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Статті в журналах з теми "Brain irradiation"

Автор: Grafiati

Опубліковано: 26 жовтня 2024

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1

Shirato, Hiroki, Akio Takamura, Masayoshi Tomita, Keishiro Suzuki, Takashi Nishioka, Toyohiko Isu, Tsutomu Kato, et al. "Stereotactic irradiation without whole-brain irradiation for single brain metastasis." International Journal of Radiation Oncology*Biology*Physics 37, no. 2 (January 1997): 385–91. http://dx.doi.org/10.1016/s0360-3016(96)00488-9.

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2

Feng, Xi, Sonali Gupta, David Chen, Zoe Boosalis, Sharon Liu, Nalin Gupta, and Susanna Rosi. "SCIDOT-04. REPLACEMENT OF MICROGLIA BY BRAIN-ENGRAFTED MACROPHAGES PREVENTS MEMORY DEFICITS AFTER THERAPEUTIC WHOLE-BRAIN IRRADIATION." Neuro-Oncology 21, Supplement_6 (November 2019): vi273. http://dx.doi.org/10.1093/neuonc/noz175.1145.

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Abstract Microglia have a distinct origin compared to blood circulating myeloid cells. Under normal physiological conditions, microglia are maintained by self-renewal, independent of hematopoietic progenitors. Following genetic or pharmacologic depletion, newborn microglia derive from the local residual pool and quickly repopulate the entire brain. The depletion of brain resident microglia during therapeutic whole-brain irradiation fully prevents irradiation-induced synaptic loss and recognition memory deficits but the mechanisms driving these protective effects are unknown. Here, we demonstrate that after CSF-1R inhibitor-mediated microglia depletion and therapeutic whole-brain irradiation, circulating monocytes engraft into the brain and replace the microglia pool. These monocyte-derived brain-engrafted macrophages have reduced phagocytic activity compared to microglia from irradiated brains, but similar to locally repopulated microglia without brain irradiation. Transcriptome comparisons reveal that brain-engrafted macrophages have both monocyte and embryonic microglia signatures. These results suggest that monocyte-derived brain-engrafted macrophages represent a novel therapeutic avenue for the treatment of brain radiotherapy-induced cognitive deficits.

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3

Feng, Xi, Sonali Gupta, David Chen, Zoe Boosalis, Sharon Liu, Nalin Gupta, and Susanna Rosi. "EXTH-08. REPLACEMENT OF MICROGLIA BY BRAIN-ENGRAFTED MACROPHAGES PREVENTS MEMORY DEFICITS AFTER THERAPEUTIC WHOLE-BRAIN IRRADIATION." Neuro-Oncology 21, Supplement_6 (November 2019): vi83—vi84. http://dx.doi.org/10.1093/neuonc/noz175.342.

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Abstract Microglia have a distinct origin compared to blood circulating myeloid cells. Under normal physiological conditions, microglia are maintained by self-renewal, independent of hematopoietic progenitors. Following genetic or pharmacologic depletion, newborn microglia derive from the local residual pool and quickly repopulate the entire brain. The depletion of brain resident microglia during therapeutic whole-brain irradiation fully prevents irradiation-induced synaptic loss and recognition memory deficits but the mechanisms driving these protective effects are unknown. Here, we demonstrate that after CSF-1R inhibitor-mediated microglia depletion and therapeutic whole-brain irradiation, circulating monocytes engraft into the brain and replace the microglia pool. These monocyte-derived brain-engrafted macrophages have reduced phagocytic activity compared to microglia from irradiated brains, but similar to locally repopulated microglia without brain irradiation. Transcriptome comparisons reveal that brain-engrafted macrophages have both monocyte and embryonic microglia signatures. These results suggest that monocyte-derived brain-engrafted macrophages represent a novel therapeutic avenue for the treatment of brain radiotherapy-induced cognitive deficits.

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4

Yuan, Hong, Judith N. Rivera, Jonathan E. Frank, Jonathan Nagel, Colette Shen, and Sha X. Chang. "Mini-Beam Spatially Fractionated Radiation Therapy for Whole-Brain Re-Irradiation—A Pilot Toxicity Study in a Healthy Mouse Model." Radiation 4, no. 2 (May 8, 2024): 125–41. http://dx.doi.org/10.3390/radiation4020010.

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For patients with recurrent brain metastases, there is an urgent need for a more effective and less toxic treatment approach. Accumulating evidence has shown that spatially fractionated radiation therapy (SFRT) is able to provide a significantly higher therapeutic ratio with lower toxicity compared to conventional radiation using a uniform dose. The purpose of this study was to explore the potential low toxicity benefit of mini-beam radiotherapy (MBRT), a form of SFRT, for whole-brain re-irradiation in a healthy mouse model. Animals first received an initial 25 Gy of uniform whole-brain irradiation. Five weeks later, they were randomized into three groups to receive three different re-irradiation treatments as follows: (1) uniform irradiation at 25 Gy; (2) MBRT at a 25 Gy volume-averaged dose (106.1/8.8 Gy for peak/valley dose, 25 Gy-MBRT); and (3) MBRT at a 43 Gy volume-averaged dose (182.5/15.1 Gy for peak/valley dose, 43 Gy-MBRT). Animal survival and changes in body weight were monitored for signs of toxicity. Brains were harvested at 5 weeks after re-irradiation for histologic evaluation and immunostaining. The study showed that 25 Gy-MBRT resulted in significantly less body weight loss than 25 Gy uniform irradiation in whole-brain re-irradiation. Mice in the 25 Gy-MBRT group had a higher level of CD11b-stained microglia but also maintained more Ki67-stained proliferative progenitor cells in the brain compared to mice in the uniform irradiation group. However, the high-dose 43 Gy-MBRT group showed severe radiation toxicity compared to the low-dose 25 Gy-MBRT and uniform irradiation groups, indicating dose-dependent toxicity. Our study demonstrates that MBRT at an appropriate dose level has the potential to provide less toxic whole-brain re-irradiation. Future studies investigating the use of MBRT for brain metastases are warranted.

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5

OKAMOTO, Shinichiro, Hajime HANDA, Junkoh YAMASHITA, Yasuhiko TOKURIKI, and Mitsuyuki ABE. "Post-irradiation Brain Tumors." Neurologia medico-chirurgica 25, no. 7 (1985): 528–33. http://dx.doi.org/10.2176/nmc.25.528.

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6

Wurm, R. E., L. Schlenger, A. Kaiser, M. Kömer, M. Fitzek, L. Röschel, D. Böhmer, G. Matnjani, M. Stuschke, and V. Budach. "Brain metastases — Radiosurgery or whole brain irradiation?" European Journal of Cancer 35 (September 1999): S129. http://dx.doi.org/10.1016/s0959-8049(99)80896-x.

