Induction by estrogens of lipid peroxidation and lipid peroxide-derived malonaldehyde-DNA adducts in male Syrian hamsters : role of lipid peroxidation in estrogen-induced kidney carcinogenesis
Estrogen-induced kidney carcinogenesis in male Syrian hamsters has previously been postulated to be mediated by free radicals generated by redox cycling of catecholestrogen metabolites. As part of our examination of this hypothesis, we have studied the induction of lipid peroxidation and lipid perox...
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| Veröffentlicht in: | Carcinogenesis (New York) 1995-08, Vol.16 (8), p.1941-1945 |
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| creator | MIAN-YING WANG LIEHR, J. G |
| description | Estrogen-induced kidney carcinogenesis in male Syrian hamsters has previously been postulated to be mediated by free radicals generated by redox cycling of catecholestrogen metabolites. As part of our examination of this hypothesis, we have studied the induction of lipid peroxidation and lipid peroxide-derived malondialdehyde (MDA)-DNA adducts in kidney and liver of hamsters treated with single injections of diethylstilbestrol (DES) or with estradiol (E2) implants for various lengths of time. Treatment of hamsters with 50 and 100 mg/kg DES increased concentrations of both lipid hydroperoxides and of MDA-DNA adducts. In hamsters treated with E2 implants for up to 50 days, lipid peroxide levels in liver were double control values 3 h after hormone implantation, and then decreased to plateau values of 30% over controls. Those in kidney rose to 2- to 3-fold above controls 3 days after hormone implantation and then decreased to plateau values of 51% above controls. MDA-DNA adduct levels were two or three times higher than those of controls in liver and kidney of hamsters treated with hormone implants for 3 and 7 days. Renal lipid peroxide concentrations were raised by chronic treatment with E2, but not by weakly carcinogenic estrogens ethinylestradiol or 2-fluoroestradiol. In contrast, MDA-DNA adduct levels were raised by all three steroidal estrogens 3 days after estrogen implantation. The increases in lipid peroxides and in MDA-DNA adducts in estrogen-treated hamsters support a mechanism of carcinogenesis by free radical generation via redox cycling of catcholestrogen metabolites. Lipid peroxides are postulated to play a dual role in estrogen-induced carcinogenesis, (i) as cofactors for cytochrome P450-mediated formation of catecholestrogen metabolites and their redox cycling, and (ii) as precursors of MDA, a DNA adduct-forming endogenous electrophile. |
| doi_str_mv | 10.1093/carcin/16.8.1941 |
| format | Article |
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G</creator><creatorcontrib>MIAN-YING WANG ; LIEHR, J. G</creatorcontrib><description>Estrogen-induced kidney carcinogenesis in male Syrian hamsters has previously been postulated to be mediated by free radicals generated by redox cycling of catecholestrogen metabolites. As part of our examination of this hypothesis, we have studied the induction of lipid peroxidation and lipid peroxide-derived malondialdehyde (MDA)-DNA adducts in kidney and liver of hamsters treated with single injections of diethylstilbestrol (DES) or with estradiol (E2) implants for various lengths of time. Treatment of hamsters with 50 and 100 mg/kg DES increased concentrations of both lipid hydroperoxides and of MDA-DNA adducts. In hamsters treated with E2 implants for up to 50 days, lipid peroxide levels in liver were double control values 3 h after hormone implantation, and then decreased to plateau values of 30% over controls. Those in kidney rose to 2- to 3-fold above controls 3 days after hormone implantation and then decreased to plateau values of 51% above controls. MDA-DNA adduct levels were two or three times higher than those of controls in liver and kidney of hamsters treated with hormone implants for 3 and 7 days. Renal lipid peroxide concentrations were raised by chronic treatment with E2, but not by weakly carcinogenic estrogens ethinylestradiol or 2-fluoroestradiol. In contrast, MDA-DNA adduct levels were raised by all three steroidal estrogens 3 days after estrogen implantation. The increases in lipid peroxides and in MDA-DNA adducts in estrogen-treated hamsters support a mechanism of carcinogenesis by free radical generation via redox cycling of catcholestrogen metabolites. Lipid peroxides are postulated to play a dual role in estrogen-induced carcinogenesis, (i) as cofactors for cytochrome P450-mediated formation of catecholestrogen metabolites and their redox cycling, and (ii) as precursors of MDA, a DNA adduct-forming endogenous electrophile.