Model of Accelerated Aging in CB6F2 Mice Induced by Ionizing Radiation
A model for accelerated aging in mice was developed: CB6F2 mice aged 39-45 days were exposed to fractionated 4-fold relatively uniform γ-radiation ( 137 Cs, 0.98 Gy/min) at a total dose of 6.8 Gy. Radiation exposure led to delayed active growth, leukopenia, and lymphopenia for over 1 year during the...
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Veröffentlicht in: | Bulletin of experimental biology and medicine 2024-07, Vol.177 (3), p.363-367 |
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creator | Yakunchikova, E. A. Yurova, M. N. Drachyov, I. S. Radetskaya, E. A. Altukhov, K. V. Semenov, A. L. Panchenko, A. V. Tyndyk, M. L. Bykov, V. N. Fedoros, E. I. |
description | A model for accelerated aging in mice was developed: CB6F2 mice aged 39-45 days were exposed to fractionated 4-fold relatively uniform γ-radiation (
137
Cs, 0.98 Gy/min) at a total dose of 6.8 Gy. Radiation exposure led to delayed active growth, leukopenia, and lymphopenia for over 1 year during the post-radiation period. The death of irradiated males and females occurred significantly earlier than in control group animals. Median lifespans in the experimental group were 35-38% lower than in the control group (
p |
doi_str_mv | 10.1007/s10517-024-06190-0 |
format | Article |
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137
Cs, 0.98 Gy/min) at a total dose of 6.8 Gy. Radiation exposure led to delayed active growth, leukopenia, and lymphopenia for over 1 year during the post-radiation period. The death of irradiated males and females occurred significantly earlier than in control group animals. Median lifespans in the experimental group were 35-38% lower than in the control group (
p
<0.001). Ionizing radiation exposure led to the early development of hair depigmentation, cachexia, and the development of aging-associated diseases. In irradiated mice, oncological pathology constituted 30-35% in the mortality structure, which is twice as often as in the control group. The developed model can be used to study the pathogenesis of accelerated aging under radiation exposure and the search for means of its prevention and treatment.</description><identifier>ISSN: 0007-4888</identifier><identifier>ISSN: 1573-8221</identifier><identifier>EISSN: 1573-8221</identifier><identifier>DOI: 10.1007/s10517-024-06190-0</identifier><identifier>PMID: 39126549</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Aging ; Aging - radiation effects ; Aging, Premature - etiology ; Aging, Premature - genetics ; Aging, Premature - pathology ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Cachexia ; Cachexia - etiology ; Cachexia - pathology ; Cell Biology ; Cell cycle ; Cesium Radioisotopes ; Drug dosages ; Female ; Females ; Gamma Rays - adverse effects ; Hematology ; Hypothesis testing ; Internal Medicine ; Ionizing radiation ; Laboratory Medicine ; Leukopenia ; Longevity - radiation effects ; Lymphopenia ; Male ; Males ; Medical research ; Mice ; Oncology ; Pathogenesis ; Pathology ; Post-radiation ; Radiation ; Radiation, Ionizing ; Research centers ; Software ; γ Radiation</subject><ispartof>Bulletin of experimental biology and medicine, 2024-07, Vol.177 (3), p.363-367</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c256t-7c37d540764fef4f401f289d6f2645a0521c4685f2ee3fd4bfb0cd59405607023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10517-024-06190-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10517-024-06190-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39126549$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yakunchikova, E. A.</creatorcontrib><creatorcontrib>Yurova, M. N.</creatorcontrib><creatorcontrib>Drachyov, I. S.</creatorcontrib><creatorcontrib>Radetskaya, E. A.</creatorcontrib><creatorcontrib>Altukhov, K. V.</creatorcontrib><creatorcontrib>Semenov, A. L.</creatorcontrib><creatorcontrib>Panchenko, A. V.</creatorcontrib><creatorcontrib>Tyndyk, M. L.</creatorcontrib><creatorcontrib>Bykov, V. N.</creatorcontrib><creatorcontrib>Fedoros, E. I.</creatorcontrib><title>Model of Accelerated Aging in CB6F2 Mice Induced by Ionizing Radiation</title><title>Bulletin of experimental biology and medicine</title><addtitle>Bull Exp Biol Med</addtitle><addtitle>Bull Exp Biol Med</addtitle><description>A model for accelerated aging in mice was developed: CB6F2 mice aged 39-45 days were exposed to fractionated 4-fold relatively uniform γ-radiation (
137
Cs, 0.98 Gy/min) at a total dose of 6.8 Gy. Radiation exposure led to delayed active growth, leukopenia, and lymphopenia for over 1 year during the post-radiation period. The death of irradiated males and females occurred significantly earlier than in control group animals. Median lifespans in the experimental group were 35-38% lower than in the control group (
p
