Folate, vitamin b12, homocysteine status and DNA damage in young Australian adults
We performed a cross-sectional study (n = 49 males, 57 females) and a randomized double-blind placebo-controlled dietary intervention study (n = 31/32 per group) to determine the effect of folate and vitamin B12 (B12) on DNA damage (micronucleus formation and DNA methylation) and plasma homocysteine...
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| Veröffentlicht in: | Carcinogenesis (New York) 1998-07, Vol.19 (7), p.1163-1171 |
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| description | We performed a cross-sectional study (n = 49 males, 57 females) and a randomized double-blind placebo-controlled dietary intervention study (n = 31/32 per group) to determine the effect of folate and vitamin B12 (B12) on DNA damage (micronucleus formation and DNA methylation) and plasma homocysteine (HC) in young Australian adults aged 18-32 years. None of the volunteers were folate deficient (i.e. red blood cell folate |
| doi_str_mv | 10.1093/carcin/19.7.1163 |
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None of the volunteers were folate deficient (i.e. red blood cell folate <136 nmol/l) and only 4.4% (all females) were vitamin B12 deficient (i.e. serum vitamin B12 <150 pmol/l). The cross-sectional study showed that (i) the frequency of micronucleated cells (MNCs) was positively correlated with plasma HC in males (R = 0.293, P < 0.05) and (ii) in females MNC frequency was negatively correlated with serum vitamin B12 (R = -0.359, P < 0.01) but (iii) there was no significant correlation between micronucleus index and folate status. The results also showed that the level of unmethylated CpG (DNA) was not significantly related to vitamin B12 or folate status. The dietary intervention involved supplementation with 3.5x the recommended dietary intake (RDI) of folate and vitamin B12 in wheat bran cereal for three months followed by ten times the RDI of these vitamins via tablets for a further three months. In the supplemented group, MNC frequency was significantly reduced during the intervention by 25.4% in those subjects with initial MNC frequency in the high 50th percentile but there was no change in those subjects in the low 50th percentile for initial MNC frequency. The reduction in MNC frequency was significantly correlated with serum vitamin B12 (R = -0.49, P < 0.0005) and plasma HC (R = 0.39, P < 0.006), but was not significantly related to red blood cell folate. DNA methylation status was not altered in the supplemented group. The greatest decrease in plasma HC (by 37%) during the intervention was observed in those subjects in the supplemented group with initial plasma HC in the high 50th percentile, and correlated significantly with increases in red blood cell folate (R = -0.64, P < 0.0001) but not with serum vitamin B12. The results from this study suggest that (i) MNC frequency is minimized when plasma HC is below 7.5 micromol/l and serum vitamin B12 is above 300 pmol/l and (ii) dietary supplement intake of 700 microg folic acid and 7 microg vitamin B12 is sufficient to minimize MNC frequency and plasma HC. Thus, it appears that elevated plasma HC, a risk factor for cardiovascular disease, may also be a risk factor for chromosome damage.]]></description><identifier>ISSN: 0143-3334</identifier><identifier>ISSN: 1460-2180</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/19.7.1163</identifier><identifier>PMID: 9683174</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Biological and medical sciences ; Chemical mutagenesis ; Chromosome Aberrations ; Cross-Sectional Studies ; Dietary Supplements ; DNA - drug effects ; DNA - metabolism ; DNA Damage ; DNA Methylation - drug effects ; Double-Blind Method ; Female ; Folic Acid - administration & dosage ; Folic Acid - blood ; Hematinics - administration & dosage ; Hematinics - blood ; Homocysteine - blood ; Humans ; Lymphocytes - drug effects ; Lymphocytes - metabolism ; Male ; Medical sciences ; Micronuclei, Chromosome-Defective - drug effects ; Placebos ; Toxicology ; Vitamin B 12 - administration & dosage ; Vitamin B 12 - blood</subject><ispartof>Carcinogenesis (New York), 1998-07, Vol.19 (7), p.1163-1171</ispartof><rights>1998 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Jul 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c489t-9c9acd06760b4d3c66a1cbde5336786e4c1950f238de68d36dac36b496ca09443</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2338528$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9683174$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FENECH, M</creatorcontrib><creatorcontrib>AITKEN, C</creatorcontrib><creatorcontrib>RINALDI, J</creatorcontrib><title>Folate, vitamin b12, homocysteine status and DNA damage in young Australian adults</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description><![CDATA[We performed a cross-sectional study (n = 