Genomic Instability in Human Lymphocytes Irradiated with Individual Charged Particles: Involvement of Tumor Necrosis Factor α in Irradiated Cells but not Bystander Cells

Cell Survival 610 Radiation Dosage Chromosomes Genomic Instability name=Radiation /dk/atira/pure/subjectarea/asjc/2700/2741 03 medical and health sciences Humans Lymphocytes name=Biophysics Cells, Cultured Chromosome Aberrations /dk/atira/pure/subjectarea/asjc/1100/1101 0303 health sciences /dk/atira/pure/subjectarea/asjc/3100/3108 Genome, Human Tumor Necrosis Factor-alpha Dose-Response Relationship, Radiation Bystander Effect name=SDG 3 - Good Health and Well-being 3. Good health name=Agricultural and Biological Sciences (miscellaneous) name=Radiology Nuclear Medicine and imaging /dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being /dk/atira/pure/subjectarea/asjc/1300/1304
DOI: 10.1667/rr3298 Publication Date: 2006-07-17T20:57:56Z
ABSTRACT
Exposure to ionizing radiation can increase the risk of cancer, which is often characterized by genomic instability. In environmental exposures to high-LET radiation (e.g. 222Ra), it is unlikely that many cells will be traversed or that any cell will be traversed by more than one alpha particle, resulting in an in vivo bystander situation, potentially involving inflammation. Here primary human lymphocytes were irradiated with precise numbers of 3He2+ ions delivered to defined cell population fractions, to as low as a single cell being traversed, resembling in vivo conditions. Also, we assessed the contribution to genomic instability of the pro-inflammatory cytokine tumor necrosis factor alpha (TNFA). Genomic instability was significantly elevated in irradiated groups (> or = two-fold over controls) and was comparable whether cells were traversed by one or two 3He2+ ions. Interestingly, substantial heterogeneity in genomic instability between experiments was observed when only one cell was traversed. Genomic instability was significantly reduced (60%) in cultures in which all cells were irradiated in the presence of TNFA antibody, but not when fractions were irradiated under the same conditions, suggesting that TNFA may have a role in the initiation of genomic instability in irradiated cells but not bystander cells. These results have implications for low-dose exposure risks and cancer.
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