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7

Natsuko, Kondo, Sakurai Yoshinori, Takayuki Kajihara, Takushi Takada, Nobuhiko Takai, Kyo Kume, Shinichi Miyatake, Shoji Oda, and Minoru Suzuki. "ET-13 CONTROL OF ACTIVATED MICROGLIA THROUGH P2X4 RECEPTOR IN RADIATION BRAIN NECROSIS." Neuro-Oncology Advances 1, Supplement_2 (December 2019): ii10. http://dx.doi.org/10.1093/noajnl/vdz039.043.

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Abstract INTRODUCTION Brain radiation necrosis (RN) is severe adverse event after radiation therapy for brain tumor patients, especially in case of re-irradiation. Although corticosteroids or vitamin E, etc. are clinically used for RN, the effect is limited and underlying mechanism is to be cleared. Therefore, we established RN mouse model with irradiating right hemisphere of mouse brain using proton beam at dose of 60 Gy [Kondo et al., 2015]. In this study, we investigated change of phospholipids and lipid mediators after irradiation using this RN model in correlation with microglia activation. METHODS After irradiation, change of phospholipids and lipid mediators in mouse brain was investigated using imaging mass spectrometry and LC-MS. Immunohistochemistry on microglia and P2X4 receptor, a receptor for lysophosphatidylcholine (LPC) was performed. RESULTS In imaging mass spectrometry, 1 and 4 months after irradiation, phosphatidylcholine (PC): (16:0/20:4), (18:0/20:4) decreased in irradiated area compared non-irradiated area. On the other hand, LPC: (16:0) increased in irradiated area compared to non-irradiated area after 1 month and 4 months irradiation. PC (16:0/20:4) is a precursor of LPC (16:0) and arachidonic acid (20:4). By LC-MS, LPC was twice higher in irradiated area compared to non-irradiated, 6 months after irradiation. Microglia was highly activated in irradiated area compared to non-irradiated from 3 months after irradiation to 8 months and strongly co-expressed P2X4 receptor was confirmed in irradiated area after 6 months. Preliminary P2X4 receptor agonist administration test prolonged the RN to 12 months after irradiation. CONCLUSION In RN, LPC may continuously activated microglia through P2X4 receptor and cause chronic inflammation after irradiation. P2X4 agonist administration test including action resolution and immunohistochemistry is ongoing.

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8

Crvenkova, S., and C. Tolevska. "314 Partial brain irradiation (PBI) or whole brain irradiation (WBI), the justified solution." European Journal of Cancer Supplements 1, no. 5 (September 2003): S96. http://dx.doi.org/10.1016/s1359-6349(03)90347-8.

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9

Romano, Mariele, Alberto Bravin, Alberto Mittone, Alicia Eckhardt, Giacomo E. Barbone, Lucie Sancey, Julien Dinkel, et al. "A Multi-Scale and Multi-Technique Approach for the Characterization of the Effects of Spatially Fractionated X-ray Radiation Therapies in a Preclinical Model." Cancers 13, no. 19 (October 1, 2021): 4953. http://dx.doi.org/10.3390/cancers13194953.

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The purpose of this study is to use a multi-technique approach to detect the effects of spatially fractionated X-ray Microbeam (MRT) and Minibeam Radiation Therapy (MB) and to compare them to seamless Broad Beam (BB) irradiation. Healthy- and Glioblastoma (GBM)-bearing male Fischer rats were irradiated in-vivo on the right brain hemisphere with MRT, MB and BB delivering three different doses for each irradiation geometry. Brains were analyzed post mortem by multi-scale X-ray Phase Contrast Imaging–Computed Tomography (XPCI-CT), histology, immunohistochemistry, X-ray Fluorescence (XRF), Small- and Wide-Angle X-ray Scattering (SAXS/WAXS). XPCI-CT discriminates with high sensitivity the effects of MRT, MB and BB irradiations on both healthy and GBM-bearing brains producing a first-time 3D visualization and morphological analysis of the radio-induced lesions, MRT and MB induced tissue ablations, the presence of hyperdense deposits within specific areas of the brain and tumor evolution or regression with respect to the evaluation made few days post-irradiation with an in-vivo magnetic resonance imaging session. Histology, immunohistochemistry, SAXS/WAXS and XRF allowed identification and classification of these deposits as hydroxyapatite crystals with the coexistence of Ca, P and Fe mineralization, and the multi-technique approach enabled the realization, for the first time, of the map of the differential radiosensitivity of the different brain areas treated with MRT and MB. 3D XPCI-CT datasets enabled also the quantification of tumor volumes and Ca/Fe deposits and their full-organ visualization. The multi-scale and multi-technique approach enabled a detailed visualization and classification in 3D of the radio-induced effects on brain tissues bringing new essential information towards the clinical implementation of the MRT and MB radiation therapy techniques.

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10

Lissoni, P., S. Meregalli, S. Curreri, G. Messina, F. Brivio, L. Fumagalli, M. Colciago, and G. Gardani. "Brain Irradiation-Induced Lymphocytosis Predicts Response in Cancer Patients with Brain Metastases." International Journal of Biological Markers 23, no. 2 (April 2008): 111–14. http://dx.doi.org/10.1177/172460080802300207.

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Lymphocytopenia is one of the main toxicities of radiotherapy and its severity is related to the irradiation dose. The occurrence of lymphocytopenia depends on the body site of radiotherapy; it is most pronounced with pelvic irradiation, whereas the effect of brain irradiation on the lymphocyte count is to be elucidated. This preliminary study was performed to evaluate changes in lymphocyte number occurring during brain irradiation in cancer patients with brain metastases. The study included 50 patients who received brain radiotherapy for single or multiple brain metastases at a total dose of 30 Gy. Overall, no significant changes in mean lymphocyte number occurred during brain radiotherapy. However, when lymphocyte variations were assessed in relation to the clinical response of brain metastases, a significant increase in the mean number of lymphocytes was found in patients who achieved objective regression of brain metastases on brain irradiation. The mean lymphocyte number decreased in nonresponding patients, albeit without a statistically significant difference with respect to the pretreatment values. The results of this study show that the efficacy of radiotherapy in the treatment of brain metastases is associated with a significant increase in mean lymphocyte number. Therefore, evidence of brain irradiation-induced lymphocytosis may predict the efficacy of radiotherapy.