49 males, 57 females) and a randomized double-blind placebo-controlled dietary intervention study (n = 31/32 per group) to determine the effect of folate and vitamin B12 (B12) on DNA damage (micronucleus formation and DNA methylation) and plasma homocysteine (HC) in young Australian adults aged 18-32 years. None of the volunteers were folate deficient (i.e. red blood cell folate <136 nmol/l) and only 4.4% (all females) were vitamin B12 deficient (i.e. serum vitamin B12 <150 pmol/l). The cross-sectional study showed that (i) the frequency of micronucleated cells (MNCs) was positively correlated with plasma HC in males (R = 0.293, P < 0.05) and (ii) in females MNC frequency was negatively correlated with serum vitamin B12 (R = -0.359, P < 0.01) but (iii) there was no significant correlation between micronucleus index and folate status. The results also showed that the level of unmethylated CpG (DNA) was not significantly related to vitamin B12 or folate status. The dietary intervention involved supplementation with 3.5x the recommended dietary intake (RDI) of folate and vitamin B12 in wheat bran cereal for three months followed by ten times the RDI of these vitamins via tablets for a further three months. In the supplemented group, MNC frequency was significantly reduced during the intervention by 25.4% in those subjects with initial MNC frequency in the high 50th percentile but there was no change in those subjects in the low 50th percentile for initial MNC frequency. The reduction in MNC frequency was significantly correlated with serum vitamin B12 (R = -0.49, P < 0.0005) and plasma HC (R = 0.39, P < 0.006), but was not significantly related to red blood cell folate. DNA methylation status was not altered in the supplemented group. The greatest decrease in plasma HC (by 37%) during the intervention was observed in those subjects in the supplemented group with initial plasma HC in the high 50th percentile, and correlated significantly with increases in red blood cell folate (R = -0.64, P < 0.0001) but not with serum vitamin B12. The results from this study suggest that (i) MNC frequency is minimized when plasma HC is below 7.5 micromol/l and serum vitamin B12 is above 300 pmol/l and (ii) dietary supplement intake of 700 microg folic acid and 7 microg vitamin B12 is sufficient to minimize MNC frequency and plasma HC. Thus, it appears that elevated plasma HC, a risk factor for cardiovascular disease, may also be a risk factor for chromosome damage.]]></description><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Chemical mutagenesis</subject><subject>Chromosome Aberrations</subject><subject>Cross-Sectional Studies</subject><subject>Dietary Supplements</subject><subject>DNA - drug effects</subject><subject>DNA - metabolism</subject><subject>DNA Damage</subject><subject>DNA Methylation - drug effects</subject><subject>Double-Blind Method</subject><subject>Female</subject><subject>Folic Acid - administration & dosage</subject><subject>Folic Acid - blood</subject><subject>Hematinics - administration & dosage</subject><subject>Hematinics - blood</subject><subject>Homocysteine - blood</subject><subject>Humans</subject><subject>Lymphocytes - drug effects</subject><subject>Lymphocytes - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Micronuclei, Chromosome-Defective - drug effects</subject><subject>Placebos</subject><subject>Toxicology</subject><subject>Vitamin B 12 - administration & dosage</subject><subject>Vitamin B 12 - blood</subject><issn>0143-3334</issn><issn>1460-2180</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkEFr3DAQhUVISbZp77kURCg9xRuNR5al45I2bSG0ENqzGEva1MGWE0kO7L-Pwy459DSH973H8DF2DmINwuCVo-T6eAVm3a4BFB6xFUglqhq0OGYrARIrRJSn7H3OD0IsSGNO2IlRGqGVK3Z3Mw1UwiV_7guNfeQd1Jf83zRObpdL6GPguVCZM6fo-ddfG-5ppPvAF3Q3zfGeb-ZcEg09RU5-Hkr-wN5tacjh4-Gesb833_5c_6huf3__eb25rZzUplTGGXJeqFaJTnp0ShG4zocGUbVaBenANGJbo_ZBaY_Kk0PVSaMcCSMlnrEv-93HND3NIRc79tmFYaAYpjlbUI3U2OgFvPgPfJjmFJffbA0G6xoaWCCxh1yack5hax9TP1LaWRD21bXdu7ZgbGtfXS-VT4fduRuDfysc5C7550NO2dGwTRRdn9-wGlE3tcYX3maGtA</recordid><startdate>19980701</startdate><enddate>19980701</enddate><creator>FENECH, M</creator><creator>AITKEN, C</creator><creator>RINALDI, J</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</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>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>19980701</creationdate><title>Folate, vitamin b12, homocysteine status and DNA damage in young Australian adults</title><author>FENECH, M ; AITKEN, C ; RINALDI, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c489t-9c9acd06760b4d3c66a1cbde5336786e4c1950f238de68d36dac36b496ca09443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Chemical mutagenesis</topic><topic>Chromosome Aberrations</topic><topic>Cross-Sectional Studies</topic><topic>Dietary Supplements</topic><topic>DNA - drug effects</topic><topic>DNA - metabolism</topic><topic>DNA Damage</topic><topic>DNA