Biology Department Seminar

Over the past century, a well established paradigm of radiation biology has been based on the "target theory" in which radiation deposits energy into the targeted cell nucleus. The deposited energy produced DNA damage, the prime target, as a linear function of dose. The DNA damage was postulated to be linearly related to the induction of mutation, chromosome aberrations and cancer. This central dogma led to the establishment of the "linear no-threshold" dose response curve and has been applied to radiation health risk and radiation protection. However, in the past two decades, there has been increasing evidence of the shift in the paradigm because dose-response curves for many biological endpoints are not straight lines following exposure to low doses of radiation. This shift comes about with the rigorous research on genomic instability, bystander effects (non-targeted effects), adaptive response, epigenetics, tissue microenvironment, and chronic inflammation. I will present biological data obtained from my laboratory, under the projects funded by the DOE and NASA, that contribute to the understanding of genomic instability, adaptive response, and chronic inflammation after radiation exposure.