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29 results on '"Matsumoto, Michiharu"'

7. Quantitative analysis of mutagenicity and carcinogenicity of 2-amino-3-methylimidazo[4,5-f]quinoline in F344 gpt delta transgenic rats

Author

Gi, Min, Fujioka, Masaki, Totsuka, Yukari, Matsumoto, Michiharu, Masumura, Kenichi, Kakehashi, Anna, Yamaguchi, Takashi, Fukushima, Shoji, Wanibuchi, Hideki, Gi, Min, Fujioka, Masaki, Totsuka, Yukari, Matsumoto, Michiharu, Masumura, Kenichi, Kakehashi, Anna, Yamaguchi, Takashi, Fukushima, Shoji, and Wanibuchi, Hideki

Abstract

Quantitative analysis of the mutagenicity and carcinogenicity of the low doses of genotoxic carcinogens present in food is of pressing concern. The purpose of the present study was to determine the mutagenicity and carcinogenicity of low doses of the dietary genotoxic carcinogen 2-amino-3-methylimidazo[4,5-f]quinoline (IQ). Male F344 gpt delta transgenic rats were fed diets supplemented with 0, 0.1, 1, 10, or 100 ppm IQ for 4 weeks....

Published
2019

19. TWO-YEAR FEED STUDY OF CARCINOGENICITY AND CHRONIC TOXICITY OF ORTHO-CHLORONITROBENZENE IN RATS AND MICE

Author

MATSUMOTO, Michiharu, primary, UMEDA, Yumi, additional, SENOH, Hideki, additional, SUZUKI, Masaaki, additional, KANO, Hirokazu, additional, KATAGIRI, Taku, additional, AISO, Shigetoshi, additional, YAMAZAKI, Kazunori, additional, ARITO, Heihaciro, additional, NAGANO, Kasuke, additional, YAMAMOTO, Seigo, additional, and MATSUSHIMA, Taijiro, additional

Published
2006
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27. Carcinogenicity of quinoline by drinking-water administration in rats and mice.

Author

Matsumoto M, Kano H, Suzuki M, Noguchi T, Umeda Y, and Fukushima S

Subjects
Administration, Oral, Animals, Carcinoma, Hepatocellular chemically induced, Female, Hemangiosarcoma chemically induced, Liver Neoplasms chemically induced, Male, Mice, Inbred Strains, Mutagenesis drug effects, Rats, Inbred F344, Specific Pathogen-Free Organisms, Drinking Water administration & dosage, Neoplasms chemically induced, Quinolines administration & dosage, Quinolines toxicity
Abstract

The carcinogenicity of quinoline was examined by administrating quinoline in the drinking water to groups of 50 F344/DuCrj rats and 50 Crj: BDF1 mice of each sex. In rats, the doses of quinoline were 0, 200, 400, and 800 ppm for males and 0, 150, 300, and 600 ppm for females. In male rats, administration of quinoline was terminated at week 96 due to high mortality caused by tumors. There were significant increases of hepatocellular adenomas, hepatocellular carcinomas, hepatocellular adenomas and/or carcinomas (combined), and liver hemangiomas, hemangiosarcomas, hemangiomas and/or hemangiosarcomas (combined) in both male and female rats, and nasal esthesioneuroepitheliomas and sarcoma NOS (not otherwise specified) in males. In mice, doses of quinoline were 0, 150, 300 and 600 ppm for both males and females. Administration of quinoline was terminated at week 65 in males and at week 50 in females due to high mortality caused by tumors. There were marked increases of hemangiomas, hemangiosarcomas, and hemangiomas and/or hemangiosarcomas (combined) in the retroperitoneum, mesenterium, and liver in males, and in the retroperitoneum, mesenterium, peritoneum, and subcutis in females. Additionally, histiocytic sarcomas were statistically increased in the livers of female mice. Thus the present studies provided clear evidence of carcinogenic activity of quinoline administered in the drinking water in both rats and mice.

Published
2018
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28. Lung carcinogenicity of inhaled multi-walled carbon nanotube in rats.

