Biomonitoring on Carcinogenic Metals and Oxidative DNA Damage in a Cross-Sectional Study
Oxidative DNA damage is mediated by reactive oxygen species and is supposed to play an important role in various diseases including cancer. The endogenous amount of reactive oxygen species may be enhanced by the exposure to genotoxic metals. A cross-sectional study was conducted from 1993 to 1994 in...
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| Veröffentlicht in: | Cancer epidemiology, biomarkers & prevention biomarkers & prevention, 2001-05, Vol.10 (5), p.515-522 |
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| creator | MERZENICH, Hiltrud HARTWIG, Andrea AHRENS, Wolfgang BEYERSMANN, Detmar SCHLEPEGRELL, Regina SCHOLZE, Martin TIMM, Jürgen JÖCKEL, Karl-Heinz |
| description | Oxidative DNA damage is mediated by reactive oxygen species and is supposed to play an important role in various diseases
including cancer. The endogenous amount of reactive oxygen species may be enhanced by the exposure to genotoxic metals. A
cross-sectional study was conducted from 1993 to 1994 in an urban population in Germany to investigate the association between
metal exposure and oxidative DNA damage.
The cross-sectional sample of 824 participants was recruited from the registry of residents in Bremen, comprising about two-third
males and one-third females with an average age of 61.1 years. A standardized questionnaire was used to obtain the occupational
and smoking history. The incorporated dose of exposure to metals was assessed by biological monitoring. Chromium, cadmium,
and nickel were measured in 593 urine samples. Lead was determined in blood samples of 227 participants. As a biomarker for
oxidative DNA damage, 7,8-dihydro-8-oxoguanine has been analyzed in lymphocytes of 201 participants. Oxidative lesions were
identified by single strand breaks induced by the bacterial formamidopyrimidine-DNA glycosylase (Fpg) in combination with
the alkaline unwinding approach.
The concentrations of metals indicate a low body load (median values: 1.0 μg nickel/l urine, 0.4 μg cadmium/l urine, and 46
μg lead/l blood; 83% of chromium measures were below the technical detection limit of 0.3 μg/l). The median level of Fpg-sensitive
DNA lesions was 0.23 lesions/10 6 bp. A positive association between nickel and the rate of oxidative DNA lesions (Fpg-sensitive sites) was observed (odds
ratio, 2.15; tertiles 1 versus 3, P < 0.05), which provides further evidence for the genotoxic effect of nickel in the general population. |
| format | Article |
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including cancer. The endogenous amount of reactive oxygen species may be enhanced by the exposure to genotoxic metals. A
cross-sectional study was conducted from 1993 to 1994 in an urban population in Germany to investigate the association between
metal exposure and oxidative DNA damage.
The cross-sectional sample of 824 participants was recruited from the registry of residents in Bremen, comprising about two-third
males and one-third females with an average age of 61.1 years. A standardized questionnaire was used to obtain the occupational
and smoking history. The incorporated dose of exposure to metals was assessed by biological monitoring. Chromium, cadmium,
and nickel were measured in 593 urine samples. Lead was determined in blood samples of 227 participants. As a biomarker for
oxidative DNA damage, 7,8-dihydro-8-oxoguanine has been analyzed in lymphocytes of 201 participants. Oxidative lesions were
identified by single strand breaks induced by the bacterial formamidopyrimidine-DNA glycosylase (Fpg) in combination with
the alkaline unwinding approach.