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11

Chura, J. C., K. Shukla, and P. A. Argenta. "Brain metastasis from cervical carcinoma." International Journal of Gynecologic Cancer 17, no. 1 (January 2007): 141–46. http://dx.doi.org/10.1111/j.1525-1438.2007.00808.x.

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The aim of this study was to describe the features of patients with brain metastasis from cervical cancer. Twelve patients with brain metastasis from cervical cancer were identified. Information regarding symptoms, treatment, and survival was analyzed. The incidence of brain metastasis in our population was 0.77%. Median patient age at initial diagnosis of cervical cancer was 43.5 years (range 29–57 years) compared with 44.5 years (range 31–58 years) at identification of brain metastasis. Six patients had FIGO stage IB disease; three had stage IIB disease; and one each had stage IIIA, IIIB, and IVB disease. The median interval from diagnosis of cervical cancer to identification of brain metastasis was 17.5 months (range 1.1–96.1 months). All but one patient presented with neurologic symptoms. Eight patients received whole-brain irradiation and steroids, three received steroids alone, and one underwent surgery, followed by irradiation. All the patients who received whole-brain irradiation experienced improvement in their symptoms. Median survival from diagnosis of brain metastasis to death was 2.3 months (range 0.3–7.9 months). Five patients who received chemotherapy after brain irradiation had a median survival of 4.4 months compared to 0.9 months for those who received no additional treatment after brain irradiation (P= .016). Most patients with brain metastasis from cervical cancer presented with neurologic sequelae. Brain irradiation improved these symptoms. Survival after diagnosis of brain metastasis was poor; however, patients who received chemotherapy after brain irradiation appeared to have improved survival.

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12

Peev, Nikolay. "DIAGNOSTIC PITFALLS OF BRAIN METASTASES AFTER BRAIN IRRADIATION." Journal of IMAB - Annual Proceeding (Scientific Papers) 16, book 3, no. 2010 (December 14, 2010): 32–37. http://dx.doi.org/10.5272/jimab.1632010_32-37.

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13

Nemoz, Christian, Astrid Kibleur, Jean Noël Hyacinthe, Gilles Berruyer, Thierry Brochard, Elke Bräuer-Krisch, Géraldine Le Duc, Emmanuel Brun, Hélène Elleaume, and Raphaël Serduc. "In vivopink-beam imaging and fast alignment procedure for rat brain tumor radiation therapy." Journal of Synchrotron Radiation 23, no. 1 (January 1, 2016): 339–43. http://dx.doi.org/10.1107/s1600577515018561.

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A fast positioning method for brain tumor microbeam irradiations for preclinical studies at third-generation X-ray sources is described. The three-dimensional alignment of the animals relative to the X-ray beam was based on the X-ray tomography multi-slices after iodine infusion. This method used pink-beam imaging produced by the ID17 wiggler. A graphical user interface has been developed in order to define the irradiation parameters: field width, height, number of angles and X-ray dose. This study is the first reporting an image guided method for soft tissue synchrotron radiotherapy. It allowed microbeam radiation therapy irradiation fields to be reduced by a factor of ∼20 compared with previous studies. It permitted more targeted, more efficient brain tumor microbeam treatments and reduces normal brain toxicity of the radiation treatment.

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14

Sano, Takashi, Kaoru Tamura, Masae Kuroha, Kazutaka Sumita, Yukika Arai, Takashi Sugawara, Motoki Inaji, Yoji Tanaka, Tadashi Nariai, and Taketoshi Maehara. "RONC-18. ANALYSIS OF BRAIN TUMOR INDUCED BY IRRADIATION IN CHILDHOOD - A SINGLE INSTITUTIONAL ANALYSIS." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii458—iii459. http://dx.doi.org/10.1093/neuonc/noaa222.787.

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Abstract BACKGROUND Radiation-induced brain tumors are rare tumors that appear during long-term follow-up after radiation therapy. Children are at greater risk for radiation -induced brain tumors than adults. The clinical characteristics of radiation-induced brain tumor treated at our hospital were retrospectively examined. PATIENTS AND METHODS Clinical characteristics of seven radiation-induced brain tumors that developed in 6 patients irradiated in their childhood at our hospital were analyzed. The background disease, age at irradiation, irradiation dose, period from irradiation to onset, pathological diagnosis, and treatment for radiation-induced brain tumor were examined. RESULTS Background diseases for irradiation were leukemia in 3 patients, germinoma in 2, medulloblastoma in 1, and the average cranial irradiation dose was 23.2 Gy. The patients tended to be young at irradiation (2–17 yeays; median:4 years old). The time between irradiation and the onset of radiation-induced brain tumors ranged from 9.5 to 39.1 years (median:28 years). Radiation-induced brain tumors comprised 6 meningioma（grade I:5, grade II:1）and 1 high-grade gliomas. All patients underwent surgical removal of the radiation-induced brain tumors and 2 received additional irradiation. During a median of 5.3 years of follow-up after the diagnosis of radiation-induced brain tumors, 2 underwent second surgery, while the remaining 4 have no recurrence. DISCUSSION: In most cases, radiation-induced brain tumors occur for a long time after irradiation in childhood. Monitoring of radiation-induced brain tumors as well as primary tumor recurrence was considered important.

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15

Levegrün, Sabine, Lan Ton, and Jürgen Debus. "Partial irradiation of the brain." Seminars in Radiation Oncology 11, no. 3 (July 2001): 259–67. http://dx.doi.org/10.1053/srao.2001.25242.

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16

Healy, John. "Mental Dysfunction After Brain Irradiation." International Journal of Radiation Oncology*Biology*Physics 72, no. 2 (October 2008): 628. http://dx.doi.org/10.1016/j.ijrobp.2008.06.1906.

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17

Toogood, A. A. "Endocrine consequences of brain irradiation." Growth Hormone & IGF Research 14 (June 2004): 118–24. http://dx.doi.org/10.1016/j.ghir.2004.03.038.

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18

Sze, Sheila, Muoi N. Tran, and Matthew Follwell. "Volumetric Whole Brain Irradiation Evaluation." Journal of Medical Imaging and Radiation Sciences 47, no. 1 (March 2016): S22—S23. http://dx.doi.org/10.1016/j.jmir.2015.12.070.

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19

Aoyama, Hidefumi. "Stereotactic irradiation for brain lesions." Annals of Oncology 28 (October 2017): ix48. http://dx.doi.org/10.1093/annonc/mdx600.

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20

Pape, H., A. Aulich, B. Bannach, A. M. Messing-Jünger, M. Glag, U. M. Carl, M. Wittkamp, and Ch Haller. "Stereotactic irradiation of brain metastases." Der Gynäkologe 32, no. 9 (September 1999): 683–88. http://dx.doi.org/10.1007/pl00003282.

