|Poulose, Shibu - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|Bielinski, Donna - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|Miller, Marshall - Duke University|
|Carrihill-knoll, Kirsty - University Of Maryland|
|Rabin, Bernard - University Of Maryland|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/30/2018
Publication Date: 7/14/2018
Citation: Shukitt Hale, B., Poulose, S.M., Bielinski, D.F., Miller, M.G., Carrihill-Knoll, K.L., Rabin, B.M. 2018. Neurochemical changes in specific regions of rat brain following partial or whole body exposures to 56Fe particles [abstract]. COSPAR 2018 Scientific Assembly Abstracts F2.1-0014-18, p. 1905.
Technical Abstract: Exposing young rats to particles of high energy and charge (HZE particles), a ground-based model for exposure to cosmic rays, disrupts cognitive performance, possibly via production of oxidative stress and inflammation and disruption of the functioning of neuronal communication in critical regions of the brain. Furthermore, these changes in neuronal function are similar to those seen in aging. Although it is known that radiation exposure can cause long-term damage to the brain, it is unknown if this exposure needs to occur directly to the brain or if hits restricted to the body will also cause residual damage. The present experiments were designed to evaluate the neuromodulation of oxidative stress and inflammation following head-only, body-only, and whole-body exposures to 56Fe particles in two areas of the brain critical for cognitive function, the hippocampus and the frontal cortex. Male, Sprague-Dawley rats were given either head-only, body-only or whole-body exposures to 56Fe (600 MeV/n; 50cGy) particles at the NASA Space Radiation Laboratory at Brookhaven National Laboratory. Tungsten bricks were used to shield either the head or the body, as required; the bricks were removed for whole body exposures. The non-irradiated control rats (0 cGy) were taken to the NSRL, but not exposed. Rats were euthanized 60 days following irradiation. Results indicated a significant (p<0.05) increase in NF-kB, a pro-inflammatory transcription factor, in the hippocampus of rats exposed to 56Fe irradiation, regardless of the target of exposure. An indication of dysfunctional autophagy (i.e., accumulation of ubiquitinated p62) was also increased in hippocampus and frontal cortex, regardless of target of exposure. Two endogenous antioxidant enzymes, GST and SOD, showed increased activation in head-only exposure, but decreased activation with body-only and further significant decrease with whole-body exposure. Nuclear factor E2-related factor 2 (Nrf2) expression, a transcription factor for antioxidant enzymes, and a possible link between oxidative stress, neuroinflammation and autophagy mechanisms, showed differential effects depending on the area of the brain and the target of exposure. These results show that exposures restricted to the body can still disrupt neuronal function, as some measures were directly affected by body-only radiation, while other measures showed greater change following whole-body exposures. Oxidative stress and inflammation caused by radiation seem to be critical factors in these neuromodulatory changes, as well as in the behavioral disruptions seen following irradiation with cosmic rays.