Updated on 2022/04/26

写真a

 
TAKUMI Shota
 
Organization
Research Field in Fisheries, Agriculture, Fisheries and Veterinary Medicine Area Faculty of Fisheries Department of Fisheries Science and Technology Associate Professor
Title
Associate Professor

Degree

  • 博士(医学) ( 2009.3   鹿児島大学 )

Research Interests

  • 食品

  • 酸化ストレス

  • 遺伝子変異

  • 亜鉛

  • マイクロシスチン

  • エピジェネティクス

Research Areas

  • Life Science / Food sciences  / 機能性、安全性

  • Life Science / Hygiene and public health (laboratory)

Research History

  • Kagoshima University   Research Field in Fisheries, Agriculture, Fisheries and Veterinary Medicine Area Faculty of Fisheries Department of Fisheries Science and Technology   Associate Professor

    2019.4

  • Kagoshima University   Faculty of Fisheries   Associate Professor

    2019.4

  • Kagoshima Women's Junior College   Department of Domestic Science   Associate Professor

    2015.4 - 2019.3

Professional Memberships

  • 日本衛生学会

    2010.4

  • 日本水産学会

    2018.4

  • 日本分子生物学会

    2015.4

  • JAPANESE SOCIETY FOR MARINE BIOTECHNOLOGY

  • THE JAPANESE SOCIETY FOR HYGIENE

  • THE JAPANESE SOCIETY OF FISHERIES SCIENCE

  • THE MOLECULAR BIOLOGY SOCIETY OF JAPAN

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Committee Memberships

  • 日本衛生学会   評議員  

    2015.4   

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    Committee type:Academic society

 

Papers

  • KOMATSU Masaharu, TAKUMI Shota .  Cyanotoxin microcystin-LR induces novel EMT-like changes to OATP1B3-expressing cells .  Annual Meeting of the Japanese Society of Toxicology47 ( 0 ) S10 - 4   2020

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    Publisher:The Japanese Society of Toxicology  

    <p>Cyanotoxin microcystin-LR (MC-LR) induces acute injury of hepatocytes through protein phosphatases PP1/PP2A inhibition. In case of its chronic exposure, MC-LR induces hepato-carcinoma caused by acceleration of cell proliferation. Previously, we demonstrated the molecular basis for hepato-selective cytotoxicity of MC-LR which is taken-up into cells mediated by hepatocyte-specifically expressing transporter OATP1B1/1B3. Recently, we demonstrated a novel function of MC-LR which induced bi-potentially changes including anoikis resistance and cytoskeleton reorganization. In this symposium, I will discuss about association with epithelial-mesenchymal transition of these cells.</p>

    DOI: 10.14869/toxpt.47.1.0_S10-4

  • Hiroyuki Yanagisawa, Yoshiko Seki, Shingo Yogosawa, Shota Takumi, Hidesuke Shimizu, Machi Suka .  Potential role of mitochondrial damage and S9 mixture including metabolic enzymes in ZnO nanoparticles-induced oxidative stress and genotoxicity in Chinese hamster lung (CHL/IU) cells. .  Mutation research. Genetic toxicology and environmental mutagenesis834   25 - 34   2018.10

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    The present study was designed to examine genotoxicity induced by 10-40 nm zinc oxide (ZnO) nanoparticles using the in vitro system. The frequency of micronuclei was significantly increased in a dose-dependent manner when cultured Chinese hamster lung (CHL/IU) cells were exposed to ZnO nanoparticles for 24, 48 and 72 h in the continuous treatment method. The maximal frequency of micronuclei was observed in exposure of CHL/IU cells to ZnO nanoparticles at a concentration of 125 μM. The frequency of micronuclei was profoundly enhanced when CHL/IU cells were exposed to ZnO nanoparticles in the presence vs. absence of S9 mixture including metabolic enzymes in the short-term treatment method, demonstrating an increase in the formation of micronuclei by S9 mixture. The maximal frequency of micronuclei was seen in exposure of CHL/IU cells to ZnO nanoparticles at a concentration of 140 μM. Similar results were obtained in chromosome aberrations, particularly structural aberrations. Surprisingly, administration of the superoxide radical scavenger, tempol, completely abolished an increase in the frequency of micronuclei in the presence or absence of S9 mixture, indicating a central role of superoxide radical in the formation of micronuclei. Indeed, reactive oxygen species (ROS) generation was elevated by simultaneous incubation of S9 mixture and ZnO nanoparticles and by exposure of CHL/IU cells to ZnO nanoparticles in the presence or absence of S9 mixture. An electron microscopic examination revealed mitochondrial damage in CHL/IU cells exposed to ZnO nanoparticles, indicating the participation of mitochondrial dysfunction in ROS generation in this setting. These observations suggest that ZnO nanoparticles evoke genotoxicity through superoxide radical-induced oxidative stress derived from mitochondrial damage in CHL/IU cells. S9 mixture appears to contribute to a further increase in genotoxicity through the generation of superoxide radical by metabolic activation of ZnO nanoparticles.

