Formation of 8-hydroxydeoxyguanosine in calf thymus DNA treated with tert-butylhydroquinone, a major metabolite of butylated hydroxyanisole
Oxidative DNA damage caused by butylated hydroxyanisole (BHA), 2- tert-butyl(1,4)hydroquinone (TBHQ, a metabolite of BHA) and 2,5-di- tert-butyl(1,4)hydroquinone (DTBHQ), as well as 2,6-di- tert-butyl(1,4)benzoquinone (BHTQ, a metabolite of butylated hydroxytoluene), was evaluated by measuring the f...
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Veröffentlicht in: | Toxicology letters 1996-12, Vol.89 (2), p.163-167 |
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creator | Nagai, Fumiko Okubo, Tomoko Ushiyama, Keiko Satoh, Kanako Kano, Itsu |
description | Oxidative DNA damage caused by butylated hydroxyanisole (BHA), 2-
tert-butyl(1,4)hydroquinone (TBHQ, a metabolite of BHA) and 2,5-di-
tert-butyl(1,4)hydroquinone (DTBHQ), as well as 2,6-di-
tert-butyl(1,4)benzoquinone (BHTQ, a metabolite of butylated hydroxytoluene), was evaluated by measuring the formation of 8-hydroxy-deoxyguanosine (80HdG) in calf thymus DNA. 80HdG formation was greatly increased by TBHQ in a concentration-dependent manner. This effect was strongly enhanced by CuCl
2 and suppressed by EDTA, bathocuproinedisulfonic acid disodium salt, methionine, glutathione reduced form or catalase, but was not affected by mannitol, sodium benzoate or sodium azide. Thus, TBHQ-induced 80HdG formation may be mediated by copper. DTBHQ also induced the formation of 80HdG, though to a much lesser extent than TBHQ, and its effect was stimulated by CuCl
2. BHA had a small enhancing effect at high concentration, only in the presence of CuCl
2, whereas in the case of BHTQ, it occurred both in the presence of CuCl
2 and FeCl
2. |
doi_str_mv | 10.1016/S0378-4274(96)03800-3 |
format | Article |
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tert-butyl(1,4)hydroquinone (TBHQ, a metabolite of BHA) and 2,5-di-
tert-butyl(1,4)hydroquinone (DTBHQ), as well as 2,6-di-
tert-butyl(1,4)benzoquinone (BHTQ, a metabolite of butylated hydroxytoluene), was evaluated by measuring the formation of 8-hydroxy-deoxyguanosine (80HdG) in calf thymus DNA. 80HdG formation was greatly increased by TBHQ in a concentration-dependent manner. This effect was strongly enhanced by CuCl
2 and suppressed by EDTA, bathocuproinedisulfonic acid disodium salt, methionine, glutathione reduced form or catalase, but was not affected by mannitol, sodium benzoate or sodium azide. Thus, TBHQ-induced 80HdG formation may be mediated by copper. DTBHQ also induced the formation of 80HdG, though to a much lesser extent than TBHQ, and its effect was stimulated by CuCl
2. BHA had a small enhancing effect at high concentration, only in the presence of CuCl
2, whereas in the case of BHTQ, it occurred both in the presence of CuCl
2 and FeCl
2.</description><identifier>ISSN: 0378-4274</identifier><identifier>EISSN: 1879-3169</identifier><identifier>DOI: 10.1016/S0378-4274(96)03800-3</identifier><identifier>PMID: 8960159</identifier><identifier>CODEN: TOLED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>2,5-Di- tert-butyl(1,4)hydroquinone ; 2,6- Di- tert-butyl- p-benzoquinone ; 2- tert-Butyl(1,4)hydroquinone ; 8-Hydroxy-2′-deoxyguanosine ; Animals ; Antioxidants - chemistry ; Biological and medical sciences ; Butylated hydroxyanisole ; Butylated Hydroxyanisole - chemistry ; Butylated Hydroxyanisole - metabolism ; Cattle ; Chemical and industrial products toxicology. Toxic occupational diseases ; Deoxyguanosine - analogs & derivatives ; Deoxyguanosine - analysis ; Deoxyguanosine - chemistry ; DNA - chemistry ; DNA Damage ; Hydroquinones - chemistry ; Medical sciences ; Thymus Gland - chemistry ; Toxicology ; Various organic compounds</subject><ispartof>Toxicology letters, 1996-12, Vol.89 (2), p.163-167</ispartof><rights>1996</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-8a89c54e34ddbbfbf94b9b6d901179c2fc45f514ee8eac7e9acfb2a840b7bae43</citedby><cites>FETCH-LOGICAL-c420t-8a89c54e34ddbbfbf94b9b6d901179c2fc45f514ee8eac7e9acfb2a840b7bae43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0378427496038003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2480590$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8960159$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nagai, Fumiko</creatorcontrib><creatorcontrib>Okubo, Tomoko</creatorcontrib><creatorcontrib>Ushiyama, Keiko</creatorcontrib><creatorcontrib>Satoh, Kanako</creatorcontrib><creatorcontrib>Kano, Itsu</creatorcontrib><title>Formation of 8-hydroxydeoxyguanosine in calf thymus DNA treated with tert-butylhydroquinone, a major metabolite of butylated hydroxyanisole</title><title>Toxicology letters</title><addtitle>Toxicol Lett</addtitle><description>Oxidative DNA damage caused by butylated hydroxyanisole (BHA), 2-
tert-butyl(1,4)hydroquinone (TBHQ, a metabolite of BHA) and 2,5-di-
tert-butyl(1,4)hydroquinone (DTBHQ), as well as 2,6-di-
tert-butyl(1,4)benzoquinone (BHTQ, a metabolite of butylated hydroxytoluene), was evaluated by measuring the formation of 8-hydroxy-deoxyguanosine (80HdG) in calf thymus DNA. 80HdG formation was greatly increased by TBHQ in a concentration-dependent manner. This effect was strongly enhanced by CuCl
2 and suppressed by EDTA, bathocuproinedisulfonic acid disodium salt, methionine, glutathione reduced form or catalase, but was not affected by mannitol, sodium benzoate or sodium azide. Thus, TBHQ-induced 80HdG formation may be mediated by copper. DTBHQ also induced the formation of 80HdG, though to a much lesser extent than TBHQ, and its effect was stimulated by CuCl
2. BHA had a small enhancing effect at high concentration, only in the presence of CuCl
2, whereas in the case of BHTQ, it occurred both in the presence of CuCl
2 and FeCl
2.</description><subject>2,5-Di- tert-butyl(1,4)hydroquinone</subject><subject>2,6- Di- tert-butyl- p-benzoquinone</subject><subject>2- tert-Butyl(1,4)hydroquinone</subject><subject>8-Hydroxy-2′-deoxyguanosine</subject><subject>Animals</subject><subject>Antioxidants - chemistry</subject><subject>Biological and medical sciences</subject><subject>Butylated hydroxyanisole</subject><subject>Butylated Hydroxyanisole - chemistry</subject><subject>Butylated Hydroxyanisole - metabolism</subject><subject>Cattle</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Deoxyguanosine - analogs & derivatives</subject><subject>Deoxyguanosine - analysis</subject><subject>Deoxyguanosine - chemistry</subject><subject>DNA - chemistry</subject><subject>DNA Damage</subject><subject>Hydroquinones - chemistry</subject><subject>Medical sciences</subject><subject>Thymus Gland - chemistry</subject><subject>Toxicology</subject><subject>Various organic compounds</subject><issn>0378-4274</issn><issn>1879-3169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1TAQRS1EVR6FT6jkBUIgkWInjmOvqqpQqFTBAlhbtjPhuUrsYjvQfAM_TZIXvS0bz2LO9R3di9A5JReUUP7-G6kaUbCyYW8kf0sqQUhRPUE7KhpZVJTLp2h3RJ6h5yndE0I44_UpOhWSE1rLHfp7E-Kgswsehw6LYj-1MTxOLczPz1H7kJwH7Dy2uu9w3k_DmPCHL1c4R9AZWvzH5T3OEHNhxjz1q_7X6Hzw8A5rPOj7EPEAWZvQuwyLywqu4s1Ne5dCDy_QSaf7BC-3eYZ-3Hz8fv25uPv66fb66q6wrCS5EFpIWzOoWNsa05lOMiMNbyWhtJG27Cyru5oyAAHaNiC17UypBSOmMRpYdYZeH_59WE6FlNXgkoW-1x7CmBStBW-qms9gfQBtDClF6NRDdIOOk6JELSWotQS1JKwkV2sJqpp155vBaAZoj6ot9Xn_atvrtOQatbcuHbGSCVJLMmOXBwzmMH47iCpZB95C6yLYrNrg_nPIP38wqI0</recordid><startdate>19961216</startdate><enddate>19961216</enddate><creator>Nagai, Fumiko</creator><creator>Okubo, Tomoko</creator><creator>Ushiyama, Keiko</creator><creator>Satoh, Kanako</creator><creator>Kano, Itsu</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Science</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>7U7</scope><scope>C1K</scope></search><sort><creationdate>19961216</creationdate><title>Formation of 8-hydroxydeoxyguanosine in calf thymus DNA treated with tert-butylhydroquinone, a major metabolite of butylated hydroxyanisole</title><author>Nagai, Fumiko ; Okubo, Tomoko ; Ushiyama, Keiko ; Satoh, Kanako ; Kano, Itsu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-8a89c54e34ddbbfbf94b9b6d901179c2fc45f514ee8eac7e9acfb2a840b7bae43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>2,5-Di- tert-butyl(1,4)hydroquinone</topic><topic>2,6- Di- tert-butyl- p-benzoquinone</topic><topic>2- tert-Butyl(1,4)hydroquinone</topic><topic>8-Hydroxy-2′-deoxyguanosine</topic><topic>Animals</topic><topic>Antioxidants - chemistry</topic><topic>Biological and medical sciences</topic><topic>Butylated hydroxyanisole</topic><topic>Butylated Hydroxyanisole - chemistry</topic><topic>Butylated Hydroxyanisole - metabolism</topic><topic>Cattle</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Deoxyguanosine - analogs & derivatives</topic><topic>Deoxyguanosine - analysis</topic><topic>Deoxyguanosine - chemistry</topic><topic>DNA - chemistry</topic><topic>DNA Damage</topic><topic>Hydroquinones - chemistry</topic><topic>Medical sciences</topic><topic>Thymus Gland - chemistry</topic><topic>Toxicology</topic><topic>Various organic compounds</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nagai, Fumiko</creatorcontrib><creatorcontrib>Okubo, Tomoko</creatorcontrib><creatorcontrib>Ushiyama, Keiko</creatorcontrib><creatorcontrib>Satoh, Kanako</creatorcontrib><creatorcontrib>Kano, Itsu</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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Toxicology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nagai, Fumiko</au><au>Okubo, Tomoko</au><au>Ushiyama, Keiko</au><au>Satoh, Kanako</au><au>Kano, Itsu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Formation of 8-hydroxydeoxyguanosine in calf thymus DNA treated with tert-butylhydroquinone, a major metabolite of butylated hydroxyanisole</atitle><jtitle>Toxicology letters</jtitle><addtitle>Toxicol Lett</addtitle><date>1996-12-16</date><risdate>1996</risdate><volume>89</volume><issue>2</issue><spage>163</spage><epage>167</epage><pages>163-167</pages><issn>0378-4274</issn><eissn>1879-3169</eissn><coden>TOLED5</coden><abstract>Oxidative DNA damage caused by butylated hydroxyanisole (BHA), 2-
tert-butyl(1,4)hydroquinone (TBHQ, a metabolite of BHA) and 2,5-di-
tert-butyl(1,4)hydroquinone (DTBHQ), as well as 2,6-di-
tert-butyl(1,4)benzoquinone (BHTQ, a metabolite of butylated hydroxytoluene), was evaluated by measuring the formation of 8-hydroxy-deoxyguanosine (80HdG) in calf thymus DNA. 80HdG formation was greatly increased by TBHQ in a concentration-dependent manner. This effect was strongly enhanced by CuCl
2 and suppressed by EDTA, bathocuproinedisulfonic acid disodium salt, methionine, glutathione reduced form or catalase, but was not affected by mannitol, sodium benzoate or sodium azide. Thus, TBHQ-induced 80HdG formation may be mediated by copper. DTBHQ also induced the formation of 80HdG, though to a much lesser extent than TBHQ, and its effect was stimulated by CuCl
2. BHA had a small enhancing effect at high concentration, only in the presence of CuCl
2, whereas in the case of BHTQ, it occurred both in the presence of CuCl
2 and FeCl
2.</abstract><cop>Shannon</cop><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>8960159</pmid><doi>10.1016/S0378-4274(96)03800-3</doi><tpages>5</tpages></addata></record> |
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issn | 0378-4274 1879-3169 |
language | eng |
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source | MEDLINE; Elsevier ScienceDirect Journals |
subjects | 2,5-Di- tert-butyl(1,4)hydroquinone 2,6- Di- tert-butyl- p-benzoquinone 2- tert-Butyl(1,4)hydroquinone 8-Hydroxy-2′-deoxyguanosine Animals Antioxidants - chemistry Biological and medical sciences Butylated hydroxyanisole Butylated Hydroxyanisole - chemistry Butylated Hydroxyanisole - metabolism Cattle Chemical and industrial products toxicology. Toxic occupational diseases Deoxyguanosine - analogs & derivatives Deoxyguanosine - analysis Deoxyguanosine - chemistry DNA - chemistry DNA Damage Hydroquinones - chemistry Medical sciences Thymus Gland - chemistry Toxicology Various organic compounds |
title | Formation of 8-hydroxydeoxyguanosine in calf thymus DNA treated with tert-butylhydroquinone, a major metabolite of butylated hydroxyanisole |
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