-off between decline in frequency of apoptotic lymphocytes and increased fractions of Chk2+ lymphocytes for doses above 1Gy was observed. The oxidation status showed a sharp reduction in the concentration of Cu/ZnSOD (at doses below 0.3 Gy) and re-distribution of free active species in favor of their most aggressive forms. We interpreted these results as a manifestation of radiation induced genomic instability. Genomic instability has developed in a small proportion of subjects who should be assigned to the group at high risk of cancer development. The application of the mechanistic modeling will allow individualization of the radiogenic risk of leukemia based on the results of the study.
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