Urinary 8-oxodeoxyguanosine, aflatoxin B1 exposure and hepatitis B virus infection and hepatocellular carcinoma in Taiwan
To evaluate the role of oxidative stress and aflatoxin exposure on risk of hepatocellular carcinoma (HCC), a case–control study nested within a community-based cohort was conducted in Taiwan. Baseline urine samples, collected from a total of 74 HCC cases and 290 matched controls, were used to determ...
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| Veröffentlicht in: | Carcinogenesis (New York) 2007-05, Vol.28 (5), p.995-999 |
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| creator | Wu, Hui-Chen Wang, Qiao Wang, Lian-Wen Yang, Hwai-I Ahsan, Habibul Tsai, Wei-Yann Wang, Li-Yu Chen, Shu-Yuan Chen, Chien-Jen Santella, Regina M. |
| description | To evaluate the role of oxidative stress and aflatoxin exposure on risk of hepatocellular carcinoma (HCC), a case–control study nested within a community-based cohort was conducted in Taiwan. Baseline urine samples, collected from a total of 74 HCC cases and 290 matched controls, were used to determine by enzyme-linked immunosorbent assays the level of urinary excretion of 8-oxodeoxyguanosine (8-oxodG), a biomarker of oxidative DNA damage and urinary aflatoxin B1 metabolites, a biomarker of aflatoxin exposure. Multivariate-adjusted linear regression analysis showed that urinary aflatoxin metabolites and gender were significantly associated with level of urinary 8-oxodG among controls. Moreover, after adjustments for potential confounding factors, there was a statistically significant positive dose–response relationship between levels of urinary 8-oxodG and urinary aflatoxin metabolites (P < 0.0001). However, when compared with subjects in the lowest quartile of 8-oxodG, there was a decrease in risk of HCC, with adjusted odds ratios (ORs) of 0.8 [95% confidence interval (CI) 0.3–2.0], 0.7 (95% CI 0.3–2.0) and 0.7 (95% CI 0.2–1.7) for subjects in the second, third and fourth quartile, respectively. The combination of level of urinary 8-oxodG below the median and hepatitis B virus infection resulted in an OR of 11.4 (95% CI 3.9–33.3), compared with those with urinary 8-oxodG above the median and hepatitis B virus surface antigen negative. These results suggest that elevated levels of urinary 8-oxodG may be related to increasing level of aflatoxin exposure but may also indicate enhanced repair of oxidative DNA damage and therefore lower risk of HCC. |
| doi_str_mv | 10.1093/carcin/bgl234 |
| format | Article |
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Baseline urine samples, collected from a total of 74 HCC cases and 290 matched controls, were used to determine by enzyme-linked immunosorbent assays the level of urinary excretion of 8-oxodeoxyguanosine (8-oxodG), a biomarker of oxidative DNA damage and urinary aflatoxin B1 metabolites, a biomarker of aflatoxin exposure. Multivariate-adjusted linear regression analysis showed that urinary aflatoxin metabolites and gender were significantly associated with level of urinary 8-oxodG among controls. Moreover, after adjustments for potential confounding factors, there was a statistically significant positive dose–response relationship between levels of urinary 8-oxodG and urinary aflatoxin metabolites (P < 0.0001). However, when compared with subjects in the lowest quartile of 8-oxodG, there was a decrease in risk of HCC, with adjusted odds ratios (ORs) of 0.8 [95% confidence interval (CI) 0.3–2.0], 0.7 (95% CI 0.3–2.0) and 0.7 (95% CI 0.2–1.7) for subjects in the second, third and fourth quartile, respectively. The combination of level of urinary 8-oxodG below the median and hepatitis B virus infection resulted in an OR of 11.4 (95% CI 3.9–33.3), compared with those with urinary 8-oxodG above the median and hepatitis B virus surface antigen negative. These results suggest that elevated levels of urinary 8-oxodG may be related to increasing level of aflatoxin exposure but may also indicate enhanced repair of oxidative DNA damage and therefore lower risk of HCC.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/bgl234</identifier><identifier>PMID: 17127712</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Aflatoxin B1 - toxicity ; Aflatoxin B1 - urine ; Biological and medical sciences ; Carcinogenesis, carcinogens and anticarcinogens ; Carcinoma, Hepatocellular - etiology ; Case-Control Studies ; Chemical agents ; Cohort Studies ; Deoxyadenine Nucleotides - urine ; DNA Damage ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Hepatitis B - complications ; Human viral diseases ; Humans ; Infectious diseases ; Liver Neoplasms - etiology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Middle Aged ; Oxidative Stress ; Plant poisons toxicology ; Risk ; Sex Factors ; Taiwan ; Toxicology ; Tumors ; Viral diseases ; Viral hepatitis</subject><ispartof>Carcinogenesis (New York), 2007-05, Vol.28 (5), p.995-999</ispartof><rights>The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org 2007</rights><rights>2007 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) May 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4394-44fc76fc6006347fcda880cb86561093054f37cf275faf503e019c5101af0143</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1584,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18733592$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17127712$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Hui-Chen</creatorcontrib><creatorcontrib>Wang, Qiao</creatorcontrib><creatorcontrib>Wang, Lian-Wen</creatorcontrib><creatorcontrib>Yang, Hwai-I</creatorcontrib><creatorcontrib>Ahsan, Habibul</creatorcontrib><creatorcontrib>Tsai, Wei-Yann</creatorcontrib><creatorcontrib>Wang, Li-Yu</creatorcontrib><creatorcontrib>Chen, Shu-Yuan</creatorcontrib><creatorcontrib>Chen, Chien-Jen</creatorcontrib><creatorcontrib>Santella, Regina M.</creatorcontrib><title>Urinary 8-oxodeoxyguanosine, aflatoxin B1 exposure and hepatitis B virus infection and hepatocellular carcinoma in Taiwan</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>To evaluate the role of oxidative stress and aflatoxin exposure on risk of hepatocellular carcinoma (HCC), a case–control study nested within a community-based cohort was conducted in Taiwan. Baseline urine samples, collected from a total of 74 HCC cases and 290 matched controls, were used to determine by enzyme-linked immunosorbent assays the level of urinary excretion of 8-oxodeoxyguanosine (8-oxodG), a biomarker of oxidative DNA damage and urinary aflatoxin B1 metabolites, a biomarker of aflatoxin exposure. Multivariate-adjusted linear regression analysis showed that urinary aflatoxin metabolites and gender were significantly associated with level of urinary 8-oxodG among controls. Moreover, after adjustments for potential confounding factors, there was a statistically significant positive dose–response relationship between levels of urinary 8-oxodG and urinary aflatoxin metabolites (P < 0.0001). However, when compared with subjects in the lowest quartile of 8-oxodG, there was a decrease in risk of HCC, with adjusted odds ratios (ORs) of 0.8 [95% confidence interval (CI) 0.3–2.0], 0.7 (95% CI 0.3–2.0) and 0.7 (95% CI 0.2–1.7) for subjects in the second, third and fourth quartile, respectively. The combination of level of urinary 8-oxodG below the median and hepatitis B virus infection resulted in an OR of 11.4 (95% CI 3.9–33.3), compared with those with urinary 8-oxodG above the median and hepatitis B virus surface antigen negative. These results suggest that elevated levels of urinary 8-oxodG may be related to increasing level of aflatoxin exposure but may also indicate enhanced repair of oxidative DNA damage and therefore lower risk of HCC.</description><subject>Adult</subject><subject>Aflatoxin B1 - toxicity</subject><subject>Aflatoxin B1 - urine</subject><subject>Biological and medical sciences</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Carcinoma, Hepatocellular - etiology</subject><subject>Case-Control Studies</subject><subject>Chemical agents</subject><subject>Cohort Studies</subject><subject>Deoxyadenine Nucleotides - urine</subject><subject>DNA Damage</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hepatitis B - complications</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Liver Neoplasms - etiology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Oxidative Stress</subject><subject>Plant poisons toxicology</subject><subject>Risk</subject><subject>Sex Factors</subject><subject>Taiwan</subject><subject>Toxicology</subject><subject>Tumors</subject><subject>Viral diseases</subject><subject>Viral hepatitis</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0U9v2yAYBnA0rVqzbsddJ1Rp0g51CwaDfWyirWlVaZdMmnZBbwh0tA64YK_Ot58tW81xB8SBn94_Dwh9ouSSkopdaYja-avtQ50z_gYtKBcky2lJ3qIFoZxljDF-it6n9EgIFayo3qFTKmkuh7NAh5_ReYgHXGahDzsT-sNDBz4k580FBltDG3rn8ZJi0zchddFg8Dv8xzTQutYlvMR_XewSdt4a3brgj-9Bm7ruaoh4mjLsYWB4A-4F_Ad0YqFO5uN8n6HN92-b1Tq7_3Fzu7q-zzRnFc84t1oKqwUhgnFp9Q7KkuhtKQoxBkAKbpnUNpeFBVsQZgitdEEJBTvuf4bOp7JNDM-dSa16DF30Q0eV04pxIooRZRPSMaQUjVVNdPshFkWJGruoaQE1xTz4z3PRbrs3u6Oecx3AlxlA0lDbCF67dHSlZMNPjO7r5ELX_LfnPKNLrelfMcQnJSSThVr_-q2WPK_WRK7UHfsHzD-kkw</recordid><startdate>200705</startdate><enddate>200705</enddate><creator>Wu, Hui-Chen</creator><creator>Wang, Qiao</creator><creator>Wang, Lian-Wen</creator><creator>Yang, Hwai-I</creator><creator>Ahsan, Habibul</creator><creator>Tsai, Wei-Yann</creator><creator>Wang, Li-Yu</creator><creator>Chen, Shu-Yuan</creator><creator>Chen, Chien-Jen</creator><creator>Santella, Regina M.