In vivo mutagenicity and initiation following oxidative DNA lesion in the kidneys of rats given potassium bromate
To clarify the role of 8‐OHdG formation as a starting point for carcinogenesis, we examined the dose‐dependence and time‐course of changes of OGG1 mRNA expression, 8‐OHdG levels and in vivo mutations in the kidneys of gpt delta rats given KBrO3 in their drinking water for 13 weeks. There were no rem...
Gespeichert in:
| Veröffentlicht in: | Cancer science 2006-09, Vol.97 (9), p.829-835 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext bestellen |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 835 |
|---|---|
| container_issue | 9 |
| container_start_page | 829 |
| container_title | Cancer science |
| container_volume | 97 |
| creator | Umemura, Takashi Kanki, Keita Kuroiwa, Yuichi Ishii, Yuji Okano, Keita Nohmi, Takehiko Nishikawa, Akiyoshi Hirose, Masao |
| description | To clarify the role of 8‐OHdG formation as a starting point for carcinogenesis, we examined the dose‐dependence and time‐course of changes of OGG1 mRNA expression, 8‐OHdG levels and in vivo mutations in the kidneys of gpt delta rats given KBrO3 in their drinking water for 13 weeks. There were no remarkable changes in OGG1 mRNA in spite of some increments being statistically significant. Increases of 8‐OHdG occurred after 1 week at 500 p.p.m. and after 13 weeks at 250 p.p.m. Elevation of Spi− mutant frequency, suggestive of deletion mutations, occurred after 9 weeks at 500 p.p.m. In a two‐stage experiment, F344 rats were given KBrO3 for 13 weeks then, after a 2‐week recovery, treated with 1% NTA in the diet for 39 weeks. The incidence and multiplicity of renal preneoplastic lesions in rats given KBrO3 at 500 p.p.m. followed by NTA treatment were significantly higher than in rats treated with NTA alone. Results suggest that a certain period of time might be required for 8‐OHdG to cause permanent mutations. The two‐step experiment shows that cells exposed to the alteration of the intranuclear status by oxidative stress including 8‐OHdG formation might be able to form tumors with appropriate promotion. (Cancer Sci 2006; 97: 829–835) |
| doi_str_mv | 10.1111/j.1349-7006.2006.00248.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_24P</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11158994</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>68757761</sourcerecordid><originalsourceid>FETCH-LOGICAL-c6218-73d53a1e2fff55c1e740ecf54a80c99e6057a2f9c53a63c735237c65d5f7e06d3</originalsourceid><addsrcrecordid>eNqNkUtvEzEUhUcIREvhLyBvYDfBHo8fIyGhKLwqVbAA1pbruU4dZuzU9qTJv8fTRC3s8MK-8vnu8ZVPVSGCF6Ssd5sFoW1XC4z5opk3jJtWLvZPqvMH4el9LeoO0-asepHSBmPK2659Xp0RLjGTDT-vbi892rldQOOU9Rq8My4fkPY9ct5lp7MLHtkwDOHO-TUKe9eXux2gj9-WaIA0y86jfAPot-s9HBIKFkWdE1oXzKNtyDolN43oOoZRZ3hZPbN6SPDqdF5Uvz5_-rn6Wl99_3K5Wl7VhjdE1oL2jGoCjbWWMUNAtBiMZa2W2HQdcMyEbmxnCsWpEZQ1VBjOemYFYN7Ti-rD0Xc7XY_QG_A56kFtoxt1PKignfpX8e5GrcNOlQ9msuva4vD25BDD7QQpq9ElA8OgPYQpKS4FE4KTAsojaGJIKYJ9eIXg2Y6ojZpzUXMuag5M3Qem9qX19d9TPjaeEirAmxOgk9GDjdoblx45iaUgQhbu_ZG7cwMc_nsAtVr-KAX9Aydps_c</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>68757761</pqid></control><display><type>article</type><title>In vivo mutagenicity and initiation following oxidative DNA lesion in the kidneys of rats given potassium bromate</title><source>Wiley Online Library Open Access</source><creator>Umemura, Takashi ; Kanki, Keita ; Kuroiwa, Yuichi ; Ishii, Yuji ; Okano, Keita ; Nohmi, Takehiko ; Nishikawa, Akiyoshi ; Hirose, Masao</creator><creatorcontrib>Umemura, Takashi ; Kanki, Keita ; Kuroiwa, Yuichi ; Ishii, Yuji ; Okano, Keita ; Nohmi, Takehiko ; Nishikawa, Akiyoshi ; Hirose, Masao</creatorcontrib><description>To clarify the role of 8‐OHdG formation as a starting point for carcinogenesis, we examined the dose‐dependence and time‐course of changes of OGG1 mRNA expression, 8‐OHdG levels and in vivo mutations in the kidneys of gpt delta rats given KBrO3 in their drinking water for 13 weeks. There were no remarkable changes in OGG1 mRNA in spite of some increments being statistically significant. Increases of 8‐OHdG occurred after 1 week at 500 p.p.m. and after 13 weeks at 250 p.p.m. Elevation of Spi− mutant frequency, suggestive of deletion mutations, occurred after 9 weeks at 500 p.p.m. In a two‐stage experiment, F344 rats were given KBrO3 for 13 weeks then, after a 2‐week recovery, treated