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effect of apigenin on cyclophosphamide and doxorubicin genotoxicity in vitro and in vivo
The aim of this study was to investigate the mutagenic and antigenotoxic effects of different doses of the flavonoid, apigenin, alone and in combination with the antitumor drugs, cyclophosphamide and doxorubicin, in vitro and in vivo. Using bacterial reverse mutation inhibition in vitro, with and wi...
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Published in: | Journal of environmental science and health. Part A, Toxic/hazardous substances & environmental engineering Toxic/hazardous substances & environmental engineering, 2011-01, Vol.46 (5), p.526-533 |
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description | The aim of this study was to investigate the mutagenic and antigenotoxic effects of different doses of the flavonoid, apigenin, alone and in combination with the antitumor drugs, cyclophosphamide and doxorubicin, in vitro and in vivo. Using bacterial reverse mutation inhibition in vitro, with and without metabolic activation, the effect of apigenin (10 – 400 μg/plate) was studied on genotoxicity induced by cyclophosphamide (800 μg/plate) and by doxorubicin (0.2 μg/plate). Subsequent to a dose-finding study in vivo, CD1 mice were treated with either cyclophosphamide (40 mg/kg, i.p.) or doxorubicin (5 mg/kg, i.p.) with or without co-administration of apigenin (1–100 mg/kg, p.o.). Micronuclei were determined microscopically in blood smears and glutathione peroxidase (GPX), superoxide dismutase (SOD) and total antioxidative status (TAS) in whole blood, erythrocytes and plasma, respectively. Apigenin decreased doxorubicin-induced, but not cyclophosphamide-induced mutagenicity in vitro. In vivo, apigenin caused a statistically significant decrease in micronucleus frequency in response to cyclophosphamide, possibly due to active flavonoid metabolite formation or inhibition of cyclophosphamide metabolic activation. In animals treated with apigenin and doxorubicin, a significant decrease in micronucleus frequency was not observed, probably due to interindividual variability. No changes in GPX, SOD or TAS were observed in response to either cytotoxic agents or the flavonoid, possibly due to limited metabolic transformation of the drugs at the doses used. The results of the present study provide further evidence for the chemo-preventative properties of apigenin. |
doi_str_mv | 10.1080/10934529.2011.551744 |
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Using bacterial reverse mutation inhibition in vitro, with and without metabolic activation, the effect of apigenin (10 – 400 μg/plate) was studied on genotoxicity induced by cyclophosphamide (800 μg/plate) and by doxorubicin (0.2 μg/plate). Subsequent to a dose-finding study in vivo, CD1 mice were treated with either cyclophosphamide (40 mg/kg, i.p.) or doxorubicin (5 mg/kg, i.p.) with or without co-administration of apigenin (1–100 mg/kg, p.o.). Micronuclei were determined microscopically in blood smears and glutathione peroxidase (GPX), superoxide dismutase (SOD) and total antioxidative status (TAS) in whole blood, erythrocytes and plasma, respectively. Apigenin decreased doxorubicin-induced, but not cyclophosphamide-induced mutagenicity in vitro. In vivo, apigenin caused a statistically significant decrease in micronucleus frequency in response to cyclophosphamide, possibly due to active flavonoid metabolite formation or inhibition of cyclophosphamide metabolic activation. In animals treated with apigenin and doxorubicin, a significant decrease in micronucleus frequency was not observed, probably due to interindividual variability. No changes in GPX, SOD or TAS were observed in response to either cytotoxic agents or the flavonoid, possibly due to limited metabolic transformation of the drugs at the doses used. The results of the present study provide further evidence for the chemo-preventative properties of apigenin.