The concentrations of metals indicate a low body load (median values: 1.0 μg nickel/l urine, 0.4 μg cadmium/l urine, and 46
μg lead/l blood; 83% of chromium measures were below the technical detection limit of 0.3 μg/l). The median level of Fpg-sensitive
DNA lesions was 0.23 lesions/10 6 bp. A positive association between nickel and the rate of oxidative DNA lesions (Fpg-sensitive sites) was observed (odds
ratio, 2.15; tertiles 1 versus 3, P < 0.05), which provides further evidence for the genotoxic effect of nickel in the general population.</description><identifier>ISSN: 1055-9965</identifier><identifier>EISSN: 1538-7755</identifier><identifier>PMID: 11352863</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Cadmium - blood ; Cadmium - urine ; Carcinogenesis, carcinogens and anticarcinogens ; Carcinogens - analysis ; Chemical agents ; Chromium - blood ; Chromium - urine ; Confidence Intervals ; Cross-Sectional Studies ; DNA Damage ; Environmental Monitoring - methods ; Environmental Pollution - adverse effects ; Environmental Pollution - analysis ; Female ; Humans ; Lead - blood ; Lead - urine ; Linear Models ; Lymphocytes - chemistry ; Male ; Medical sciences ; Metals - blood ; Metals - urine ; Middle Aged ; Monitoring, Physiologic ; Nickel - blood ; Nickel - urine ; Odds Ratio ; Oxidative Stress ; Risk Assessment ; Sampling Studies ; Sensitivity and Specificity ; Tumors</subject><ispartof>Cancer epidemiology, biomarkers & prevention, 2001-05, Vol.10 (5), p.515-522</ispartof><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14137151$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11352863$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MERZENICH, Hiltrud</creatorcontrib><creatorcontrib>HARTWIG, Andrea</creatorcontrib><creatorcontrib>AHRENS, Wolfgang</creatorcontrib><creatorcontrib>BEYERSMANN, Detmar</creatorcontrib><creatorcontrib>SCHLEPEGRELL, Regina</creatorcontrib><creatorcontrib>SCHOLZE, Martin</creatorcontrib><creatorcontrib>TIMM, Jürgen</creatorcontrib><creatorcontrib>JÖCKEL, Karl-Heinz</creatorcontrib><title>Biomonitoring on Carcinogenic Metals and Oxidative DNA Damage in a Cross-Sectional Study</title><title>Cancer epidemiology, biomarkers & prevention</title><addtitle>Cancer Epidemiol Biomarkers Prev</addtitle><description>Oxidative DNA damage is mediated by reactive oxygen species and is supposed to play an important role in various diseases
including cancer. The endogenous amount of reactive oxygen species may be enhanced by the exposure to genotoxic metals. A
cross-sectional study was conducted from 1993 to 1994 in an urban population in Germany to investigate the association between
metal exposure and oxidative DNA damage.
The cross-sectional sample of 824 participants was recruited from the registry of residents in Bremen, comprising about two-third
males and one-third females with an average age of 61.1 years. A standardized questionnaire was used to obtain the occupational
and smoking history. The incorporated dose of exposure to metals was assessed by biological monitoring. Chromium, cadmium,
and nickel were measured in 593 urine samples. Lead was determined in blood samples of 227 participants. As a biomarker for
oxidative DNA damage, 7,8-dihydro-8-oxoguanine has been analyzed in lymphocytes of 201 participants. Oxidative lesions were
identified by single strand breaks induced by the bacterial formamidopyrimidine-DNA glycosylase (Fpg) in combination with
the alkaline unwinding approach.