with 1% NTA in the diet for 39 weeks. The incidence and multiplicity of renal preneoplastic lesions in rats given KBrO3 at 500 p.p.m. followed by NTA treatment were significantly higher than in rats treated with NTA alone. Results suggest that a certain period of time might be required for 8‐OHdG to cause permanent mutations. The two‐step experiment shows that cells exposed to the alteration of the intranuclear status by oxidative stress including 8‐OHdG formation might be able to form tumors with appropriate promotion. (Cancer Sci 2006; 97: 829–835)</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/j.1349-7006.2006.00248.x</identifier><identifier>PMID: 16805826</identifier><language>eng</language><publisher>Melbourne, Australia: Blackwell Publishing Asia</publisher><subject>8-Hydroxy-2'-Deoxyguanosine ; Animal tumors. Experimental tumors ; Animals ; Animals, Genetically Modified ; Biological and medical sciences ; Bromates - toxicity ; Carcinogens - toxicity ; Cell Transformation, Neoplastic - drug effects ; Cell Transformation, Neoplastic - metabolism ; Deoxyguanosine - analogs & derivatives ; Deoxyguanosine - biosynthesis ; DNA Damage - drug effects ; DNA Glycosylases - biosynthesis ; DNA Glycosylases - drug effects ; Dose-Response Relationship, Drug ; Experimental renal and urinary tract tumors ; Kidney - drug effects ; Kidney - pathology ; Kidney Neoplasms - chemically induced ; Kidney Neoplasms - genetics ; Kidney Neoplasms - pathology ; Male ; Medical sciences ; Mutation ; Nitrilotriacetic Acid - toxicity ; Original ; Oxidative Stress - drug effects ; Precancerous Conditions - chemically induced ; Precancerous Conditions - genetics ; Precancerous Conditions - pathology ; Rats ; Rats, Inbred F344 ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - analysis ; Time Factors ; Tumors</subject><ispartof>Cancer science, 2006-09, Vol.97 (9), p.829-835</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6218-73d53a1e2fff55c1e740ecf54a80c99e6057a2f9c53a63c735237c65d5f7e06d3</citedby><cites>FETCH-LOGICAL-c6218-73d53a1e2fff55c1e740ecf54a80c99e6057a2f9c53a63c735237c65d5f7e06d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11158994/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11158994/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1349-7006.2006.00248.x$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18087178$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16805826$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Umemura, Takashi</creatorcontrib><creatorcontrib>Kanki, Keita</creatorcontrib><creatorcontrib>Kuroiwa, Yuichi</creatorcontrib><creatorcontrib>Ishii, Yuji</creatorcontrib><creatorcontrib>Okano, Keita</creatorcontrib><creatorcontrib>Nohmi, Takehiko</creatorcontrib><creatorcontrib>Nishikawa, Akiyoshi</creatorcontrib><creatorcontrib>Hirose, Masao</creatorcontrib><title>In vivo mutagenicity and initiation following oxidative DNA lesion in the kidneys of rats given potassium bromate</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>To clarify the role of 8‐OHdG formation as a starting point for carcinogenesis, we examined the dose‐dependence and time‐course of changes of OGG1 mRNA expression, 8‐OHdG levels and in vivo mutations in the kidneys of gpt delta rats given KBrO3 in their drinking water for 13 weeks. There were no remarkable changes in OGG1 mRNA in spite of some increments being statistically significant. Increases of 8‐OHdG occurred after 1 week at 500 p.p.m. and after 13 weeks at 250 p.p.m. Elevation of Spi− mutant frequency, suggestive of deletion mutations, occurred after 9 weeks at 500 p.p.m. In a two‐stage experiment, F344 rats were given KBrO3 for 13 weeks then, after a 2‐week recovery, treated with 1% NTA in the diet for 39 weeks. The incidence and multiplicity of renal preneoplastic lesions in rats given KBrO3 at 500 p.p.m. followed by NTA treatment were significantly higher than in rats treated with NTA alone. Results suggest that a certain period of time might be required for 8‐OHdG to cause permanent mutations. The two‐step experiment shows that cells exposed to the alteration of the intranuclear status by oxidative stress including 8‐OHdG formation might be able to form tumors with appropriate promotion. (Cancer Sci 2006; 97: 829–835)</description><subject>8-Hydroxy-2'-Deoxyguanosine</subject><subject>Animal tumors. Experimental