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21

Windsor, P. "Re-irradiation of the Brain." Clinical Oncology 30, no. 7 (July 2018): 456–57. http://dx.doi.org/10.1016/j.clon.2018.03.011.

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22

Larson, David A., Philip H. Gutin, Steven A. Leibel, Theodore L. Phillips, Penny K. Sneed, and William M. Wara. "Stereotaxic irradiation of brain tumors." Cancer 65, S3 (February 1, 1990): 792–99. http://dx.doi.org/10.1002/1097-0142(19900201)65:3+<792::aid-cncr2820651327>3.0.co;2-p.

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23

Olzowy, Bernhard, Cornelia S. Hundt, Susanne Stocker, Karl Bise, Hans Jürgen Reulen, and Walter Stummer. "Photoirradiation therapy of experimental malignant glioma with 5-aminolevulinic acid." Journal of Neurosurgery 97, no. 4 (October 2002): 970–76. http://dx.doi.org/10.3171/jns.2002.97.4.0970.

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Object. Accumulation of protoporphyrin IX (PPIX) in malignant gliomas is induced by 5-aminolevulinic acid (5-ALA). Because PPIX is a potent photosensitizer, the authors sought to discover whether its accumulation might be exploited for use in photoirradiation therapy of experimental brain tumors, without injuring normal or edematous brain. Methods. Thirty rats underwent craniotomy and were randomized to the following groups: 1) photoirradiation of cortex (200 J/cm2, 635-nm argon-dye laser); 2) photoirradiation of cortex (200 J/cm2) 6 hours after intravenous administration of 5-ALA (100 mg/kg body weight); 3) cortical cold injury for edema induction; 4) cortical cold injury with simultaneous administration of 5-ALA (100 mg/kg body weight) and photoirradiation of cortex (200 J/cm2) 6 hours later; or 5) irradiation of cortex (200 J/cm2) 6 hours after intravenous administration of Photofrin II (5 mg/kg body weight). Tumors were induced by cortical inoculation of C6 cells and 9 days later, magnetic resonance (MR) images were obtained. On Day 10, animals were given 5-ALA (100 mg/kg body weight) and their brains were irradiated (100 J/cm2) 3 or 6 hours later. Seventy-two hours after irradiation, the brains were removed for histological examination. Irradiation of brains after administration of 5-ALA resulted in superficial cortical damage, the effects of which were not different from those of the irradiation alone. Induction of cold injury in combination with 5-ALA and irradiation slightly increased the depth of damage. In the group that received irradiation after intravenous administration of Photofrin II the depth of damage inflicted was significantly greater. The extent of damage in response to 5-ALA and irradiation in brains harboring C6 tumors corresponded to the extent of tumor determined from pretreatment MR images. Conclusions. Photoirradiation therapy in combination with 5-ALA appears to damage experimental brain tumors selectively, with negligible damage to normal or perifocal edematous tissue.

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24

Kohzuki, Hidehiro, Ai Muroi, Masashi Mizumoto, Hideaki Sakurai, Eiichi Ishikawa, and Akira Matsumura. "GCT-60. DEVELOPMENT OF MICROBLEEDING AFTER PROTON THERAPY FOR PATIENTS WITH GERM CELL TUMOR." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii340. http://dx.doi.org/10.1093/neuonc/noaa222.277.

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Abstract BACKGROUND Proton therapy has been increasingly used to treat pediatric brain tumor. However, there were few reports about radiation-induced cerebral microbleeds(CMBs) and cavernous malformation among these patients. Here we evaluate the incidence and risk factor of CMBs with MR imaging. MATERIAL AND METHOD We retrospectively identified patients with germ cell tumor treated with whole ventricle irradiation of 30.6 Gy using proton therapy at the Tsukuba University Hospital between 2004 and 2017. CMBs were characterized by examination of MR imaging scan including susceptibility-weighted imaging and T2* weighed gradient-recalled echo sequence. RESULT The mean age at the time of proton therapy was 14.5 years. The median follow-up duration was 62.3 months. Three patients were treated by local boost in addition to whole ventricle irradiation. CMBs were found in 78% at 5 years, and 88% at 10 years from irradiation. Over 80% of CMBs occurred in area of the brain exposed to 30 Gy. CONCLUSION This study indicated over 30 Gy irradiation may become a risk factor for development of CMBs. Although the correlation between development of CMBs and cognitive function, proton therapy might have an advantage to reduce late sequelae with decreasing irradiating dose to surrounding normal brain tissue.

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25

Zhirnik, A. S., A. V. Rodina, Yu P. Semochkina, O. V. Vysotskaya, O. D. Smirnova, M. G. Ratushnyak, and E. Yu Moskaleva. "COGNITIVE DISTURBANCES AND THE STATE OF BRAIN GLIAL CELLS IN MICE EXPOSED TO FRACTIONATED WHOLE-BRAIN IRRADIATION." MEDICAL RADIOLOGY AND RADIATION SAFETY 67, no. 5 (October 2022): 10–17. http://dx.doi.org/10.33266/1024-6177-2022-67-5-10-17.

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Purpose: To investigate the effect of fractionated whole-brain γ-irradiation at a cumulative dose of 20 Gy on cognitive functions, the state of brain glial cells and expression of multiple cytokines in mice 2 months after exposure. Material and methods: Male C57Bl/6 mice were exposed to fractionated head γ-irradiation with 5 doses of 4 Gy. Two months after irradiation the behavior and cognitive functions of animals were assessed. After isolation of cells from mice brains the content of resting and activated microglia, microglial cells with M1- and M2-phenotype, astrocytes, proliferating cells were evaluated, and the hippocampal mRNA levels of pro- and anti-inflammatory cytokines (TNFα, IL-1β, IL-6, IL-4, TGFβ) were determined. Results: It was shown that fractionated head γ-irradiation didn’t alter the locomotor activity and associative (context fear) memory, but reduced the episodic memory in novel object recognition test (discrimination index was 0.44 ± 0.08 и 0.02 ± 0.09 in control and irradiated groups, respectively) and spatial memory in Morris water maze (time in target quadrant was 46,8 ± 2,4 % and 37,4 ± 2,8 % in control and irradiated groups, respectively). Exposure of γ-radiation significantly reduced the brain contents of microglial cells (Iba1+) and astrocytes (GFAP+) with concurrent 2.5 times increase in proportion of activated microglia (from 2.0 ± 0.2 % in control to 4.9 ± 0.5 % in irradiated mice), changed the M1- / M2-microglia ratio and significantly decreased the number of proliferating cells (BrdU+) and proliferating microglial cells (BrdU+/Iba1+). An increase in mRNA level of pro-inflammatory cytokine TNFα, a decrease in mRNA level of anti-inflammatory cytokine TGFβ and concurrent increase in mRNA level of IL-4 were detected in hippocampus 2 months after irradiation. Conclusion: We show that fractionated head γ-irradiation at a cumulative dose of 20 Gy reduces the episodic and spatial memory in mice 2 months after exposure. Cognitive dysfunctions detected are associated with neuroinflammation characterized by increasing proportion of activated brain microglia and altered hippocampal pro- and anti-inflammatory cytokine profile.

