In vivo genotoxicity of furan in F344 rats at cancer bioassay doses
Furan, a potent rodent liver carcinogen, is found in many cooked food items and thus represents a human cancer risk. Mechanisms for furan carcinogenicity were investigated in male F344 rats using the in vivo Comet and micronucleus assays, combined with analysis of histopathological and gene expressi...
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| Published in | Toxicology and applied pharmacology Vol. 261; no. 2; pp. 164 - 171 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Amsterdam
Elsevier Inc
01.06.2012
Elsevier |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0041-008X 1096-0333 1096-0333 |
| DOI | 10.1016/j.taap.2012.03.021 |
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| Abstract | Furan, a potent rodent liver carcinogen, is found in many cooked food items and thus represents a human cancer risk. Mechanisms for furan carcinogenicity were investigated in male F344 rats using the in vivo Comet and micronucleus assays, combined with analysis of histopathological and gene expression changes. In addition, formamidopyrimidine DNA glycosylase (Fpg) and endonuclease III (EndoIII)-sensitive DNA damage was monitored as a measure of oxidative DNA damage. Rats were treated by gavage on four consecutive days with 2, 4, and 8mg/kg bw furan, doses that were tumorigenic in 2-year cancer bioassays, and with two higher doses, 12 and 16mg/kg. Rats were killed 3h after the last dose, a time established as producing maximum levels of DNA damage in livers of furan-treated rats. Liver Comet assays indicated that both DNA strand breaks and oxidized purines and pyrimidines increased in a near-linear dose-responsive fashion, with statistically significant increases detected at cancer bioassay doses. No DNA damage was detected in bone marrow, a non-target tissue for cancer, and peripheral blood micronucleus assays were negative. Histopathological evaluation of liver from furan-exposed animals produced evidence of inflammation, single-cell necrosis, apoptosis, and cell proliferation. In addition, genes related to apoptosis, cell-cycle checkpoints, and DNA-repair were expressed at a slightly lower level in the furan-treated livers. Although a mixed mode of action involving direct DNA binding cannot be ruled out, the data suggest that furan induces cancer in rat livers mainly through a secondary genotoxic mechanism involving oxidative stress, accompanied by inflammation, cell proliferation, and toxicity.
► Furan is a potent rodent liver carcinogen and represents a human cancer risk. ► Furan induces DNA damage in rat liver at cancer bioassay doses. ► Furan induces oxidative stress, inflammation and cell proliferation in rat liver. ► Expression of DNA damage repair-related genes is reduced in furan-treated rat livers. ► Furan induces rat liver cancer mainly through a secondary genotoxic mechanism. |
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| AbstractList | Furan, a potent rodent liver carcinogen, is found in many cooked food items and thus represents a human cancer risk. Mechanisms for furan carcinogenicity were investigated in male F344 rats using the in vivo Comet and micronucleus assays, combined with analysis of histopathological and gene expression changes. In addition, formamidopyrimidine DNA glycosylase (Fpg) and endonuclease III (EndoIII)-sensitive DNA damage was monitored as a measure of oxidative DNA damage. Rats were treated by gavage on four consecutive days with 2, 4, and 8mg/kg bw furan, doses that were tumorigenic in 2-year cancer bioassays, and with two higher doses, 12 and 16mg/kg. Rats were killed 3h after the last dose, a time established as producing maximum levels of DNA damage in livers of furan-treated rats. Liver Comet assays indicated that both DNA strand breaks and oxidized purines and pyrimidines increased in a near-linear dose-responsive fashion, with statistically significant increases detected at cancer bioassay doses. No DNA damage was detected in bone marrow, a non-target tissue for cancer, and peripheral blood micronucleus assays were negative. Histopathological evaluation of liver from furan-exposed animals produced evidence of inflammation, single-cell necrosis, apoptosis, and cell proliferation. In addition, genes related to apoptosis, cell-cycle checkpoints, and DNA-repair were expressed at a slightly lower level in the furan-treated livers. Although a mixed mode of action involving direct DNA binding cannot be ruled out, the data suggest that furan induces cancer in rat livers mainly through a secondary genotoxic mechanism involving oxidative stress, accompanied by inflammation, cell proliferation, and toxicity.
