{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1390282680616005248.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.11513/jrrsabst.2008.0.18.0"}},{"identifier":{"@type":"NAID","@value":"130006999204"}}],"dc:title":[{"@language":"en","@value":"Mitochondrial Function and cell transformation"},{"@language":"ja","@value":"ミトコンドリア機能と細胞がん化"}],"dc:language":"ja","description":[{"type":"abstract","notation":[{"@language":"en","@value":"Reactive oxygen species, produced in energy production, or by exposed stresses such as radiation, is thought to be involved in the critical cause of life-style related disease, aging and cancer. We have reported that irradiated cells are accumulated genetic instability such as unstable telomere, or hypoxically-cultured cells are prevented genetic instability, and we predict that oxidative stresses are closely involved in genetic instability. On the other hand, there is clear difference in transformation sensitivity between human and rodent cells. Therefore this study was carried out to the intervention of mitochondrial function in cell transformation.\nWe cultured human, mouse, and hamster cells obtained from carcass of embryos under 0.5, 2, and 20% oxygen. As a result, mitochondria number or membrane potential was not change in human cells, and they never immortalized or transformed under all the oxygen conditions. Meanwhile, mouse cells spontaneously overcame replicative senescence easily and transformed. Moreover, intracellular oxidative levels of hypoxic-cultured mouse cells were significantly higher, and the tendency to immortalization was increased. This suggests that the response to the oxygen stress via mitochondria involve in cell immortalization and transformation. Additionally, there is a critical difference in responsibility to oxygen stress, between human and rodent cells, and increase of intracellular oxidative stress result in cell immortalization and malignant transformation. We will present the relation of cell transformation and mitochondrial function."},{"@language":"ja","@value":"エネルギー代謝副産物としてミトコンドリアで発生する活性酸素や放射線などの外的ストレスによって誘導される酸化ストレスは、動脈硬化や心筋梗塞などの生活習慣病発症とともに老化促進や癌など遺伝的不安定化の原因になると考えられている。我々は、これまでに、放射線照射された細胞では酸化状態が亢進しテロメア不安定性といった遺伝的不安定が増強されること、低酸素下で培養された細胞で遺伝的不安定性が抑制されることなどを発見し、酸化ストレスが遺伝的不安定性誘導に密接に関与していると予想している。一方、ヒト細胞とげっ歯類細胞とでは細胞がん化感受性は明らかに異なる。しかし、その感受性差を生ずる原因は明らかではない。そこで、本研究では、ヒトおよびげっ歯類細胞の細胞がん化感受性の違いがミトコンドリア機能の違いに起因するかどうかを検討することを目的とした。\n本研究では、ほぼ同じ発生段階にあるヒト、マウスおよびハムスター胎児カーカス由来初代培養細胞を用い様々な酸素圧下で培養した。その結果、ヒト細胞は、培養酸素圧の違いに依らずミトコンドリア機能は大きく変動せず不老化や細胞がん化することはなかった。一方、マウス細胞は、全ての酸素圧下で容易に老化を乗り越え不死化し、一部の細胞で細胞がん化形質を発現することがわかった。マウス細胞では、低酸素圧で培養されるとミトコンドリアの数や膜電位に変動はないものの、細胞内酸化度が高くなり、細胞がん化形質の発現が強まる傾向が認められた。このことは細胞の不死化とがん化過程にミトコンドリアを介した酸素ストレス応答能が深く関与しており、ヒト細胞に比べげっ歯類細胞では、ミトコンドリア機能恒常性維持機能が低く、細胞内酸化度の上昇が容易に起きることが細胞不死化とそれに続く細胞がん化形質の発現が高頻度で起きる原因であると予想される。本発表では細胞がん化とミトコンドリア機能との関係を考察する。"}],"abstractLicenseFlag":"disallow"}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1410009221721405696","@type":"Researcher","personIdentifier":[{"@type":"NRID","@value":"9000391976635"}],"foaf:name":[{"@language":"en","@value":"YOSHII Hanako"},{"@language":"ja","@value":"吉居 華子"}],"jpcoar:affiliationName":[{"@language":"en","@value":"Radiati. Bio., Radiat. Life Science, Res. React. Instit., Kyoto Univ."},{"@language":"ja","@value":"京大・原子炉・放射線生命・粒子線生物"}]},{"@id":"https://cir.nii.ac.jp/crid/1410009221721405697","@type":"Researcher","personIdentifier":[{"@type":"NRID","@value":"9000391976636"}],"foaf:name":[{"@language":"en","@value":"WATANABE Masami"},{"@language":"ja","@value":"渡邉 正己"}],"jpcoar:affiliationName":[{"@language":"en","@value":"Radiati. Bio., Radiat. Life Science, Res. React. Instit., Kyoto Univ."},{"@language":"ja","@value":"京大・原子炉・放射線生命・粒子線生物"}]}],"publication":{"prism:publicationName":[{"@language":"en","@value":"The Japan Radiation Research Society Annual Meeting Abstracts"},{"@language":"ja","@value":"日本放射線影響学会大会講演要旨集"},{"@language":"en","@value":"JRRS Annual Meeting Abstracts"},{"@language":"ja","@value":"日本放射線影響学会大会講演要旨集"}],"dc:publisher":[{"@language":"en","@value":"The Japanese Radiation Research Society"},{"@language":"ja","@value":"一般社団法人 日本放射線影響学会"}],"prism:publicationDate":"2008","prism:volume":"2008","prism:number":"0","prism:startingPage":"18","prism:endingPage":"18"},"availableAt":"2008","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=transformation","dc:title":"transformation"},{"@id":"https://cir.nii.ac.jp/all?q=immortalization","dc:title":"immortalization"},{"@id":"https://cir.nii.ac.jp/all?q=mitochondrial%20function","dc:title":"mitochondrial function"},{"@id":"https://cir.nii.ac.jp/all?q=%E7%B4%B0%E8%83%9E%E3%81%8C%E3%82%93%E5%8C%96","dc:title":"細胞がん化"},{"@id":"https://cir.nii.ac.jp/all?q=%E7%B4%B0%E8%83%9E%E4%B8%8D%E6%AD%BB%E5%8C%96","dc:title":"細胞不死化"},{"@id":"https://cir.nii.ac.jp/all?q=%E3%83%9F%E3%83%88%E3%82%B3%E3%83%B3%E3%83%89%E3%83%AA%E3%82%A2%E6%A9%9F%E8%83%BD","dc:title":"ミトコンドリア機能"}],"dataSourceIdentifier":[{"@type":"JALC","@value":"oai:japanlinkcenter.org:1003202013"},{"@type":"CIA","@value":"130006999204"}]}