tumors</subject><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Biological and medical sciences</subject><subject>Bromates - toxicity</subject><subject>Carcinogens - toxicity</subject><subject>Cell Transformation, Neoplastic - drug effects</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Deoxyguanosine - analogs & derivatives</subject><subject>Deoxyguanosine - biosynthesis</subject><subject>DNA Damage - drug effects</subject><subject>DNA Glycosylases - biosynthesis</subject><subject>DNA Glycosylases - drug effects</subject><subject>Dose-Response Relationship, Drug</subject><subject>Experimental renal and urinary tract tumors</subject><subject>Kidney - drug effects</subject><subject>Kidney - pathology</subject><subject>Kidney Neoplasms - chemically induced</subject><subject>Kidney Neoplasms - genetics</subject><subject>Kidney Neoplasms - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mutation</subject><subject>Nitrilotriacetic Acid - toxicity</subject><subject>Original</subject><subject>Oxidative Stress - drug effects</subject><subject>Precancerous Conditions - chemically induced</subject><subject>Precancerous Conditions - genetics</subject><subject>Precancerous Conditions - pathology</subject><subject>Rats</subject><subject>Rats, Inbred F344</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - analysis</subject><subject>Time Factors</subject><subject>Tumors</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUtvEzEUhUcIREvhLyBvYDfBHo8fIyGhKLwqVbAA1pbruU4dZuzU9qTJv8fTRC3s8MK-8vnu8ZVPVSGCF6Ssd5sFoW1XC4z5opk3jJtWLvZPqvMH4el9LeoO0-asepHSBmPK2659Xp0RLjGTDT-vbi892rldQOOU9Rq8My4fkPY9ct5lp7MLHtkwDOHO-TUKe9eXux2gj9-WaIA0y86jfAPot-s9HBIKFkWdE1oXzKNtyDolN43oOoZRZ3hZPbN6SPDqdF5Uvz5_-rn6Wl99_3K5Wl7VhjdE1oL2jGoCjbWWMUNAtBiMZa2W2HQdcMyEbmxnCsWpEZQ1VBjOemYFYN7Ti-rD0Xc7XY_QG_A56kFtoxt1PKignfpX8e5GrcNOlQ9msuva4vD25BDD7QQpq9ElA8OgPYQpKS4FE4KTAsojaGJIKYJ9eIXg2Y6ojZpzUXMuag5M3Qem9qX19d9TPjaeEirAmxOgk9GDjdoblx45iaUgQhbu_ZG7cwMc_nsAtVr-KAX9Aydps_c</recordid><startdate>200609</startdate><enddate>200609</enddate><creator>Umemura, Takashi</creator><creator>Kanki, Keita</creator><creator>Kuroiwa, Yuichi</creator><creator>Ishii, Yuji</creator><creator>Okano, Keita</creator><creator>Nohmi, Takehiko</creator><creator>Nishikawa, Akiyoshi</creator><creator>Hirose, Masao</creator><general>Blackwell Publishing Asia</general><general>Blackwell</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200609</creationdate><title>In vivo mutagenicity and initiation following oxidative DNA lesion in the kidneys of rats given potassium bromate</title><author>Umemura, Takashi ; Kanki, Keita ; Kuroiwa, Yuichi ; Ishii, Yuji ; Okano, Keita ; Nohmi, Takehiko ; Nishikawa, Akiyoshi ; Hirose, Masao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6218-73d53a1e2fff55c1e740ecf54a80c99e6057a2f9c53a63c735237c65d5f7e06d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>8-Hydroxy-2'-Deoxyguanosine</topic><topic>Animal tumors. Experimental tumors</topic><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>Biological and medical sciences</topic><topic>Bromates - toxicity</topic><topic>Carcinogens - toxicity</topic><topic>Cell Transformation, Neoplastic - drug effects</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Deoxyguanosine - analogs & derivatives</topic><topic>Deoxyguanosine - biosynthesis</topic><topic>DNA Damage - drug effects</topic><topic>DNA Glycosylases - biosynthesis</topic><topic>DNA Glycosylases - drug effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>Experimental renal and urinary tract tumors</topic><topic>Kidney - drug effects</topic><topic>Kidney - pathology</topic><topic>Kidney Neoplasms - chemically induced</topic><topic>Kidney Neoplasms - genetics</topic><topic>Kidney Neoplasms - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mutation</topic><topic>Nitrilotriacetic Acid - toxicity</topic><topic>Original</topic><topic>Oxidative Stress - drug effects</topic><topic>Precancerous Conditions - chemically induced</topic><topic>Precancerous Conditions - genetics</topic><topic>Precancerous Conditions - pathology</topic><topic>Rats</topic><topic>Rats, Inbred F344</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - analysis</topic><topic>Time