</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>200705</creationdate><title>Urinary 8-oxodeoxyguanosine, aflatoxin B1 exposure and hepatitis B virus infection and hepatocellular carcinoma in Taiwan</title><author>Wu, Hui-Chen ; Wang, Qiao ; Wang, Lian-Wen ; Yang, Hwai-I ; Ahsan, Habibul ; Tsai, Wei-Yann ; Wang, Li-Yu ; Chen, Shu-Yuan ; Chen, Chien-Jen ; Santella, Regina M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4394-44fc76fc6006347fcda880cb86561093054f37cf275faf503e019c5101af0143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Aflatoxin B1 - toxicity</topic><topic>Aflatoxin B1 - urine</topic><topic>Biological and medical sciences</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Carcinoma, Hepatocellular - etiology</topic><topic>Case-Control Studies</topic><topic>Chemical agents</topic><topic>Cohort Studies</topic><topic>Deoxyadenine Nucleotides - urine</topic><topic>DNA Damage</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hepatitis B - complications</topic><topic>Human viral diseases</topic><topic>Humans</topic><topic>Infectious diseases</topic><topic>Liver Neoplasms - etiology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Oxidative Stress</topic><topic>Plant poisons toxicology</topic><topic>Risk</topic><topic>Sex Factors</topic><topic>Taiwan</topic><topic>Toxicology</topic><topic>Tumors</topic><topic>Viral diseases</topic><topic>Viral hepatitis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Hui-Chen</creatorcontrib><creatorcontrib>Wang, Qiao</creatorcontrib><creatorcontrib>Wang, Lian-Wen</creatorcontrib><creatorcontrib>Yang, Hwai-I</creatorcontrib><creatorcontrib>Ahsan, Habibul</creatorcontrib><creatorcontrib>Tsai, Wei-Yann</creatorcontrib><creatorcontrib>Wang, Li-Yu</creatorcontrib><creatorcontrib>Chen, Shu-Yuan</creatorcontrib><creatorcontrib>Chen, Chien-Jen</creatorcontrib><creatorcontrib>Santella, Regina M.</creatorcontrib><collection>Istex</collection><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>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Hui-Chen</au><au>Wang, Qiao</au><au>Wang, Lian-Wen</au><au>Yang, Hwai-I</au><au>Ahsan, Habibul</au><au>Tsai, Wei-Yann</au><au>Wang, Li-Yu</au><au>Chen, Shu-Yuan</au><au>Chen, Chien-Jen</au><au>Santella, Regina M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Urinary 8-oxodeoxyguanosine, aflatoxin B1 exposure and hepatitis B virus infection and hepatocellular carcinoma in Taiwan</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2007-05</date><risdate>2007</risdate><volume>28</volume><issue>5</issue><spage>995</spage><epage>999</epage><pages>995-999</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>To evaluate the role of oxidative stress and aflatoxin exposure on risk of hepatocellular carcinoma (HCC), a case–control study nested within a community-based cohort was conducted in Taiwan. Baseline urine samples, collected from a total of 74 HCC cases and 290 matched controls, were used to determine by enzyme-linked immunosorbent assays the level of urinary excretion of 8-oxodeoxyguanosine (8-oxodG), a biomarker of oxidative DNA damage and urinary aflatoxin B1 metabolites, a biomarker of aflatoxin exposure. Multivariate-adjusted linear regression analysis showed that urinary aflatoxin metabolites and gender were significantly associated with level of urinary 8-oxodG among controls. Moreover, after adjustments for potential confounding factors, there was a statistically significant positive dose–response relationship between levels of urinary 8-oxodG and urinary aflatoxin metabolites (P < 0.0001). However, when compared with subjects in the lowest quartile of 8-oxodG, there was a decrease in risk of HCC, with adjusted odds ratios (ORs) of 0.8 [95% confidence interval (CI) 0.3–2.0], 0.7 (95% CI 0.3–2.0) and 0.7 (95% CI 0.2–1.7) for subjects in the second, third and fourth quartile, respectively. The combination of level of urinary 8-oxodG below the median and hepatitis B virus infection resulted in an OR of 11.4 (95% CI 3.9–33.3), compared with those with urinary 8-oxodG above the median and hepatitis B virus surface antigen negative. These results suggest that elevated levels of urinary 8-oxodG may be related to increasing level of aflatoxin exposure but may also indicate enhanced repair of oxidative DNA damage and therefore lower risk of HCC.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>17127712</pmid><doi>10.1093/carcin/bgl234</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aflatoxin B1 - toxicity Aflatoxin B1 - urine Biological and medical sciences Carcinogenesis, carcinogens and anticarcinogens Carcinoma, Hepatocellular - etiology Case-Control Studies Chemical agents Cohort Studies Deoxyadenine Nucleotides - urine DNA Damage Female Gastroenterology. Liver. Pancreas. Abdomen Hepatitis B - complications Human viral diseases Humans Infectious diseases Liver Neoplasms - etiology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Middle Aged Oxidative Stress Plant poisons toxicology Risk Sex Factors Taiwan Toxicology Tumors Viral diseases Viral hepatitis |
| title | Urinary 8-oxodeoxyguanosine, aflatoxin B1 exposure and hepatitis B virus infection and hepatocellular carcinoma in Taiwan |
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