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/16.8.1941</identifier><identifier>PMID: 7634425</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Animal tumors. Experimental tumors ; Animals ; Biological and medical sciences ; Cricetinae ; Diethylstilbestrol - toxicity ; DNA Adducts - analysis ; Estradiol - toxicity ; Estrogens - toxicity ; Experimental renal and urinary tract tumors ; Kidney Neoplasms - chemically induced ; Lipid Peroxidation - drug effects ; Male ; Malondialdehyde - metabolism ; Medical sciences ; Mesocricetus ; Tumors</subject><ispartof>Carcinogenesis (New York), 1995-08, Vol.16 (8), p.1941-1945</ispartof><rights>1995 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3635297$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7634425$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MIAN-YING WANG</creatorcontrib><creatorcontrib>LIEHR, J. G</creatorcontrib><title>Induction by estrogens of lipid peroxidation and lipid peroxide-derived malonaldehyde-DNA adducts in male Syrian hamsters : role of lipid peroxidation in estrogen-induced kidney carcinogenesis</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>Estrogen-induced kidney carcinogenesis in male Syrian hamsters has previously been postulated to be mediated by free radicals generated by redox cycling of catecholestrogen metabolites. As part of our examination of this hypothesis, we have studied the induction of lipid peroxidation and lipid peroxide-derived malondialdehyde (MDA)-DNA adducts in kidney and liver of hamsters treated with single injections of diethylstilbestrol (DES) or with estradiol (E2) implants for various lengths of time. Treatment of hamsters with 50 and 100 mg/kg DES increased concentrations of both lipid hydroperoxides and of MDA-DNA adducts. In hamsters treated with E2 implants for up to 50 days, lipid peroxide levels in liver were double control values 3 h after hormone implantation, and then decreased to plateau values of 30% over controls. Those in kidney rose to 2- to 3-fold above controls 3 days after hormone implantation and then decreased to plateau values of 51% above controls. MDA-DNA adduct levels were two or three times higher than those of controls in liver and kidney of hamsters treated with hormone implants for 3 and 7 days. Renal lipid peroxide concentrations were raised by chronic treatment with E2, but not by weakly carcinogenic estrogens ethinylestradiol or 2-fluoroestradiol. In contrast, MDA-DNA adduct levels were raised by all three steroidal estrogens 3 days after estrogen implantation. The increases in lipid peroxides and in MDA-DNA adducts in estrogen-treated hamsters support a mechanism of carcinogenesis by free radical generation via redox cycling of catcholestrogen metabolites. Lipid peroxides are postulated to play a dual role in estrogen-induced carcinogenesis, (i) as cofactors for cytochrome P450-mediated formation of catecholestrogen metabolites and their redox cycling, and (ii) as precursors of MDA, a DNA adduct-forming endogenous electrophile.</description><subject>Animal tumors. Experimental tumors</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cricetinae</subject><subject>Diethylstilbestrol - toxicity</subject><subject>DNA Adducts - analysis</subject><subject>Estradiol - toxicity</subject><subject>Estrogens - toxicity</subject><subject>Experimental renal and urinary tract tumors</subject><subject>Kidney Neoplasms - chemically induced</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Medical sciences</subject><subject>Mesocricetus</subject><subject>Tumors</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptUMtOwzAQtBColMKdC5IPXNPasfMwt6q8KiE40Hu1iTfUkDiRnSLyd3waCS1ISJxWmpmdnR1CzjmbcqbELAeXGzvj8TSdciX5ARlzGbMg5Ck7JGPGpQiEEPKYnHj_yhiPRaRGZJTEQsowGpPPpdXbvDW1pVlH0beufkHraV3Q0jRG0wZd_WE0fEvA6r8wBhqdeUdNKyhrC6XGTdej149zCnpw9tTYgUT63DkDlm6g8i06T6-oq3v4_0v90k-YwAwR-xNvRlvs6O7ngUFv_Ck5KqD0eLafE7K6vVkt7oOHp7vlYv4QNDxO2gBUyCKVYxImWay5ygolcy4gjETEUUWi0AK1FCmoDHosyjIIpS4gFWmIWkzIxc622WYV6nXjTAWuW--L7PnLPQ8-h7JwYHPjf2Wi7z1UifgCjseIpQ</recordid><startdate>19950801</startdate><enddate>19950801</enddate><creator>MIAN-YING WANG</creator><creator>LIEHR, J. G</creator><general>Oxford University Press</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>19950801</creationdate><title>Induction by estrogens of lipid peroxidation and lipid peroxide-derived