Factors</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Umemura, Takashi</creatorcontrib><creatorcontrib>Kanki, Keita</creatorcontrib><creatorcontrib>Kuroiwa, Yuichi</creatorcontrib><creatorcontrib>Ishii, Yuji</creatorcontrib><creatorcontrib>Okano, Keita</creatorcontrib><creatorcontrib>Nohmi, Takehiko</creatorcontrib><creatorcontrib>Nishikawa, Akiyoshi</creatorcontrib><creatorcontrib>Hirose, Masao</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Umemura, Takashi</au><au>Kanki, Keita</au><au>Kuroiwa, Yuichi</au><au>Ishii, Yuji</au><au>Okano, Keita</au><au>Nohmi, Takehiko</au><au>Nishikawa, Akiyoshi</au><au>Hirose, Masao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In vivo mutagenicity and initiation following oxidative DNA lesion in the kidneys of rats given potassium bromate</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2006-09</date><risdate>2006</risdate><volume>97</volume><issue>9</issue><spage>829</spage><epage>835</epage><pages>829-835</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>To clarify the role of 8‐OHdG formation as a starting point for carcinogenesis, we examined the dose‐dependence and time‐course of changes of OGG1 mRNA expression, 8‐OHdG levels and in vivo mutations in the kidneys of gpt delta rats given KBrO3 in their drinking water for 13 weeks. There were no remarkable changes in OGG1 mRNA in spite of some increments being statistically significant. Increases of 8‐OHdG occurred after 1 week at 500 p.p.m. and after 13 weeks at 250 p.p.m. Elevation of Spi− mutant frequency, suggestive of deletion mutations, occurred after 9 weeks at 500 p.p.m. In a two‐stage experiment, F344 rats were given KBrO3 for 13 weeks then, after a 2‐week recovery, treated with 1% NTA in the diet for 39 weeks. The incidence and multiplicity of renal preneoplastic lesions in rats given KBrO3 at 500 p.p.m. followed by NTA treatment were significantly higher than in rats treated with NTA alone. Results suggest that a certain period of time might be required for 8‐OHdG to cause permanent mutations. The two‐step experiment shows that cells exposed to the alteration of the intranuclear status by oxidative stress including 8‐OHdG formation might be able to form tumors with appropriate promotion. (Cancer Sci 2006; 97: 829–835)</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Publishing Asia</pub><pmid>16805826</pmid><doi>10.1111/j.1349-7006.2006.00248.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext_linktorsrc |
| identifier | ISSN: 1347-9032 |
| ispartof | Cancer science, 2006-09, Vol.97 (9), p.829-835 |
| issn | 1347-9032 1349-7006 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11158994 |
| source | Wiley Online Library Open Access |
| subjects | 8-Hydroxy-2'-Deoxyguanosine Animal tumors. Experimental tumors Animals Animals, Genetically Modified Biological and medical sciences Bromates - toxicity Carcinogens - toxicity Cell Transformation, Neoplastic - drug effects Cell Transformation, Neoplastic - metabolism Deoxyguanosine - analogs & derivatives Deoxyguanosine - biosynthesis DNA Damage - drug effects DNA Glycosylases - biosynthesis DNA Glycosylases - drug effects Dose-Response Relationship, Drug Experimental renal and urinary tract tumors Kidney - drug effects Kidney - pathology Kidney Neoplasms - chemically induced Kidney Neoplasms - genetics Kidney Neoplasms - pathology Male Medical sciences Mutation Nitrilotriacetic Acid - toxicity Original Oxidative Stress - drug effects Precancerous Conditions - chemically induced Precancerous Conditions - genetics Precancerous Conditions - pathology Rats Rats, Inbred F344 Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - analysis Time Factors Tumors |
| title | In vivo mutagenicity and initiation following oxidative DNA lesion in the kidneys of rats given potassium bromate |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-09T07%3A46%3A23IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_24P&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=In%20vivo%20mutagenicity%20and%20initiation%20following%20oxidative%20DNA%20lesion%20in%20the%20kidneys%20of%20rats%20given%20potassium%20bromate&rft.jtitle=Cancer%20science&rft.au=Umemura,%20Takashi&rft.date=2006-09&rft.volume=97&rft.issue=9&rft.spage=829&rft.epage=835&rft.pages=829-835&rft.issn=1347-9032&rft.eissn=1349-7006&rft_id=info:doi/10.1111/j.1349-7006.2006.00248.x&rft_dat=%3Cproquest_24P%3E68757761%3C/proquest_24P%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=68757761&rft_id=info:pmid/16805826&rfr_iscdi=true |