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Description:
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Ionizing radiation (IR ) can initiate a large spectrum of damage which leads to the induction of DNA protective and repair pathways . Historically , IR studies have assessed the effects of high dose , acute exposures ; however a recent shift in radiation biology has focused its efforts to cellular responses of low dose IR exposure . We used the radioactive environment surrounding the Chornobyl Nuclear Power Plant to assess the potential for the development of radioresistance in exposed animals and the possible molecular mechanisms that maybe responsible . To better understand the phenomenon of radioresistance , we exposed male BALB /c mice externally to a priming (pr ) dose of 10cGy at two dose rates (6 .94x10 -4cGy min -1 and 0 .5cGy min -1 ) followed by a subsequent 1 .5Gy challenge (ch ) dose (6 .25x10 -3Gy min -1 ) . We measured absolute mRNA levels using quantitative real -time polymerase chain reaction (QRT -PCR ) of enzymes and proteins believed to maintain genome integrity under increased levels of oxidative stress . Twenty four hours post exposure there was no induction of Apex1 and Polb (Base Excision Repair [BER] ) , Ercc1 and Ercc2 (Nucleotide Excision Repair [NER] ) and Gpx1 (Reactive Oxygen Species [ROS] scavenging ) . We were able to detect a significant amount of differential expression in two of our exposure groups for the Sod1 (ROS scavenging ) gene . When compared to micronucleus (MN ) data as a measurement of radioadaption of these same mice , the high expression levels of Sod1 suggest a temporal -dependent component . Therefore , we conclude that Sod1 expression levels suggest a role in radioadaption at ultra -low dose rates . |