</description><identifier>ISSN: 1532-4117</identifier><identifier>ISSN: 1093-4529</identifier><identifier>EISSN: 1532-4117</identifier><identifier>DOI: 10.1080/10934529.2011.551744</identifier><identifier>PMID: 21469013</identifier><language>eng</language><publisher>Philadelphia, PA: Taylor & Francis Group</publisher><subject>Ames test ; Animals ; Antineoplastic Agents - toxicity ; Antioxidants - chemistry ; antitumor drugs ; Apigenin ; Apigenin - pharmacology ; Applied sciences ; Bacteria ; Chemical compounds ; cyclophosphamide ; Cyclophosphamide - toxicity ; cytotoxicity ; DNA Damage ; doxorubicin ; Doxorubicin - toxicity ; Environmental science ; erythrocytes ; Exact sciences and technology ; flavonoids ; genotoxicity ; glutathione peroxidase ; Glutathione Peroxidase - blood ; in vivo studies ; Metabolites ; Mice ; micronucleus test ; Mutagenesis ; mutagenicity ; Mutagenicity Tests ; Mutation ; Pollution ; Salmonella typhimurium ; superoxide dismutase ; Superoxide Dismutase - blood ; Toxicity</subject><ispartof>Journal of environmental science and health. 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Part A, Toxic/hazardous substances & environmental engineering</title><addtitle>J Environ Sci Health A Tox Hazard Subst Environ Eng</addtitle><description>The aim of this study was to investigate the mutagenic and antigenotoxic effects of different doses of the flavonoid, apigenin, alone and in combination with the antitumor drugs, cyclophosphamide and doxorubicin, in vitro and in vivo. Using bacterial reverse mutation inhibition in vitro, with and without metabolic activation, the effect of apigenin (10 – 400 μg/plate) was studied on genotoxicity induced by cyclophosphamide (800 μg/plate) and by doxorubicin (0.2 μg/plate). Subsequent to a dose-finding study in vivo, CD1 mice were treated with either cyclophosphamide (40 mg/kg, i.p.) or doxorubicin (5 mg/kg, i.p.) with or without co-administration of apigenin (1–100 mg/kg, p.o.). Micronuclei were determined microscopically in blood smears and glutathione peroxidase (GPX), superoxide dismutase (SOD) and total antioxidative status (TAS) in whole blood, erythrocytes and plasma, respectively. Apigenin decreased doxorubicin-induced, but not cyclophosphamide-induced mutagenicity in vitro. In vivo, apigenin caused a statistically significant decrease in micronucleus frequency in response to cyclophosphamide, possibly due to active flavonoid metabolite formation or inhibition of cyclophosphamide metabolic activation. In animals treated with apigenin and doxorubicin, a significant decrease in micronucleus frequency was not observed, probably due to interindividual variability. No changes in GPX, SOD or TAS were observed in response to either cytotoxic agents or the flavonoid, possibly due to limited metabolic transformation of the drugs at the doses used. The results of the present study provide further evidence for the chemo-preventative properties of apigenin.</description><subject>Ames test</subject><subject>Animals</subject><subject>Antineoplastic Agents - toxicity</subject><subject>Antioxidants - chemistry</subject><subject>antitumor drugs</subject><subject>Apigenin</subject><subject>Apigenin - pharmacology</subject><subject>Applied sciences</subject><subject>Bacteria</subject><subject>Chemical compounds</subject><subject>cyclophosphamide</subject><subject>Cyclophosphamide - toxicity</subject><subject>cytotoxicity</subject><subject>DNA Damage</subject><subject>doxorubicin</subject><subject>Doxorubicin - toxicity</subject><subject>Environmental science</subject><subject>erythrocytes</subject><subject>Exact sciences and technology</subject><subject>flavonoids</subject><subject>genotoxicity</subject><subject>glutathione peroxidase</subject><subject>Glutathione Peroxidase - blood</subject><subject>in vivo studies</subject><subject>Metabolites</subject><subject>Mice</subject><subject>micronucleus test</subject><subject>Mutagenesis</subject><subject>mutagenicity</subject><subject>Mutagenicity Tests</subject><subject>Mutation</subject><subject>Pollution</subject><subject>Salmonella typhimurium</subject><subject>superoxide dismutase</subject><subject>Superoxide Dismutase - blood</subject><subject>Toxicity</subject><issn>1532-4117</issn><issn>1093-4529</issn><issn>1532-4117</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqF0UuLFDEQB_AgiruufgPRRhBPM6by7tMiiy9Y8KAL3kImj90s3Z026V53vr2Z6RkVL55SBb8qin8Qeg54DVjht4Bbyjhp1wQDrDkHydgDdAqckhUDkA__qk_Qk1JuMQZFgT9GJwSYaDHQU_Tdh-Dt1KTQmDFe-yEOTRoau7VdGm9SGW9MH51vzOAal-5TnjfRVlNlmtJ9radtU_u7OOW0V_vmLj1Fj4Lpin92eM_Q1Yf33y4-rS6_fPx88e5yZRmj00oFQYMSihuOCTjZCiIMBCy5US2hoDhsmHTBt4x44zkRgjouCHjnCZWWnqE3y94xpx-zL5PuY7G-68zg01y0ElhJhVuo8tU_8jbNeajHVSSIIiBlRWxBNqdSsg96zLE3easB613u-pi73uWul9zr2IvD7nnTe_d76Bh0Ba8PwBRrupDNYGP549gOElXd-eLiEFLuzc-UO6cns-1SPg7R_5zyctkQTNLmOteBq68VsP3305bTX1yopko</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>BOKULIC, Ana</creator><creator>GARAJ-VRHOVAC, Verica</creator><creator>BRAJSA, Karmen</creator><creator>DURIC, Koraljka</creator><creator>GLOJNARIC, Ines</creator><creator>SITUM, Kristina</creator><general>Taylor & Francis Group</general><general>Taylor & Francis</general><general>Taylor & Francis Ltd</general><scope>FBQ</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>7QF</scope><scope>7QQ</scope><scope>7SC</scope><scope>7SE</scope><scope>7SP</scope><scope>7SR</scope><scope>7ST</scope><scope>7T7</scope><scope>7TA</scope><scope>7TB</scope><scope>7U5</scope><scope>7U7</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>JG9</scope><scope>JQ2</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>P64</scope><scope>SOI</scope><scope>7X8</scope></search><sort><creationdate>20110101</creationdate><title>effect of apigenin on cyclophosphamide and doxorubicin genotoxicity in vitro and in vivo</title><author>BOKULIC, Ana ; 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Part A, Toxic/hazardous substances & environmental engineering</jtitle><addtitle>J Environ Sci Health A Tox Hazard Subst Environ Eng</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>46</volume><issue>5</issue><spage>526</spage><epage>533</epage><pages>526-533</pages><issn>1532-4117</issn><issn>1093-4529</issn><eissn>1532-4117</eissn><abstract>The aim of this study was to investigate the mutagenic and antigenotoxic effects of different doses of the flavonoid, apigenin, alone and in combination with the antitumor drugs, cyclophosphamide and doxorubicin, in vitro and in vivo. Using bacterial reverse mutation inhibition in vitro, with and without metabolic activation, the effect of apigenin (10 – 400 μg/plate) was studied on genotoxicity induced by cyclophosphamide (800 μg/plate) and by doxorubicin (0.2 μg/plate). Subsequent to a dose-finding study in vivo, CD1 mice were treated with either cyclophosphamide (40 mg/kg, i.p.) or doxorubicin (5 mg/kg, i.p.) with or without co-administration of apigenin (1–100 mg/kg, p.o.). Micronuclei were determined microscopically in blood smears and glutathione peroxidase (GPX), superoxide dismutase (SOD) and total antioxidative status (TAS) in whole blood, erythrocytes and plasma, respectively. Apigenin decreased doxorubicin-induced, but not cyclophosphamide-induced mutagenicity in vitro. In vivo, apigenin caused a statistically significant decrease in micronucleus frequency in response to cyclophosphamide, possibly due to active flavonoid metabolite formation or inhibition of cyclophosphamide metabolic activation. In animals treated with apigenin and doxorubicin, a significant decrease in micronucleus frequency was not observed, probably due to interindividual variability. No changes in GPX, SOD or TAS were observed in response to either cytotoxic agents or the flavonoid, possibly due to limited metabolic transformation of the drugs at the doses used. The results of the present study provide further evidence for the chemo-preventative properties of apigenin.</abstract><cop>Philadelphia, PA</cop><pub>Taylor & Francis Group</pub><pmid>21469013</pmid><doi>10.1080/10934529.2011.551744</doi><tpages>8</tpages></addata></record> |
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subjects | Ames test Animals Antineoplastic Agents - toxicity Antioxidants - chemistry antitumor drugs Apigenin Apigenin - pharmacology Applied sciences Bacteria Chemical compounds cyclophosphamide Cyclophosphamide - toxicity cytotoxicity DNA Damage doxorubicin Doxorubicin - toxicity Environmental science erythrocytes Exact sciences and technology flavonoids genotoxicity glutathione peroxidase Glutathione Peroxidase - blood in vivo studies Metabolites Mice micronucleus test Mutagenesis mutagenicity Mutagenicity Tests Mutation Pollution Salmonella typhimurium superoxide dismutase Superoxide Dismutase - blood Toxicity |
title | effect of apigenin on cyclophosphamide and doxorubicin genotoxicity in vitro and in vivo |
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