    DOI: 10.1016/j.mrgentox.2018.07.003

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  • Yanagisawa H, Seki Y, Yogosawa S, Takumi S, Shimizu H, Suka M. .  Potential role of mitochondrial damage and S9 mixture including metabolic enzymes in ZnO nanoparticles-induced oxidative stress and genotoxicity in Chinese hamster lung (CHL/IU) cells. .  Mutat Res Genet Toxicol Environ Mutagen.   2018.8Potential role of mitochondrial damage and S9 mixture including metabolic enzymes in ZnO nanoparticles-induced oxidative stress and genotoxicity in Chinese hamster lung (CHL/IU) cells.Reviewed

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    Language:English   Publishing type:Research paper (scientific journal)  

  • Takumi S, Shimono T, Ikema S, Hotta Y, Chigwechokha PK, Shiozaki K, Sugiyama Y, Hashimoto M, Furukawa T, Komatsu M. .  Overexpression of carboxylesterase contributes to the attenuation of cyanotoxin microcystin-LR toxicity. .  Comp Biochem Physiol C Toxicol Pharmacol   2017.4Overexpression of carboxylesterase contributes to the attenuation of cyanotoxin microcystin-LR toxicity.Reviewed

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    Language:English   Publishing type:Research paper (scientific journal)  

  • Shota Takumi, Tai Shimono, Satoshi Ikema, Yuki Hotta, Petros K. Chigwechokha, Kazuhiro Shiozaki, Yasumasa Sugiyama, Mitsuru Hashimoto, Tatsuhiko Furukawa, Masaharu Komatsu .  Overexpression of carboxylesterase contributes to the attenuation of cyanotoxin microcystin-LR toxicity .  COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY194   22 - 27   2017.4

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    Publisher:ELSEVIER SCIENCE INC  

    Microcystin-LR is a hepatotoxin produced by several cyanobacteria. Its toxicity is mainly due to a inhibition of protein phosphatase, PP1 and PP2A. Previously, we used a cell line stably expressing uptake transporter for microcystin-LR, OATPIB3 (HEK293-OATP1B3 cells). In this study, to determine whether overexpression of carboxylesterase (CES), which degrades ester-group and amide-group, attenuates the cytotoxicity of microcystin-LR, we generated the HEK293-OATPIB3/CES2 double-transfected cells. HEK293-OATP1B3/CES2 cells showed high hydrolysis activity of p-nitrophenyl acetate (PNPA), which is an authentic substrate for esterase. CES activity in HEK293-OATP1B3/CES2 cells was approximately 3-fold higher than that in the HEK293-OATP1B3 cells. HEK293-0ATP1B3/CES2 cells (IC50: 25.4 +/- 7.7 nM) showed approximately 2.1-fold resistance to microcystin-LR than HEK293-OATP1B3 cells (IC50: 12.0 +/- 1.5 nM). Moreover, the CES inhibition assay and microcystin-agarose pull down assay showed the possibility of the interaction between CES2 and microcystin-LR. Our results indicated that the overexpression of CES2 attenuates the cytotoxicity of microcystin-LR via interaction with microcystin-LR. (C) 2017 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.cbpc.2017.01.008

    Web of Science

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  • Nohara K, Suzuki T, Okamura K, Matsushita J, Takumi S. .  Tumor-augmenting effects of gestational arsenic exposure on F1 and F2 in mice. .  Genes Environ.   2017.3Tumor-augmenting effects of gestational arsenic exposure on F1 and F2 in mice.Reviewed

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    Language:English   Publishing type:Research paper (scientific journal)  

  • Keiko Nohara, Takehiro Suzuki, Kazuyuki Okamura, Junya Matsushita, Shota Takumi .  Tumor-augmenting effects of gestational arsenic exposure on F1 and F2 in mice .  Genes and Environment39 ( 1 ) 3   2017

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    Publisher:BioMed Central Ltd.  

