T
Tomoe Negishi
Researcher at Okayama University
Publications - 76
Citations - 1889
Tomoe Negishi is an academic researcher from Okayama University. The author has contributed to research in topics: Chlorophyllin & DNA damage. The author has an hindex of 19, co-authored 74 publications receiving 1797 citations. Previous affiliations of Tomoe Negishi include Nihon Pharmaceutical University.
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Journal ArticleDOI
Dietary inhibitors of mutagenesis and carcinogenesis.
TL;DR: In this chapter, inhibitors of mutagenesis and carcinogenesis that can arise as components of diet have been reviewed and most of the inhibitors have been demonstrated to be effective against a specific class of mutagens or carcinogens.
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Chemopreventive properties of chlorophylls towards aflatoxin B1: a review of the antimutagenicity and anticarcinogenicity data in rainbow trout
Roderick H. Dashwood,Tomoe Negishi,Hikoya Hayatsu,Vibeke Breinholt,Jerry D. Hendricks,George S. Bailey +5 more
TL;DR: Co-injection of inhibitor and AFB1 into trout embryos established that CHL was more effective than chlorophyll a in reducing AFB1-DNA adducts 2 weeks after injection, and liver tumors after 1 year.
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Inhibitory effect of chlorophyll on the genotoxicity of 3-amino-1-methyl-5H-pyrido[4,3-b indole (Trp-P-2)
TL;DR: Using the wing hair spot test, it is found that the formation of mutant hairs in adult flies as a result of feeding them with Trp-P-2 in their larval stage was efficiently inhibited by coadministration of chlorophyll.
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Inhibition of the mutagenicity of amino acid pyrolysis products by hemin and other biological pyrrole pigments
TL;DR: Hemin appears to interact with the metabolically activated form of Trp-P-1 and as a result to inhibit the mutagenicity and was the most effective among these pigments.
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Suppression of genotoxicity of carcinogens by (-)-epigallocatechin gallate
Hikoya Hayatsu,Naomi Inada,Toshifumi Kakutani,Sakae Arimoto,Tomoe Negishi,Kazuko Mori,Takuo Okuda,Isao Sakata +7 more
TL;DR: The mechanism of inhibition may not have resulted from direct interaction between E GCG and the mutagens, but rather from indirect interception of mutagen action by EGCG.