The concentrations of metals indicate a low body load (median values: 1.0 μg nickel/l urine, 0.4 μg cadmium/l urine, and 46
μg lead/l blood; 83% of chromium measures were below the technical detection limit of 0.3 μg/l). The median level of Fpg-sensitive
DNA lesions was 0.23 lesions/10 6 bp. A positive association between nickel and the rate of oxidative DNA lesions (Fpg-sensitive sites) was observed (odds
ratio, 2.15; tertiles 1 versus 3, P < 0.05), which provides further evidence for the genotoxic effect of nickel in the general population.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Cadmium - blood</subject><subject>Cadmium - urine</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Carcinogens - analysis</subject><subject>Chemical agents</subject><subject>Chromium - blood</subject><subject>Chromium - urine</subject><subject>Confidence Intervals</subject><subject>Cross-Sectional Studies</subject><subject>DNA Damage</subject><subject>Environmental Monitoring - methods</subject><subject>Environmental Pollution - adverse effects</subject><subject>Environmental Pollution - analysis</subject><subject>Female</subject><subject>Humans</subject><subject>Lead - blood</subject><subject>Lead - urine</subject><subject>Linear Models</subject><subject>Lymphocytes - chemistry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metals - blood</subject><subject>Metals - urine</subject><subject>Middle Aged</subject><subject>Monitoring, Physiologic</subject><subject>Nickel - blood</subject><subject>Nickel - urine</subject><subject>Odds Ratio</subject><subject>Oxidative Stress</subject><subject>Risk Assessment</subject><subject>Sampling Studies</subject><subject>Sensitivity and Specificity</subject><subject>Tumors</subject><issn>1055-9965</issn><issn>1538-7755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0E1PwzAMBuAKgdgY_AWUC-JUKWnrpjmOji9psMNA4la5SdoGremUdMD-PZE2xMk-PLbl9ySaMkiLmHOA09BTgFiIHCbRhfeflFIuAM6jCWMpJEWeTqOPOzP0gzXj4IxtyWBJiU4aO7TaGkle9IgbT9AqsvoxCkfzpcnidU4W2GOribEESekG7-O1lqMZLG7Ietyp_WV01oRRfXWss-j94f6tfIqXq8fncr6MuyQXYwzIRSZRochSzmqsVYpUKMho3rAikY1IshrqOsekkI3SOWOKF5yzQlJW51k6i64Pe7e7uteq2jrTo9tXfy8GcHME6CVuGodWGv_vMhYOAwvu9uA603bfxulKBqmd016HSLqK0QoqCPn-Aj8saJg</recordid><startdate>20010501</startdate><enddate>20010501</enddate><creator>MERZENICH, Hiltrud</creator><creator>HARTWIG, Andrea</creator><creator>AHRENS, Wolfgang</creator><creator>BEYERSMANN, Detmar</creator><creator>SCHLEPEGRELL, Regina</creator><creator>SCHOLZE, Martin</creator><creator>TIMM, Jürgen</creator><creator>JÖCKEL, Karl-Heinz</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20010501</creationdate><title>Biomonitoring on Carcinogenic Metals and Oxidative DNA Damage in a Cross-Sectional Study</title><author>MERZENICH, Hiltrud ; HARTWIG, Andrea ; AHRENS, Wolfgang ; BEYERSMANN, Detmar ; SCHLEPEGRELL, Regina ; SCHOLZE, Martin ; TIMM, Jürgen ; JÖCKEL, Karl-Heinz</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h269t-5a794cada94371babd3a09d5406f182cf924b5bb6a28cfde611d787718c01b643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Cadmium - blood</topic><topic>Cadmium - urine</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Carcinogens - analysis</topic><topic>Chemical agents</topic><topic>Chromium - blood</topic><topic>Chromium - urine</topic><topic>Confidence Intervals</topic><topic>Cross-Sectional Studies</topic><topic>DNA Damage</topic><topic>Environmental Monitoring - methods</topic><topic>Environmental Pollution - adverse effects</topic><topic>Environmental Pollution - analysis</topic><topic>Female</topic><topic>Humans</topic><topic>Lead - blood</topic><topic>Lead - urine</topic><topic>Linear Models</topic><topic>Lymphocytes - chemistry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metals - blood</topic><topic>Metals - urine</topic><topic>Middle Aged</topic><topic>Monitoring, Physiologic</topic><topic>Nickel - blood</topic><topic>Nickel - urine</topic><topic>Odds Ratio</topic><topic>Oxidative Stress</topic><topic>Risk Assessment</topic><topic>Sampling Studies</topic><topic>Sensitivity and