<0.001). Ionizing radiation exposure led to the early development of hair depigmentation, cachexia, and the development of aging-associated diseases. In irradiated mice, oncological pathology constituted 30-35% in the mortality structure, which is twice as often as in the control group. The developed model can be used to study the pathogenesis of accelerated aging under radiation exposure and the search for means of its prevention and treatment.</description><subject>Aging</subject><subject>Aging - radiation effects</subject><subject>Aging, Premature - etiology</subject><subject>Aging, Premature - genetics</subject><subject>Aging, Premature - pathology</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cachexia</subject><subject>Cachexia - etiology</subject><subject>Cachexia - pathology</subject><subject>Cell Biology</subject><subject>Cell cycle</subject><subject>Cesium Radioisotopes</subject><subject>Drug dosages</subject><subject>Female</subject><subject>Females</subject><subject>Gamma Rays - adverse effects</subject><subject>Hematology</subject><subject>Hypothesis testing</subject><subject>Internal Medicine</subject><subject>Ionizing radiation</subject><subject>Laboratory Medicine</subject><subject>Leukopenia</subject><subject>Longevity - radiation effects</subject><subject>Lymphopenia</subject><subject>Male</subject><subject>Males</subject><subject>Medical research</subject><subject>Mice</subject><subject>Oncology</subject><subject>Pathogenesis</subject><subject>Pathology</subject><subject>Post-radiation</subject><subject>Radiation</subject><subject>Radiation, Ionizing</subject><subject>Research centers</subject><subject>Software</subject><subject>γ Radiation</subject><issn>0007-4888</issn><issn>1573-8221</issn><issn>1573-8221</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9LwzAYh4Mobk6_gAcJePESfZMmaXucw-lgQxA9hzZ_RkfXzqY9zE9vaqeCB08hvM_7yy8PQpcUbilAfOcpCBoTYJyApCkQOEJjKuKIJIzRYzSGQBGeJMkInXm_6a8BPEWjKKVMCp6O0XxVG1vi2uGp1ra0TdZag6frolrjosKzezlneFVoixeV6XSY5Xu8qKvioydeMlNkbVFX5-jEZaW3F4dzgt7mD6-zJ7J8flzMpkuimZAtiXUUG8EhltxZxx0H6liSGumY5CIDwajmMhGOWRs5w3OXgzYi5SBk6M6iCboZcndN_d5Z36pt4UPvMqts3XkVQfhZEssIAnr9B93UXVOFdj0Vi4Rx0VNsoHRTe99Yp3ZNsc2avaKgestqsKyCZfVlWfVLV4foLt9a87PyrTUA0QD4MKrWtvl9-5_YTwyrg70</recordid><startdate>20240701</startdate><enddate>20240701</enddate><creator>Yakunchikova, E. A.</creator><creator>Yurova, M. N.</creator><creator>Drachyov, I. S.</creator><creator>Radetskaya, E. A.</creator><creator>Altukhov, K. V.</creator><creator>Semenov, A. L.</creator><creator>Panchenko, A. V.</creator><creator>Tyndyk, M. L.</creator><creator>Bykov, V. N.</creator><creator>Fedoros, E. I.</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20240701</creationdate><title>Model of Accelerated Aging in CB6F2 Mice Induced by Ionizing Radiation</title><author>Yakunchikova, E. A. ; Yurova, M. N. ; Drachyov, I. S. ; Radetskaya, E. A. ; Altukhov, K. V. ; Semenov, A. L. ; Panchenko, A. V. ; Tyndyk, M. L. ; Bykov, V. N. ; Fedoros, E. 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A.</au><au>Yurova, M. N.</au><au>Drachyov, I. S.</au><au>Radetskaya, E. A.</au><au>Altukhov, K. V.</au><au>Semenov, A. L.</au><au>Panchenko, A. V.</au><au>Tyndyk, M. L.</au><au>Bykov, V. N.</au><au>Fedoros, E. I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Model of Accelerated Aging in CB6F2 Mice Induced by Ionizing Radiation</atitle><jtitle>Bulletin of experimental biology and medicine</jtitle><stitle>Bull Exp Biol Med</stitle><addtitle>Bull Exp Biol Med</addtitle><date>2024-07-01</date><risdate>2024</risdate><volume>177</volume><issue>3</issue><spage>363</spage><epage>367</epage><pages>363-367</pages><issn>0007-4888</issn><issn>1573-8221</issn><eissn>1573-8221</eissn><abstract>A model for accelerated aging in mice was developed: CB6F2 mice aged 39-45 days were exposed to fractionated 4-fold relatively uniform γ-radiation (
137
Cs, 0.98 Gy/min) at a total dose of 6.8 Gy. Radiation exposure led to delayed active growth, leukopenia, and lymphopenia for over 1 year during the post-radiation period. The death of irradiated males and females occurred significantly earlier than in control group animals. Median lifespans in the experimental group were 35-38% lower than in the control group (
p
<0.001). Ionizing radiation exposure led to the early development of hair depigmentation, cachexia, and the development of aging-associated diseases. In irradiated mice, oncological pathology constituted 30-35% in the mortality structure, which is twice as often as in the control group. The developed model can be used to study the pathogenesis of accelerated aging under radiation exposure and the search for means of its prevention and treatment.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>39126549</pmid><doi>10.1007/s10517-024-06190-0</doi><tpages>5</tpages></addata></record> |
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subjects | Aging Aging - radiation effects Aging, Premature - etiology Aging, Premature - genetics Aging, Premature - pathology Animals Biomedical and Life Sciences Biomedicine Cachexia Cachexia - etiology Cachexia - pathology Cell Biology Cell cycle Cesium Radioisotopes Drug dosages Female Females Gamma Rays - adverse effects Hematology Hypothesis testing Internal Medicine Ionizing radiation Laboratory Medicine Leukopenia Longevity - radiation effects Lymphopenia Male Males Medical research Mice Oncology Pathogenesis Pathology Post-radiation Radiation Radiation, Ionizing Research centers Software γ Radiation |
title | Model of Accelerated Aging in CB6F2 Mice Induced by Ionizing Radiation |
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