Author

Kasai T, Umeda Y, Ohnishi M, Mine T, Kondo H, Takeuchi T, Matsumoto M, and Fukushima S

Subjects
Animals, Body Weight drug effects, Bronchoalveolar Lavage Fluid, Female, Inhalation Exposure, Lung Neoplasms pathology, Male, Organ Size drug effects, Rats, Rats, Inbred F344, Lung Neoplasms chemically induced, Nanotubes, Carbon toxicity
Abstract

Background: Multi-walled carbon nanotubes (MWCNTs) constitute one of the most promising types of nanomaterials in industry today. With their increasing use, the potential toxicity and carcinogenicity of MWCNT needs to be evaluated in bioassay studies using rodents. Since humans are mainly exposed to MWCNT by inhalation, we performed a 104-week carcinogenicity study using whole-body inhalation exposure chambers with a fibrous straight type of MWCNT at concentrations of 0, 0.02, 0.2, and 2 mg/m 3 using male and female F344 rats., Results: Lung carcinomas, mainly bronchiolo-alveolar carcinoma, and combined carcinomas and adenomas were significantly increased in males exposed to 0.2 and 2 mg/m 3 MWNT-7 and in females exposed to 2 mg/m 3 MWNT-7 compared to the clean air control group. However, no development of pleural mesothelioma was observed. Concentration-dependent toxic effects in the lung such as epithelial hyperplasia, granulomatous change, localized fibrosis, and alteration in BALF parameters were found in MWNT-7 treatment groups of both sexes. There were no MWNT-7-specific macroscopic findings in the other organs, including the pleura and peritoneum. Absolute and relative lung weights were significantly elevated in male rats exposed to 0.2 and 2 mg/m 3 MWNT-7 and in all exposed female groups. The lung burdens of MWNT-7 were clearly increased in a concentration-dependent as well as a duration-dependent manner., Conclusion: There is clear evidence that MWNT-7 is carcinogenic to the lungs of male and female F344 rats, however no plural mesothelioma was observed.

Published
2016
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29. Qualitative and quantitative approaches in the dose-response assessment of genotoxic carcinogens.

Author

Fukushima S, Gi M, Kakehashi A, Wanibuchi H, and Matsumoto M

Subjects
Animals, Carcinogens toxicity, DNA drug effects, Dose-Response Relationship, Drug, Female, Glutathione Transferase, Guanosine analogs & derivatives, Guanosine analysis, Humans, Liver metabolism, Male, Mice, Mutagenicity Tests, Mutagens toxicity, Quinolines analysis, Rats, Rats, Inbred F344, Carcinogenicity Tests methods, DNA Adducts analysis, Diethylnitrosamine toxicity, Liver drug effects, Quinolines toxicity, Quinoxalines toxicity
Abstract

Qualitative and quantitative approaches are important issues in field of carcinogenic risk assessment of the genotoxic carcinogens. Herein, we provide quantitative data on low-dose hepatocarcinogenicity studies for three genotoxic hepatocarcinogens: 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and N-nitrosodiethylamine (DEN). Hepatocarcinogenicity was examined by quantitative analysis of glutathione S-transferase placental form (GST-P) positive foci, which are the preneoplastic lesions in rat hepatocarcinogenesis and the endpoint carcinogenic marker in the rat liver medium-term carcinogenicity bioassay. We also examined DNA damage and gene mutations which occurred through the initiation stage of carcinogenesis. For the establishment of points of departure (PoD) from which the cancer-related risk can be estimated, we analyzed the above events by quantitative no-observed-effect level and benchmark dose approaches. MeIQx at low doses induced formation of DNA-MeIQx adducts; somewhat higher doses caused elevation of 8-hydroxy-2'-deoxyquanosine levels; at still higher doses gene mutations occurred; and the highest dose induced formation of GST-P positive foci. These data indicate that early genotoxic events in the pathway to carcinogenesis showed the expected trend of lower PoDs for earlier events in the carcinogenic process. Similarly, only the highest dose of IQ caused an increase in the number of GST-P positive foci in the liver, while IQ-DNA adduct formation was observed with low doses. Moreover, treatment with DEN at low doses had no effect on development of GST-P positive foci in the liver. These data on PoDs for the markers contribute to understand whether genotoxic carcinogens have a threshold for their carcinogenicity. The most appropriate approach to use in low dose-response assessment must be approved on the basis of scientific judgment., (© The Author 2015. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Published
2016
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