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26

Kaushal, V., M. Bidmead, L. Hill, and M. Brada. "Radiotherapy of brain tumours: Reduced irradiation of normal brain." Clinical Oncology 2, no. 6 (November 1990): 338–42. http://dx.doi.org/10.1016/s0936-6555(05)80997-5.

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27

Guo, S., C. A. Reddy, S. T. Chao, and J. H. Suh. "Repeat Whole Brain Irradiation for Patients with Brain Metastases." International Journal of Radiation Oncology*Biology*Physics 81, no. 2 (October 2011): S645. http://dx.doi.org/10.1016/j.ijrobp.2011.06.1906.

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Contreras-Zarate, Maria, Karen Alvarez-Eraso, Zachary Littrell, Nicole Tsuji, Sana Karam, D. Ryan Ormond, Peter Kabos, and Diana Cittelly. "BSCI-18 ESTROGEN-DEPLETION DECREASES PROGRESSION OF ER¯ BRAIN METASTASES BY PROMOTING AN ANTI-TUMORAL LOCAL IMMUNE RESPONSE." Neuro-Oncology Advances 4, Supplement_1 (August 1, 2022): i4. http://dx.doi.org/10.1093/noajnl/vdac078.016.

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Abstract We have shown that 17-β-Estradiol (E2) promotes brain metastasis (BM) of estrogen receptor negative (ER¯) BC cells by inducing neuroinflammatory ER+ astrocytes in the brain niche to secrete pro-metastatic factors critical for early brain colonization. E2-depletion prevented brain colonization of human xenografts (MDA231BR/NSG) and syngeneic (E0711/C57Bl6, 4T1/Balb-c) ER¯ models. Yet, whether E2-depletion can be used to decrease progression of established BM and how E2-dependent modulation of brain immune response contributes to the pro-metastatic effects of E2 remains unclear. To assess whether E2-depletion could decrease BM progression in a model that mimics standard of care for BM, E0771-GFP-luc cells were injected intracardially in syngeneic ovariectomized (OVX)-female C57Bl6 mice supplemented with E2. Seven days after injection (when micrometastases are established), mice received a single 15Gy dose brain irradiation and were randomized to continue receiving E2, E2 withdrawal (E2WD) or E2WD plus the aromatase-inhibitor letrozole (EWD+LET). Endpoint BM (but not systemic metastases) were significantly decreased in E2WD+Letrozole treated mice as compared to E2-treated mice. This effect was abolished when E0711 cells were injected in severely immunocompromised NSG mice or in the absence of brain irradiation, suggesting EWD+LET decreases BM progression through boosting radiation-induced anti-tumor immunity. Accordingly, there were no differences in BM progression in E2, EWD or E2WD+let treated mice in a xenograft model (F2-7 TNBC cells) in NSG mice, even in the presence of brain irradiation. Brain immune-profiling of brain irradiated E2, EWD and EWD+Let C57BL6 mice carrying E0771 BMs shows that brains of EWD+LET-treated mice had a significantly lower fraction of CD4 T cells and an increase in CD8 T cells, suggesting that EWD+letrozole decrease brain metastatic burden in part through modulation of T cells. These results suggest E2-depletion therapies could be used in combination with brain irradiation to decrease progression of BMs and promote an anti-tumoral immune response.

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Kim, Jin-Woong, Ji-Ae Park, Nitish Katoch, Ji-ung Yang, Seungwoo Park, Bup-Kyung Choi, Sang-Gook Song, Tae-Hoon Kim, and Hyung-Joong Kim. "Image-Based Evaluation of Irradiation Effects in Brain Tissues by Measuring Absolute Electrical Conductivity Using MRI." Cancers 13, no. 21 (October 31, 2021): 5490. http://dx.doi.org/10.3390/cancers13215490.

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Radiation-induced injury is damage to normal tissues caused by unintentional exposure to ionizing radiation. Image-based evaluation of tissue damage by irradiation has an advantage for the early assessment of therapeutic effects by providing sensitive information on minute tissue responses in situ. Recent magnetic resonance (MR)-based electrical conductivity imaging has shown potential as an effective early imaging biomarker for treatment response and radiation-induced injury. However, to be a tool for evaluating therapeutic effects, validation of its reliability and sensitivity according to various irradiation conditions is required. We performed MR-based electrical conductivity imaging on designed phantoms to confirm the effect of ionizing radiation at different doses and on in vivo mouse brains to distinguish tissue response depending on different doses and the elapsed time after irradiation. To quantify the irradiation effects, we measured the absolute conductivity of brain tissues and calculated relative conductivity changes based on the value of pre-irradiation. The conductivity of the phantoms with the distilled water and saline solution increased linearly with the irradiation doses. The conductivity of in vivo mouse brains showed different time-course variations and residual contrast depending on the irradiation doses. Future studies will focus on validation at long-term time points, including early and late delayed response and evaluation of irradiation effects in various tissue types.

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30

Mechanick, Jeffrey I., Fred H. Hochberg, and Alan LaRocque. "Hypothalamic dysfunction following whole-brain irradiation." Journal of Neurosurgery 65, no. 4 (October 1986): 490–94. http://dx.doi.org/10.3171/jns.1986.65.4.0490.

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✓ The authors describe 15 cases with evidence of hypothalamic dysfunction 2 to 9 years following megavoltage whole-brain x-irradiation for primary glial neoplasm. The patients received 4000 to 5000 rads in 180- to 200-rad fractions. Dysfunction occurred in the absence of computerized tomography-delineated radiation necrosis or hypothalamic invasion by tumor, and antedated the onset of dementia. Fourteen patients displayed symptoms reflecting disturbances of personality, libido, thirst, appetite, or sleep. Hyperprolactinemia (with prolactin levels up to 70 ng/ml) was present in all of the nine patients so tested. Of seven patients tested with thyrotropin-releasing hormone, one demonstrated an abnormal pituitary gland response consistent with a hypothalamic disorder. Seven patients developed cognitive abnormalities. Computerized tomography scans performed a median of 4 years after tumor diagnosis revealed no hypothalamic tumor or diminished density of the hypothalamus. Cortical atrophy was present in 50% of cases and third ventricular dilatation in 58%. Hypothalamic dysfunction, heralded by endocrine, behavioral, and cognitive impairment, represents a common, subtle form of radiation damage.