    The consequences of early-life exposure to chemicals in the environment are emerging concerns. Chronic exposure to naturally occurring inorganic arsenic has been known to cause various adverse health effects, including cancers, in humans. On the other hand, animal studies by Dr. M. Waalkes’ group reported that arsenite exposure of pregnant F0 females, only from gestational day 8 to 18, increased hepatic tumors in the F1 (arsenite-F1) males of C3H mice, whose males tend to develop spontaneous hepatic tumors later in life. Since this mice model illuminated novel unidentified consequences of arsenic exposure, we wished to further investigate the background mechanisms. In the same experimental model, we identified a variety of factors that were affected by gestational arsenic exposure, including epigenetic and genetic changes, as possible constituents of multiple steps of late-onset hepatic tumor augmentation in arsenite-F1 males. Furthermore, our study discovered that the F2 males born to arsenite-F1 males developed hepatic tumors at a significantly higher rate than the control F2 males. The results imply that the tumor augmenting effect is inherited by arsenite-F2 males through the sperm of arsenite-F1. In this article, we summarized our studies on the consequences of gestational arsenite exposure in F1 and F2 mice to discuss novel aspects of biological effects of gestational arsenic exposure.

    DOI: 10.1186/s41021-016-0069-1

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  • Funahashi A, Komatsu M, Furukawa T, Yoshizono Y, Yoshizono H, Orikawa Y, Takumi S, Shiozaki K, Hayashi S, Kaminishi Y, Itakura T. .  Eel green fluorescent protein is associated with resistance to oxidative stress. .  Comp Biochem Physiol C Toxicol Pharmacol.   2016.3Eel green fluorescent protein is associated with resistance to oxidative stress.Reviewed

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    Language:English   Publishing type:Research paper (scientific journal)  

  • Ikema S, Takumi S, Maeda Y, Kurimoto T, Bohda S, Chigwechokha PK, Sugiyama Y, Shiozaki K, Furukawa T, Komatsu M. .  Okadaic acid is taken-up into the cells mediated by human hepatocytes transporter OATP1B3. .  Food Chem Toxicol.   2015.9Okadaic acid is taken-up into the cells mediated by human hepatocytes transporter OATP1B3.Reviewed

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    Language:English   Publishing type:Research paper (scientific journal)  

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Books

  • 健康・栄養科学シリーズ 食べ物と健康 食品の科学 改訂第3版

    内匠正太(分担執筆) ( Role: Contributor)

    南江堂  2022.3 

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    Total pages:335   Responsible for pages:233-242   Language:Japanese Book type:Textbook, survey, introduction

  • Eel Serum Synergistically Enhances Growth of Fish Cell Line GAKS Reviewed

    ( Role: Joint author)

    Memoirs of Faculty of Fisheries Kagoshima University  2021 

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    Language:English

  • ニホンウナギ産卵回遊中の代謝に関する考察ービリルビン結合型UnaGの産卵回遊における生理的意義ー

    林征一、小松正治、内匠正太( Role: Joint author)

    生物の科学 遺伝  2020 

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    Language:Japanese

  • 健康・栄養科学シリーズ 食べ物と健康 食品の科学 改訂第2版

    内匠正太(分担執筆) ( Role: Contributor)

    南江堂  2018.1 

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    Total pages:331   Responsible for pages:232-241   Language:Japanese Book type:Textbook, survey, introduction

MISC

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Presentations

  • 西 優弥,古川龍彦,内匠正太,小松正治   無機ヒ素により誘発される細胞内コレステロール蓄積にクルクミンが及ぼす影響  

    第42回 日本分子生物学会年会 

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    Event date: 2019.12

    Language:English   Presentation type:Poster presentation  

  • 内匠正太、大榮 薫、古川龍彦、西 優弥、塩崎一弘、小松正治   ヒジキに含有される無機ヒ素の細胞毒性及びその細胞膜コレステロール輸送系への影響  

    日本水産学会九州支部大会 

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    Event date: 2018.12

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 富岡 優,嶋 祐介,濱口真理奈,塩崎一弘,内匠正太,小松正治   アオコ毒microcystin-LRの上皮間葉転換様作用  