Specificity</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MERZENICH, Hiltrud</creatorcontrib><creatorcontrib>HARTWIG, Andrea</creatorcontrib><creatorcontrib>AHRENS, Wolfgang</creatorcontrib><creatorcontrib>BEYERSMANN, Detmar</creatorcontrib><creatorcontrib>SCHLEPEGRELL, Regina</creatorcontrib><creatorcontrib>SCHOLZE, Martin</creatorcontrib><creatorcontrib>TIMM, Jürgen</creatorcontrib><creatorcontrib>JÖCKEL, Karl-Heinz</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Cancer epidemiology, biomarkers & prevention</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MERZENICH, Hiltrud</au><au>HARTWIG, Andrea</au><au>AHRENS, Wolfgang</au><au>BEYERSMANN, Detmar</au><au>SCHLEPEGRELL, Regina</au><au>SCHOLZE, Martin</au><au>TIMM, Jürgen</au><au>JÖCKEL, Karl-Heinz</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biomonitoring on Carcinogenic Metals and Oxidative DNA Damage in a Cross-Sectional Study</atitle><jtitle>Cancer epidemiology, biomarkers & prevention</jtitle><addtitle>Cancer Epidemiol Biomarkers Prev</addtitle><date>2001-05-01</date><risdate>2001</risdate><volume>10</volume><issue>5</issue><spage>515</spage><epage>522</epage><pages>515-522</pages><issn>1055-9965</issn><eissn>1538-7755</eissn><abstract>Oxidative DNA damage is mediated by reactive oxygen species and is supposed to play an important role in various diseases
including cancer. The endogenous amount of reactive oxygen species may be enhanced by the exposure to genotoxic metals. A
cross-sectional study was conducted from 1993 to 1994 in an urban population in Germany to investigate the association between
metal exposure and oxidative DNA damage.
The cross-sectional sample of 824 participants was recruited from the registry of residents in Bremen, comprising about two-third
males and one-third females with an average age of 61.1 years. A standardized questionnaire was used to obtain the occupational
and smoking history. The incorporated dose of exposure to metals was assessed by biological monitoring. Chromium, cadmium,
and nickel were measured in 593 urine samples. Lead was determined in blood samples of 227 participants. As a biomarker for
oxidative DNA damage, 7,8-dihydro-8-oxoguanine has been analyzed in lymphocytes of 201 participants. Oxidative lesions were
identified by single strand breaks induced by the bacterial formamidopyrimidine-DNA glycosylase (Fpg) in combination with
the alkaline unwinding approach.
The concentrations of metals indicate a low body load (median values: 1.0 μg nickel/l urine, 0.4 μg cadmium/l urine, and 46
μg lead/l blood; 83% of chromium measures were below the technical detection limit of 0.3 μg/l). The median level of Fpg-sensitive
DNA lesions was 0.23 lesions/10 6 bp. A positive association between nickel and the rate of oxidative DNA lesions (Fpg-sensitive sites) was observed (odds
ratio, 2.15; tertiles 1 versus 3, P < 0.05), which provides further evidence for the genotoxic effect of nickel in the general population.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>11352863</pmid><tpages>8</tpages></addata></record> |
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| ispartof | Cancer epidemiology, biomarkers & prevention, 2001-05, Vol.10 (5), p.515-522 |
| issn | 1055-9965 1538-7755 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; American Association for Cancer Research |
| subjects | Adult Aged Aged, 80 and over Biological and medical sciences Cadmium - blood Cadmium - urine Carcinogenesis, carcinogens and anticarcinogens Carcinogens - analysis Chemical agents Chromium - blood Chromium - urine Confidence Intervals Cross-Sectional Studies DNA Damage Environmental Monitoring - methods Environmental Pollution - adverse effects Environmental Pollution - analysis Female Humans Lead - blood Lead - urine Linear Models Lymphocytes - chemistry Male Medical sciences Metals - blood Metals - urine Middle Aged Monitoring, Physiologic Nickel - blood Nickel - urine Odds Ratio Oxidative Stress Risk Assessment Sampling Studies Sensitivity and Specificity Tumors |
| title | Biomonitoring on Carcinogenic Metals and Oxidative DNA Damage in a Cross-Sectional Study |
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