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31

Perrin, Andrew J., and Jeff C. Donovan. "Lichen planopilaris following whole brain irradiation." International Journal of Dermatology 53, no. 10 (June 5, 2014): e468-e470. http://dx.doi.org/10.1111/ijd.12576.

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32

CHIANG, J.-H. HONG, A. STALDER, J.-, C. S. "Delayed molecular responses to brain irradiation." International Journal of Radiation Biology 72, no. 1 (January 1997): 45–53. http://dx.doi.org/10.1080/095530097143527.

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33

Lawler, Sean E., E. Antonio Chiocca, and Charles H. Cook. "Cytomegalovirus Encephalopathy during Brain Tumor Irradiation." Clinical Cancer Research 26, no. 13 (April 10, 2020): 3077–78. http://dx.doi.org/10.1158/1078-0432.ccr-20-0646.

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34

Stewart-Amidei, Chris. "Delayed Effects of Therapeutic Brain Irradiation." Critical Care Nursing Clinics of North America 7, no. 1 (March 1995): 125–33. http://dx.doi.org/10.1016/s0899-5885(18)30430-1.

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35

Deprez, S. "SP-0338 Neurocognition and brain irradiation." Radiotherapy and Oncology 133 (April 2019): S172. http://dx.doi.org/10.1016/s0167-8140(19)30758-3.

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36

Sze, Sheila, Matthew Follwell, and Muoi N. Tran. "188: Volumetric Whole Brain Irradiation Evaluation." Radiotherapy and Oncology 120 (September 2016): S69. http://dx.doi.org/10.1016/s0167-8140(16)33587-3.

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37

Ford, Judith. "Whole Brain Irradiation at Lower Doses." International Journal of Radiation Oncology*Biology*Physics 103, no. 5 (April 2019): 1286–87. http://dx.doi.org/10.1016/j.ijrobp.2018.12.003.

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38

Rades, D., J. D. Kueter, J. Gliemroth, T. Veninga, A. Pluemer, and S. E. Schild. "Resection plus whole-brain irradiation versus resection plus whole-brain irradiation plus boost for the treatment of single brain metastasis." Strahlentherapie und Onkologie 188, no. 2 (January 12, 2012): 143–47. http://dx.doi.org/10.1007/s00066-011-0024-9.

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39

Zanni, Giulia, Kai Zhou, Ilse Riebe, Cuicui Xie, Changlian Zhu, Eric Hanse, and Klas Blomgren. "Irradiation of the Juvenile Brain Provokes a Shift from Long-Term Potentiation to Long-Term Depression." Developmental Neuroscience 37, no. 3 (2015): 263–72. http://dx.doi.org/10.1159/000430435.

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Radiotherapy is common in the treatment of brain tumors in children but often causes deleterious, late-appearing sequelae, including cognitive decline. This is thought to be caused, at least partly, by the suppression of hippocampal neurogenesis. However, the changes in neuronal network properties in the dentate gyrus (DG) following the irradiation of the young, growing brain are still poorly understood. We characterized the long-lasting effects of irradiation on the electrophysiological properties of the DG after a single dose of 6-Gy whole-brain irradiation on postnatal day 11 in male Wistar rats. The assessment of the basal excitatory transmission in the medial perforant pathway (MPP) by an examination of the field excitatory postsynaptic potential/volley ratio showed an increase of the synaptic efficacy per axon in irradiated animals compared to sham controls. The paired-pulse ratio at the MPP granule cell synapses was not affected by irradiation, suggesting that the release probability of neurotransmitters was not altered. Surprisingly, the induction of long-term synaptic plasticity in the DG by applying 4 trains of high-frequency stimulation provoked a shift from long-term potentiation (LTP) to long-term depression (LTD) in irradiated animals compared to sham controls. The morphological changes consisted in a virtually complete ablation of neurogenesis following irradiation, as judged by doublecortin immunostaining, while the inhibitory network of parvalbumin interneurons was intact. These data suggest that the irradiation of the juvenile brain caused permanent changes in synaptic plasticity that would seem consistent with an impairment of declarative learning. Unlike in our previous study in mice, lithium treatment did unfortunately not ameliorate any of the studied parameters. For the first time, we show that the effects of cranial irradiation on long-term synaptic plasticity is different in the juvenile compared with the adult brain, such that while irradiation of the adult brain will only cause a reduction in LTP, irradiation of the juvenile brain goes further and causes LTD. Although the mechanisms underlying the synaptic alterations need to be elucidated, these findings provide a better understanding of the effects of irradiation in the developing brain and the cognitive deficits observed in young patients who have been subjected to cranial radiotherapy.

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40

Eggert, Hans R., Marika Kiessling, and Paul Kleihues. "Time Course and Spatial Distribution of Neodymium: Yttrium-Aluminum-Garnet (Nd:YAG) Laser-induced Lesions in the Rat Brain." Neurosurgery 16, no. 4 (April 1, 1985): 443–48. http://dx.doi.org/10.1097/00006123-198504000-00001.

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Abstract Cerebral lesions made by focal neodymium: yttrium-aluminum-garnet (Nd: YAG) laser irradiation of the rat forebrain were studied in adult Wistar rats. For the analysis of time-dependent changes, the brains of 28 animals were irradiated with a constant energy density of 461 J/cm2. In this series, survival time ranged from 0.5 hours to 80 days. Immediately after irradiation, a circular lesion appeared on the surface of the brain. This lesion was surrounded by an edematous area intensively stained with Evans blue. At energy levels higher than 30 J, this circular edema contained numerous thrombosed vessels. Histopathologically, the lesion consisted of three distinct zones: the central coagulation necrosis was surrounded by a zone of delayed colliquation necrosis and by perifocal edema. At approximately 80 days after irradiation, the resulting cortical defect was covered by a pial membrane. Edematous changes of the brain cortex and the adjacent white matter were observed as early as 1 hour after irradiation. Within 16 hours, the perifocal edema spread over the white matter of both hemispheres, and it had disappeared by the 5th day after irradiation. In a second experiment, the energy density varied from 231 to 3077 J/cm2. This series consisted of 84 animals that were allowed to survive 48 hours. The size of the lesion depended on the level of energy applied, but the depth of the lesion varied less than the diameter at the brain surface. The depth ranged from 1.3 mm at 20 J to 3.1 mm at 140 J, and the diameter of the lesion at the brain surface varied from 1.3 mm at 15 J to 5.8 mm at 140 J. The results obtained suggest that the Nd: YAG laser can be used for tumor coagulation with minimal risk of adverse effects on the adjacent brain.