► Furan is a potent rodent liver carcinogen and represents a human cancer risk. ► Furan induces DNA damage in rat liver at cancer bioassay doses. ► Furan induces oxidative stress, inflammation and cell proliferation in rat liver. ► Expression of DNA damage repair-related genes is reduced in furan-treated rat livers. ► Furan induces rat liver cancer mainly through a secondary genotoxic mechanism. Furan, a potent rodent liver carcinogen, is found in many cooked food items and thus represents a human cancer risk. Mechanisms for furan carcinogenicity were investigated in male F344 rats using the in vivo Comet and micronucleus assays, combined with analysis of histopathological and gene expression changes. In addition, formamidopyrimidine DNA glycosylase (Fpg) and endonuclease III (EndoIII)-sensitive DNA damage was monitored as a measure of oxidative DNA damage. Rats were treated by gavage on four consecutive days with 2, 4, and 8mg/kg bw furan, doses that were tumorigenic in 2-year cancer bioassays, and with two higher doses, 12 and 16mg/kg. Rats were killed 3h after the last dose, a time established as producing maximum levels of DNA damage in livers of furan-treated rats. Liver Comet assays indicated that both DNA strand breaks and oxidized purines and pyrimidines increased in a near-linear dose-responsive fashion, with statistically significant increases detected at cancer bioassay doses. No DNA damage was detected in bone marrow, a non-target tissue for cancer, and peripheral blood micronucleus assays were negative. Histopathological evaluation of liver from furan-exposed animals produced evidence of inflammation, single-cell necrosis, apoptosis, and cell proliferation. In addition, genes related to apoptosis, cell-cycle checkpoints, and DNA-repair were expressed at a slightly lower level in the furan-treated livers. Although a mixed mode of action involving direct DNA binding cannot be ruled out, the data suggest that furan induces cancer in rat livers mainly through a secondary genotoxic mechanism involving oxidative stress, accompanied by inflammation, cell proliferation, and toxicity. Furan, a potent rodent liver carcinogen, is found in many cooked food items and thus represents a human cancer risk. Mechanisms for furan carcinogenicity were investigated in male F344 rats using the in vivo Comet and micronucleus assays, combined with analysis of histopathological and gene expression changes. In addition, formamidopyrimidine DNA glycosylase (Fpg) and endonuclease III (EndoIII)-sensitive DNA damage was monitored as a measure of oxidative DNA damage. Rats were treated by gavage on four consecutive days with 2, 4, and 8mg/kg bw furan, doses that were tumorigenic in 2-year cancer bioassays, and with two higher doses, 12 and 16mg/kg. Rats were killed 3h after the last dose, a time established as producing maximum levels of DNA damage in livers of furan-treated rats. Liver Comet assays indicated that both DNA strand breaks and oxidized purines and pyrimidines increased in a near-linear dose-responsive fashion, with statistically significant increases detected at cancer bioassay doses. No DNA damage was detected in bone marrow, a non-target tissue for cancer, and peripheral blood micronucleus assays were negative. Histopathological evaluation of liver from furan-exposed animals produced evidence of inflammation, single-cell necrosis, apoptosis, and cell proliferation. In addition, genes related to apoptosis, cell-cycle checkpoints, and DNA-repair were expressed at a slightly lower level in the furan-treated livers. Although a mixed mode of action involving direct DNA binding cannot be ruled out, the data suggest that furan induces cancer in rat livers mainly through a secondary genotoxic mechanism involving oxidative stress, accompanied by inflammation, cell proliferation, and toxicity.Furan, a potent rodent liver carcinogen, is found in many cooked food items and thus represents a human cancer risk. Mechanisms for furan carcinogenicity were investigated in male F344 rats using the in vivo Comet and micronucleus assays, combined with analysis of histopathological and gene expression changes. In addition, formamidopyrimidine DNA glycosylase (Fpg) and endonuclease III (EndoIII)-sensitive DNA damage was monitored as a measure of oxidative DNA damage. Rats were treated by gavage on four consecutive days with 2, 4, and 8mg/kg bw furan, doses that were tumorigenic in 2-year cancer bioassays, and with two higher doses, 12 and 16mg/kg. Rats were killed 3h after the last dose, a time established as producing maximum levels of DNA damage in livers of furan-treated rats. Liver Comet assays indicated that both DNA strand breaks and oxidized purines and pyrimidines increased in a near-linear dose-responsive fashion, with statistically significant increases detected at cancer bioassay doses. No DNA damage was detected in bone marrow, a non-target tissue for cancer, and peripheral blood micronucleus assays were negative. Histopathological evaluation of liver from furan-exposed animals produced evidence of inflammation, single-cell necrosis, apoptosis, and cell proliferation. In addition, genes related to apoptosis, cell-cycle checkpoints, and DNA-repair were expressed at a slightly lower level in the furan-treated livers. Although a mixed mode of action involving direct DNA binding cannot be ruled out, the data suggest that furan induces cancer in rat livers mainly through a secondary genotoxic mechanism involving oxidative stress, accompanied by inflammation, cell proliferation, and toxicity. Furan, a potent rodent liver carcinogen, is found in many cooked food items and thus represents a human cancer risk. Mechanisms for furan carcinogenicity were investigated in male F344 rats using the in vivo Comet and micronucleus assays, combined with analysis of histopathological and gene expression changes. In addition, formamidopyrimidine DNA glycosylase (Fpg) and endonuclease III (EndoIII)-sensitive DNA damage was monitored as a measure of oxidative DNA damage. Rats were treated by gavage on four consecutive days with 2, 4, and 8 mg/kg bw furan, doses that were tumorigenic in 2-year cancer bioassays, and with two higher doses, 12 and 16 mg/kg. Rats were killed 3 h after the last dose, a time established as producing maximum levels of DNA damage in livers of furan-treated rats. Liver Comet assays indicated that both DNA strand breaks and oxidized purines and pyrimidines increased in a near-linear dose-responsive fashion, with statistically significant increases detected at cancer bioassay doses. No DNA damage was detected in bone marrow, a non-target tissue for cancer, and peripheral blood micronucleus assays were negative. Histopathological evaluation of liver from furan-exposed animals produced evidence of inflammation, single-cell necrosis, apoptosis, and cell proliferation. In addition, genes related to apoptosis, cell-cycle checkpoints, and DNA-repair were expressed at a slightly lower level in the furan-treated livers. Although a mixed mode of action involving direct DNA binding cannot be ruled out, the data suggest that furan induces cancer in rat livers mainly through a secondary genotoxic mechanism involving oxidative stress, accompanied by inflammation, cell proliferation, and toxicity. -- Highlights: ► Furan is a potent rodent liver carcinogen and represents a human cancer risk. ► Furan induces DNA damage in rat liver at cancer bioassay doses. ► Furan induces oxidative stress, inflammation and cell proliferation in rat liver. ► Expression of DNA damage repair-related genes is reduced in furan-treated rat livers. ► Furan induces rat liver cancer mainly through a secondary genotoxic mechanism. |
| Author | Manjanatha, Mugimane G. Aidoo, Anane Pearce, Mason G. Bishop, Michelle E. Chang, Ching-Wei Mittelstaedt, Roberta A. Latendresse, John R. Heflich, Robert H. Doerge, Daniel R. White, Gene A. Shaddock, Joseph G. McDaniel, Lea P. Ding, Wei Petibone, Dayton M. Muskhelishvili, Levan Morris, Suzanne M. |