Methylation - drug effects</topic><topic>Double-Blind Method</topic><topic>Female</topic><topic>Folic Acid - administration & dosage</topic><topic>Folic Acid - blood</topic><topic>Hematinics - administration & dosage</topic><topic>Hematinics - blood</topic><topic>Homocysteine - blood</topic><topic>Humans</topic><topic>Lymphocytes - drug effects</topic><topic>Lymphocytes - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Micronuclei, Chromosome-Defective - drug effects</topic><topic>Placebos</topic><topic>Toxicology</topic><topic>Vitamin B 12 - administration & dosage</topic><topic>Vitamin B 12 - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FENECH, M</creatorcontrib><creatorcontrib>AITKEN, C</creatorcontrib><creatorcontrib>RINALDI, J</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>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>FENECH, M</au><au>AITKEN, C</au><au>RINALDI, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Folate, vitamin b12, homocysteine status and DNA damage in young Australian adults</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>1998-07-01</date><risdate>1998</risdate><volume>19</volume><issue>7</issue><spage>1163</spage><epage>1171</epage><pages>1163-1171</pages><issn>0143-3334</issn><issn>1460-2180</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract><![CDATA[We performed a cross-sectional study (n = 49 males, 57 females) and a randomized double-blind placebo-controlled dietary intervention study (n = 31/32 per group) to determine the effect of folate and vitamin B12 (B12) on DNA damage (micronucleus formation and DNA methylation) and plasma homocysteine (HC) in young Australian adults aged 18-32 years. None of the volunteers were folate deficient (i.e. red blood cell folate <136 nmol/l) and only 4.4% (all females) were vitamin B12 deficient (i.e. serum vitamin B12 <150 pmol/l). The cross-sectional study showed that (i) the frequency of micronucleated cells (MNCs) was positively correlated with plasma HC in males (R = 0.293, P < 0.05) and (ii) in females MNC frequency was negatively correlated with serum vitamin B12 (R = -0.359, P < 0.01) but (iii) there was no significant correlation between micronucleus index and folate status. The results also showed that the level of unmethylated CpG (DNA) was not significantly related to vitamin B12 or folate status. The dietary intervention involved supplementation with 3.5x the recommended dietary intake (RDI) of folate and vitamin B12 in wheat bran cereal for three months followed by ten times the RDI of these vitamins via tablets for a further three months. In the supplemented group, MNC frequency was significantly reduced during the intervention by 25.4% in those subjects with initial MNC frequency in the high 50th percentile but there was no change in those subjects in the low 50th percentile for initial MNC frequency. The reduction in MNC frequency was significantly correlated with serum vitamin B12 (R = -0.49, P < 0.0005) and plasma HC (R = 0.39, P < 0.006), but was not significantly related to red blood cell folate. DNA methylation status was not altered in the supplemented group. The greatest decrease in plasma HC (by 37%) during the intervention was observed in those subjects in the supplemented group with initial plasma HC in the high 50th percentile, and correlated significantly with increases in red blood cell folate (R = -0.64, P < 0.0001) but not with serum vitamin B12. The results from this study suggest that (i) MNC frequency is minimized when plasma HC is below 7.5 micromol/l and serum vitamin B12 is above 300 pmol/l and (ii) dietary supplement intake of 700 microg folic acid and 7 microg vitamin B12 is sufficient to minimize MNC frequency and plasma HC. Thus, it appears that elevated plasma HC, a risk factor for cardiovascular disease, may also be a risk factor for chromosome damage.]]></abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>9683174</pmid><doi>10.1093/carcin/19.7.1163</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0143-3334 |
| ispartof | Carcinogenesis (New York), 1998-07, Vol.19 (7), p.1163-1171 |
| issn | 0143-3334 1460-2180 1460-2180 |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adult Biological and medical sciences Chemical mutagenesis Chromosome Aberrations Cross-Sectional Studies Dietary Supplements DNA - drug effects DNA - metabolism DNA Damage DNA Methylation - drug effects Double-Blind Method Female Folic Acid - administration & dosage Folic Acid - blood Hematinics - administration & dosage Hematinics - blood Homocysteine - blood Humans Lymphocytes - drug effects Lymphocytes - metabolism Male Medical sciences Micronuclei, Chromosome-Defective - drug effects Placebos Toxicology Vitamin B 12 - administration & dosage Vitamin B 12 - blood |
| title | Folate, vitamin b12, homocysteine status and DNA damage in young Australian adults |
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