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41

Park, Ji Ae, Youngsung Kim, Jiung Yang, Bup Kyung Choi, Nitish Katoch, Seungwoo Park, Young Hoe Hur, Jin Woong Kim, Hyung Joong Kim, and Hyun Chul Kim. "Effects of Irradiation on Brain Tumors Using MR-Based Electrical Conductivity Imaging." Cancers 15, no. 1 (December 20, 2022): 22. http://dx.doi.org/10.3390/cancers15010022.

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Ionizing radiation delivers sufficient energy inside the human body to create ions, which kills cancerous tissues either by damaging the DNA directly or by creating charged particles that can damage the DNA. Recent magnetic resonance (MR)-based conductivity imaging shows higher sensitivity than other MR techniques for evaluating the responses of normal tissues immediately after irradiation. However, it is still necessary to verify the responses of cancer tissues to irradiation by conductivity imaging for it to become a reliable tool in evaluating therapeutic effects in clinical practice. In this study, we applied MR-based conductivity imaging to mouse brain tumors to evaluate the responses in irradiated and non-irradiated tissues during the peri-irradiation period. Absolute conductivities of brain tissues were measured to quantify the irradiation effects, and the percentage changes were determined to estimate the degree of response. The conductivity of brain tissues with irradiation was higher than that without irradiation for all tissue types. The percentage changes of tumor tissues with irradiation were clearly different than those without irradiation. The measured conductivity and percentage changes between tumor rims and cores to irradiation were clearly distinguished. The contrast of the conductivity images following irradiation may reflect the response to the changes in cellularity and the amounts of electrolytes in tumor tissues.

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42

Akiba, T., E. Kunieda, A. Kogawa, T. Komatsu, Y. Tamai, and Y. Ohizumi. "Re-irradiation for Metastatic Brain Tumors with Whole-brain Radiotherapy." Japanese Journal of Clinical Oncology 42, no. 4 (February 9, 2012): 264–69. http://dx.doi.org/10.1093/jjco/hys007.

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43

Sadikov, E., A. Bezjak, Q. L. Yi, W. Wells, L. Dawson, and N. Laperriere. "48 Value of Whole Brain Re-Irradiation for Brain Metastases." Radiotherapy and Oncology 76 (September 2005): S15. http://dx.doi.org/10.1016/s0167-8140(05)80209-9.

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44

Sundgren, Pia C., and Yue Cao. "Brain Irradiation: Effects on Normal Brain Parenchyma and Radiation Injury." Neuroimaging Clinics of North America 19, no. 4 (November 2009): 657–68. http://dx.doi.org/10.1016/j.nic.2009.08.014.

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45

Brockmann, Silke, Peter Grummich, Oliver Ganslandt, Rainer Fietkau, and Sabine Semrau. "Reorganization of Functional Areas of the Brain After Brain Irradiation." Journal of Clinical Oncology 29, no. 12 (April 20, 2011): e321-e323. http://dx.doi.org/10.1200/jco.2010.32.7890.

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46

Li, Wenxin, Chi Zhang, Shuhei Aramaki, Lili Xu, Shogo Tsuge, Takumi Sakamoto, Md Al Mamun, et al. "Lipid Polyunsaturated Fatty Acid Chains in Mouse Kidneys Were Increased within 5 min of a Single High Dose Whole Body Irradiation." International Journal of Molecular Sciences 24, no. 15 (August 4, 2023): 12439. http://dx.doi.org/10.3390/ijms241512439.

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To understand the ultra-early reaction of normal organ lipids during irradiation, we investigated the response of lipids, including polyunsaturated fatty acid (PUFA) chains, which are particularly susceptible to damage by ROS, in mice’s kidneys, lungs, brains, and livers within 5 min of single high-dose irradiation. In this study, we set up three groups of C56BL/6 male mice and conducted whole-body irradiation with 0 Gy, 10 Gy, and 20 Gy single doses. Kidney, lung, brain, and liver tissues were collected within 5 min of irradiation. PUFA-targeted and whole lipidomic analyses were conducted using liquid chromatography–tandem mass spectrometry (LC-MS/MS). The results showed that PUFA chains of kidney phosphatidylcholine (PC), phosphatidylethanolamine (PE), and triacylglycerol (TG) significantly increased within 5 min of 10 Gy and 20 Gy irradiation. The main components of increased PUFA chains in PC and PE were C18:2, C20:4, and C22:6, and in TG the main component was C18:2. The kidney lipidomes also showed significant changes from the perspective of lipid species, mainly dominated by an increase in PC, PE, TG, and signal lipids, while lipidomes of the lung, brain, and liver were slightly changed. Our results revealed that acute PUFA chains increase and other lipidomic changes in the kidney upon whole-body irradiation within 5 min of irradiation. The significantly increased lipids also showed a consistent preference for possessing PUFA chains. The lipidomic changes varied from organ to organ, which indicates that the response upon irradiation within a short time is tissue-specific.

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47

Alrefae, M. A., D. Roberge, and L. Souhami. "Short-course irradiation as adjuvant treatment of surgically resected single brain metastases." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 2067. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.2067.

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2067 Background: Surgical resection followed by whole-brain irradiation is a standard treatment approach for patients with a single brain metastasis from solid tumours. As short-course hypofractionated irradiation has proven equivalent to more protracted schedules for the palliative treatment of brain metastasis, it has been commonly applied in the adjuvant setting. Methods: By reviewing our pathology database, we identified patients having undergone complete neurosurgical resection of a single brain metastasis followed by short-course (4–6 fractions) whole-brain irradiation. Irradiation was delivered using standard lateral-opposed megavoltage radiation portals. Local failure and new brain metastases were identified by chart and imaging study reviews. All outcomes were calculated actuarially. Results: Between March 2000 and August 2005, 50 patients received short-course whole-brain irradiation (20 Gy in 5 fractions in 41 of 50 cases) following complete surgical resection of a single brain metastasis. The most common primary malignancies were lung (66%), breast (14%), and cancer of unknown primary origin (10%). Median age was 60 years. Imaging studies were available for all patients and a preoperative MRI was reviewed in 94% of cases. Median follow-up for living patients was 30.0 months. The median overall survival was 10.92 months (29% at 2 years). Following radiation, failure at the surgical site was seen in 51% and 79% of patients at 1 and 2 years. New metastases elsewhere in the brain developed in 26% and 53% of these patients at 1 and 2 years. Conclusions: When calculated actuarially, local failure and new brain metastases were common following surgery and short-course whole-brain radiation therapy. In part, this may represent inefficacy of the short hypofractionated radiation scheme. Further investigation into the local and systemic treatment of these patients is warranted. No significant financial relationships to disclose.