| Author_xml | – sequence: 1 givenname: Wei surname: Ding fullname: Ding, Wei email: Wei.Ding@fda.hhs.gov organization: Division of Genetic and Molecular Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 2 givenname: Dayton M. surname: Petibone fullname: Petibone, Dayton M. organization: Division of Genetic and Molecular Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 3 givenname: John R. surname: Latendresse fullname: Latendresse, John R. organization: Toxicologic Pathology Associates, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 4 givenname: Mason G. surname: Pearce fullname: Pearce, Mason G. organization: Division of Genetic and Molecular Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 5 givenname: Levan surname: Muskhelishvili fullname: Muskhelishvili, Levan organization: Toxicologic Pathology Associates, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 6 givenname: Gene A. surname: White fullname: White, Gene A. organization: Toxicologic Pathology Associates, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 7 givenname: Ching-Wei surname: Chang fullname: Chang, Ching-Wei organization: Division of Personalized Nutrition and Medicine, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 8 givenname: Roberta A. surname: Mittelstaedt fullname: Mittelstaedt, Roberta A. organization: Division of Genetic and Molecular Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 9 givenname: Joseph G. surname: Shaddock fullname: Shaddock, Joseph G. organization: Division of Genetic and Molecular Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 10 givenname: Lea P. surname: McDaniel fullname: McDaniel, Lea P. organization: Division of Genetic and Molecular Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 11 givenname: Daniel R. surname: Doerge fullname: Doerge, Daniel R. organization: Division of Biochemical Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 12 givenname: Suzanne M. surname: Morris fullname: Morris, Suzanne M. organization: Division of Genetic and Molecular Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 13 givenname: Michelle E. surname: Bishop fullname: Bishop, Michelle E. organization: Division of Genetic and Molecular Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 14 givenname: Mugimane G. surname: Manjanatha fullname: Manjanatha, Mugimane G. organization: Division of Genetic and Molecular Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 15 givenname: Anane surname: Aidoo fullname: Aidoo, Anane organization: Division of Genetic and Molecular Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA – sequence: 16 givenname: Robert H. surname: Heflich fullname: Heflich, Robert H. organization: Division of Genetic and Molecular Toxicology, US FDA/National Center for Toxicological Research, Jefferson, AR 72079, USA |
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| Keywords | Cell proliferation MN Oxidative stress EndoIII Liver DNA damage Inflammation NTP BER In vivo Comet assay MMR ROS NER Fpg GSH BDA MOA DSBR Furan Bioassay Rat Digestive system Toxicity Rodentia Genotoxicity Malignant tumor Comet assay In vivo Vertebrata Mammalia Animal DNA Lesion Dose Cancer Genotoxity test |
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| Snippet | Furan, a potent rodent liver carcinogen, is found in many cooked food items and thus represents a human cancer risk. Mechanisms for furan carcinogenicity were... |
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| SubjectTerms | 60 APPLIED LIFE SCIENCES Animals Apoptosis BIOASSAY bioassays Biological and medical sciences blood BONE MARROW Bone Marrow - drug effects BUTENES Cancer Carcinogenicity Carcinogenicity Tests Carcinogens cell cycle CELL PROLIFERATION DNA DNA Damage DNA glycosylase DNA repair Dose-Response Relationship, Drug DOSES EXCISION REPAIR Food FURANS Furans - toxicity Gene expression gene expression regulation genes Genotoxicity GLUTATHIONE histopathology humans In vivo Comet assay INFLAMMATION LIVER Liver - drug effects Liver - pathology Male males mechanism of action Medical sciences Micronuclei, Chromosome-Defective Mutagenicity Tests necrosis NEOPLASMS OXIDATION Oxidative stress OXYGEN Peripheral blood purines pyrimidines RATS Rats, Inbred F344 risk Statistical analysis STRAND BREAKS Toxicity Toxicology |
| Title | In vivo genotoxicity of furan in F344 rats at cancer bioassay doses |
| URI | https://dx.doi.org/10.1016/j.taap.2012.03.021 https://www.ncbi.nlm.nih.gov/pubmed/22507866 https://www.proquest.com/docview/1015246420 https://www.proquest.com/docview/1020850576 https://www.proquest.com/docview/1733546073 https://www.osti.gov/biblio/22215325 |
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