| Project/Area Number |
10680507
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Environmental dynamic analysis
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| Research Institution | TOKYO UNIVERSITY OF PHARMACY AND LIFE SCIENCES |
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Principal Investigator |
KAISE Toshikazu TOKYO UNIVERSITY OF PHARMACY AND LIFE SCIENCE, SCHOOL OF LIFE SCIENCES, ENVIRONMENTAL CHEMISTRY, ASSOCIATE PROFESSOR, 生命科学部・環境衛生化学研究室, 助教授 (20266894)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Shoko TOKYO UNIVERSITY OF PHARMACY AND LIFE SCIENCE, SCHOOL OF LIFE SCIENCES, PLANT PHYSIOLOGY, ASSISTANT PROFESSOR, 生命科学部・環境衛生化学研究室, 講師 (30266895)
SAKURAI Teruaki TOKYO UNIVERSITY OF PHARMACY AND LIFE SCIENCE, SCHOOL OF LIFE SCIENCES, ENVIRONMENTAL CHEMISTRY, ASSISTANT (30266902)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | arsenic / aquatic ecosystem / biomethylation / dimethylasinic aci / Chlamydomonas reinhardtii / arseno-sugar / ジメチルアルソン酸 |
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| Research Abstract |
(1)A wall-less cell strain (CW-15) of Chlamydomonas reinhardtii proliferated in a low level arsenic-containing medium (0.01-0.1 mmol dmィイD1-3ィエD1). Although the growth of the algal cells was only slightly more inhibited in a growth medium containing arsenic at a concentration of 1.0 mmol dmィイD1-3ィエD1 than that in an arsenic-free medium, it was completely inhibited at concentrations of 10 and 100 mmol dmィイD1-3ィエD1. Furthermore, transformed strains were obtained by random introduction of plasmid pJD67, carrying an ArgィイD1+ィエD1 gene, into a wall-less cell ArgィイD1+ィエD1 mutant CC425 strain. Finally we selected a strain AS1, among the transformed CC425 of the arsenic-sensitive group. The accumulation of arsenic by the AS1 strain was about three-fold higher than that by the CW-15 strain and 80〜90% of the inorganic arsenic was transformed into a dimethylarsenic compound. (2)The intracellular concentrations of arsenic in the mutants were determined with an atomic absorption spectrophotometer. The intracellular levels of arsenic in the arsenate-resistant mutants were all lower than that of the parent strain CC425. Some of the arsenate-sensitive mutants, AS1 and AS3, showed obviously higher levels of arsenic than that of CC425, while other sensitive mutant, AS2, did not accumulate arsenic so much. Analysis of the chemical species of arsenic suggested that inorganic arsenic was converted to dimethylarsinic acid (DMAA) in CC425. However, DMAA was hardly detected in AS2. The mechanisms of the resistance to arsenate are discussed on its uptake and detoxification.
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