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48

Kiessling, Marika, Eberhard Herchenhan, and Hans R. Eggert. "Cerebrovascular and metabolic effects on the rat brain of focal Nd:YAG laser irradiation." Journal of Neurosurgery 73, no. 6 (December 1990): 909–17. http://dx.doi.org/10.3171/jns.1990.73.6.0909.

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✓ To investigate the effects of focal neodymium:yttrium-aluminum-garnet (Nd:YAG) laser irradiation (λ = 1060 nm) on regional cerebral blood flow, cerebral protein synthesis, and blood-brain barrier permeability, the parietal brain surface of 44 rats was irradiated with a focused laser beam at a constant output energy of 30 J. Survival times ranged from 5 minutes to 48 hours. Laser irradiation immediately caused well-defined cortical coagulation necrosis. Within 5 minutes after unilateral irradiation, 14C-iodoantipyrine autoradiographs demonstrated severely reduced blood flow to the irradiation site and perilesional neocortex, but a distinct reactive hyperemia in all other areas of the forebrain. Apart from a persistent ischemic focus in the vicinity of the cortical coagulation necrosis, blood flow alterations in remote areas of the brain subsided within 3 hours after irradiation. Autoradiographic assessment of 3H-tyrosine incorporation into brain proteins revealed rapid onset and prolonged duration of protein synthesis inhibition in perifocal morphologically intact cortical and subcortical structures. Impairment of amino acid incorporation proved to be completely reversible within 48 hours. Immunoautoradiographic visualization of extravasated plasma proteins using 3H-labeled rabbit anti-rat immunoglobulins showed that, up to 1 hour after irradiation, immunoreactive proteins were confined to the neocortex at the irradiation site. At 4 hours, vasogenic edema was present in the vicinity of the irradiation site and the subcortical white matter, and, at later stages (16 to 36 hours), also extended into the contralateral hemisphere. Although this was followed by a gradual decrease in labeling intensity, resolution of edema was still not complete after 48 hours. Analysis of sequential functional changes in conjunction with morphological alterations indicates that the evolution of morphological damage after laser irradiation does not correlate with the time course and spatial distribution of protein synthesis inhibition or vasogenic edema. Although the central coagulation necrosis represents a direct effect of radiation, the final size of the laser-induced lesion is determined by a delayed colliquation necrosis due to persistent perifocal ischemia. Extent and severity of ischemia in a zone with initial preservation of neuroglial cells can be explained by the optical properties of the Nd:YAG laser; extensive scattering of light within brain parenchyma associated with a high blood-to-brain absorption ratio selectively affects blood vessels outside the irradiation focus.

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Yuen, Nili, Kamila U. Szulc-Lerch, Yu-Qing Li, Cindi M. Morshead, Donald J. Mabbott, C. Shun Wong, and Brian J. Nieman. "Metformin effects on brain development following cranial irradiation in a mouse model." Neuro-Oncology 23, no. 9 (May 27, 2021): 1523–36. http://dx.doi.org/10.1093/neuonc/noab131.

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Abstract Background Cranial radiation therapy (CRT) is a mainstay of treatment for malignant pediatric brain tumors and high-risk leukemia. Although CRT improves survival, it has been shown to disrupt normal brain development and result in cognitive impairments in cancer survivors. Animal studies suggest that there is potential to promote brain recovery after injury using metformin. Our aim was to evaluate whether metformin can restore brain volume outcomes in a mouse model of CRT. Methods C57BL/6J mice were irradiated with a whole-brain radiation dose of 7 Gy during infancy. Two weeks of metformin treatment started either on the day of or 3 days after irradiation. In vivo magnetic resonance imaging was performed prior to irradiation and at 3 subsequent time points to evaluate the effects of radiation and metformin on brain development. Results Widespread volume loss in the irradiated brain appeared within 1 week of irradiation with limited subsequent recovery in volume outcomes. In many structures, metformin administration starting on the day of irradiation exacerbated radiation-induced injury, particularly in male mice. Metformin treatment starting 3 days after irradiation improved brain volume outcomes in subcortical regions, the olfactory bulbs, and structures of the brainstem and cerebellum. Conclusions Our results show that metformin treatment has the potential to improve neuroanatomical outcomes after CRT. However, both timing of metformin administration and subject sex affect structure outcomes, and metformin may also be deleterious. Our results highlight important considerations in determining the potential benefits of metformin treatment after CRT and emphasize the need for caution in repurposing metformin in clinical studies.

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Abdel-Aziz, Nahed, Ahmed A. Elkady, and Eman M. Elgazzar. "Effect of Low-Dose Gamma Radiation and Lipoic Acid on High- Radiation-Dose Induced Rat Brain Injuries." Dose-Response 19, no. 4 (October 2021): 155932582110448. http://dx.doi.org/10.1177/15593258211044845.

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Aim This work aims to investigate the possible radio-adaptive mechanisms induced by low-dose (LD) whole-body γ-irradiation alone or combined with alpha-lipoic acid (ALA) administration in modulating high-dose (HD) head irradiation–induced brain injury in rats. Materials and Methods Rats were irradiated with LD (.25 Gy) 24 hours prior HD (20 Gy), and subjected to ALA (100 mg/kg/day) 5 minutes after HD and continued for 10 days. At the end of the experiment, animals were sacrificed and brain samples were dissected for biochemical and histopathological examinations. Results HD irradiation-induced brain injury as manifested by elevation of oxidative stress, DNA damage, apoptotic, and inflammatory markers in brain tissue. Histological examination of brain sections showed marked alterations. However, LD alone or combined with ALA ameliorated the changes induced by HD. Conclusion Under the present experimental conditions, LD whole-body irradiation exhibited neuroprotective activity against detrimental effects of a subsequent HD head irradiation. This effect might be due to the adaptive response induced by LD that activated the anti-oxidative, anti-apoptotic, and anti-inflammatory mechanisms in the affected animals making them able to cope with the subsequent high-dose exposure. However, the combined LD exposure and ALA supplementation produced a further modulating effect in the HD-irradiated rats.

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