    令和元年度 日本水産学会九州支部会大会 

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    Event date: 2019.12

    Language:Japanese   Presentation type:Oral presentation (general)  

  • 瀬戸祥太,河野和樹,内匠正太,小松正治   ウナギ緑色蛍光タンパク質eelGP発現細胞の酸化ストレス応答  

    第42回 日本分子生物学会年会 

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    Event date: 2019.12

    Language:English   Presentation type:Poster presentation  

  • 富岡 優,藤田理子,山本歩加,塩崎一弘,古川龍彦,内匠正太,小松正治   Microcystin-LRが誘導するEMT様形質転換細胞の細胞内シグナリングの解析  

    第42回 日本分子生物学会年会 

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    Event date: 2019.12

    Language:English   Presentation type:Poster presentation  

  • 瀬戸 祥太, 内匠 正太, 塩崎 一弘, 安樂 和彦, 小松 正治   細胞の酸化ストレス抵抗性を賦与するウナギ緑色蛍光タンパク質eeIGFP  

    中毒研究  2020.9  (株)へるす出版

  • 小松 正治, 内匠 正太   海産毒リビジテッド2.0 アオコ毒マイクロシスチンLRの新奇機能性の発見  

    The Journal of Toxicological Sciences  2020.6  (一社)日本毒性学会

  • 内匠 正太, 山下 優香, 小松 正治, 柳澤 裕之   ヒ素曝露による細胞内コレステロールの蓄積  

    日本衛生学雑誌  2017.3  (一社)日本衛生学会

  • 富岡 優, 内匠 正太, 杉山 靖正, 塩崎 一弘, 古川 龍彦, 小松 正治   NodularinはOATP1B3発現細胞に対して上皮間葉転換様の形質転換を誘導する  

    生命科学系学会合同年次大会  2017.12  生命科学系学会合同年次大会運営事務局

  • 内匠 正太, 木戸 尊將, 関 良子, 柳澤 裕之   亜鉛欠乏におけるSirt1の役割  

    産業衛生学雑誌  2017.5  (公社)日本産業衛生学会

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Research Projects

  • 食品成分による動脈硬化症予防法の開発

    2016.4 - 2020.3

    科学研究費補助金  基盤研究(C)

  • ヒ素によるコレステロール代謝異常誘発メカニズムの解明

    2014.4 - 2016.3

    科学研究費補助金  若手研究(B)

  • 酸化ストレスによるDNA脱メチル化酵素の発現誘導メカニズムの解明

    2012.4 - 2013.3

    科学研究費補助金  若手研究(B)

  • ヒ素代謝物が脂質代謝経路へ及ぼす影響

    2020.4 - 2021.3

    民間財団等  サンケイ科学振興財団研究助成金 

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    Grant type:Competitive

  • 食品成分による動脈硬化症予防法の開発

    2016.4 - 2019.3

    文部科学省科学研究費  基盤研究(C) 

    内匠正太

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  • 亜鉛欠乏食による病態発症における Sirt1 の役割

    2015.4 - 2016.3

    民間財団等  上原記念生命科学財団 研究奨励金 

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    Grant type:Competitive

  • ヒ素によるコレステロール代謝異常誘発メカニズムの解明

    2014.4 - 2017.3

    文部科学省科学研究費  若手研究(B) 

    内匠正太

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Teaching Experience

  • 食品化学

    Institution:鹿児島大学

  • 食品科学基礎実験

    Institution:鹿児島大学

  • 公衆衛生学

    Institution:志學館大学

  • 公衆衛生学I

    Institution:鹿児島女子短期大学

  • 衛生学

    Institution:志學館大学

  • 食品学各論

    Institution:鹿児島女子短期大学

  • 資源利用化学実験

    Institution:鹿児島大学

  • 衛生学

    Institution:志學館大学

  • 公衆衛生学

    Institution:鹿児島女子短期大学

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