malonaldehyde-DNA adducts in male Syrian hamsters : role of lipid peroxidation in estrogen-induced kidney carcinogenesis</title><author>MIAN-YING WANG ; LIEHR, J. G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p167t-a92059ce727b6d19bf94c13a25351e953fd3ed438a9ba5355bba24dfa8382ed3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animal tumors. Experimental tumors</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cricetinae</topic><topic>Diethylstilbestrol - toxicity</topic><topic>DNA Adducts - analysis</topic><topic>Estradiol - toxicity</topic><topic>Estrogens - toxicity</topic><topic>Experimental renal and urinary tract tumors</topic><topic>Kidney Neoplasms - chemically induced</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>Malondialdehyde - metabolism</topic><topic>Medical sciences</topic><topic>Mesocricetus</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MIAN-YING WANG</creatorcontrib><creatorcontrib>LIEHR, J. G</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>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MIAN-YING WANG</au><au>LIEHR, J. G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Induction by estrogens of lipid peroxidation and lipid peroxide-derived malonaldehyde-DNA adducts in male Syrian hamsters : role of lipid peroxidation in estrogen-induced kidney carcinogenesis</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>1995-08-01</date><risdate>1995</risdate><volume>16</volume><issue>8</issue><spage>1941</spage><epage>1945</epage><pages>1941-1945</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>Estrogen-induced kidney carcinogenesis in male Syrian hamsters has previously been postulated to be mediated by free radicals generated by redox cycling of catecholestrogen metabolites. As part of our examination of this hypothesis, we have studied the induction of lipid peroxidation and lipid peroxide-derived malondialdehyde (MDA)-DNA adducts in kidney and liver of hamsters treated with single injections of diethylstilbestrol (DES) or with estradiol (E2) implants for various lengths of time. Treatment of hamsters with 50 and 100 mg/kg DES increased concentrations of both lipid hydroperoxides and of MDA-DNA adducts. In hamsters treated with E2 implants for up to 50 days, lipid peroxide levels in liver were double control values 3 h after hormone implantation, and then decreased to plateau values of 30% over controls. Those in kidney rose to 2- to 3-fold above controls 3 days after hormone implantation and then decreased to plateau values of 51% above controls. MDA-DNA adduct levels were two or three times higher than those of controls in liver and kidney of hamsters treated with hormone implants for 3 and 7 days. Renal lipid peroxide concentrations were raised by chronic treatment with E2, but not by weakly carcinogenic estrogens ethinylestradiol or 2-fluoroestradiol. In contrast, MDA-DNA adduct levels were raised by all three steroidal estrogens 3 days after estrogen implantation. The increases in lipid peroxides and in MDA-DNA adducts in estrogen-treated hamsters support a mechanism of carcinogenesis by free radical generation via redox cycling of catcholestrogen metabolites. Lipid peroxides are postulated to play a dual role in estrogen-induced carcinogenesis, (i) as cofactors for cytochrome P450-mediated formation of catecholestrogen metabolites and their redox cycling, and (ii) as precursors of MDA, a DNA adduct-forming endogenous electrophile.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>7634425</pmid><doi>10.1093/carcin/16.8.1941</doi><tpages>5</tpages></addata></record> |
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| ispartof | Carcinogenesis (New York), 1995-08, Vol.16 (8), p.1941-1945 |
| issn | 0143-3334 1460-2180 |
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| source | MEDLINE; Oxford University Press Journals Digital Archive Legacy |
| subjects | Animal tumors. Experimental tumors Animals Biological and medical sciences Cricetinae Diethylstilbestrol - toxicity DNA Adducts - analysis Estradiol - toxicity Estrogens - toxicity Experimental renal and urinary tract tumors Kidney Neoplasms - chemically induced Lipid Peroxidation - drug effects Male Malondialdehyde - metabolism Medical sciences Mesocricetus Tumors |
| title | Induction by estrogens of lipid peroxidation and lipid peroxide-derived malonaldehyde-DNA adducts in male Syrian hamsters : role of lipid peroxidation in estrogen-induced kidney carcinogenesis |
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