Ameliorative role of naringenin against lead‐induced genetic damage and oxidative stress in cultured human lymphocytes
Lead (Pb) is a ubiquitous toxic heavy metal that is known to induce damage to major macromolecules (lipids, proteins, and nucleic acids) by enhancing the level of reactive oxygen species (ROS). Naringenin, a predominant flavonoid primarily found in citrus fruits has attained increasing attention due...
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| Veröffentlicht in: | Journal of biochemical and molecular toxicology 2022-06, Vol.36 (6), p.e23036-n/a |
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| creator | Yadav, Bharti Vishwakarma, Veena Kumar, Sunil Aggarwal, Neeraj K. Gupta, Ranjan Yadav, Anita |
| description | Lead (Pb) is a ubiquitous toxic heavy metal that is known to induce damage to major macromolecules (lipids, proteins, and nucleic acids) by enhancing the level of reactive oxygen species (ROS). Naringenin, a predominant flavonoid primarily found in citrus fruits has attained increasing attention due to its various pharmacological properties. Thus, the present investigation aimed to explore the ameliorative role of naringenin against Pb‐induced toxicity in human peripheral blood lymphocytes (PBLs) under in vitro conditions. For this purpose, PBLs were exposed to Pb (350 µg/ml) alone as well in combination with naringenin (10 and 30 µg/ml). Sister chromatid exchange (SCE) and alkaline comet assay were used as genotoxic indices to evaluate the genotoxic and antigenotoxic activity of Pb and naringenin, respectively. Lipid peroxidation (LPO), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) assays were used as oxidative damage markers. The results revealed that Pb induced a significant (p |
| doi_str_mv | 10.1002/jbt.23036 |
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Naringenin, a predominant flavonoid primarily found in citrus fruits has attained increasing attention due to its various pharmacological properties. Thus, the present investigation aimed to explore the ameliorative role of naringenin against Pb‐induced toxicity in human peripheral blood lymphocytes (PBLs) under in vitro conditions. For this purpose, PBLs were exposed to Pb (350 µg/ml) alone as well in combination with naringenin (10 and 30 µg/ml). Sister chromatid exchange (SCE) and alkaline comet assay were used as genotoxic indices to evaluate the genotoxic and antigenotoxic activity of Pb and naringenin, respectively. Lipid peroxidation (LPO), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) assays were used as oxidative damage markers. The results revealed that Pb induced a significant (p < 0.05) increase in genetic and oxidative damage as compared with the untreated sample whereas the treatment of cells along with naringenin (10 and 30 µg/ml) and Pb (350 µg/ml) caused a significant reduction in genetic damage and elevation in SOD, GPx, and CAT activities and GSH level, accompanied by a significant reduction in LPO level as compared with Pb alone treated sample. So, the present investigation revealed that naringenin might be used as a protective agent against Pb‐induced toxicity due to its antigenotoxic and antioxidative properties.</description><identifier>ISSN: 1095-6670</identifier><identifier>EISSN: 1099-0461</identifier><identifier>DOI: 10.1002/jbt.23036</identifier><identifier>PMID: 35289026</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>antioxidant ; Antioxidants - metabolism ; Antioxidants - pharmacology ; Bioassays ; Catalase ; Catalase - metabolism ; Chromosome aberrations ; Citrus fruits ; Comet assay ; Damage ; Flavanones ; Flavonoids ; Genotoxicity ; Glutathione ; Glutathione - metabolism ; Glutathione peroxidase ; Glutathione Peroxidase - metabolism ; Heavy metals ; Humans ; Lead ; Lead - toxicity ; Lipid Peroxidation ; Lipids ; Lymphocytes ; Lymphocytes - metabolism ; Macromolecules ; Naringenin ; Nucleic acids ; Oxidative Stress ; Peripheral blood ; Peroxidase ; Peroxidation ; Reactive oxygen species ; Sister chromatid exchange ; Superoxide dismutase ; Superoxide Dismutase - metabolism ; Toxicity</subject><ispartof>Journal of biochemical and molecular toxicology, 2022-06, Vol.36 (6), p.e23036-n/a</ispartof><rights>2022 Wiley Periodicals LLC</rights><rights>2022 Wiley Periodicals LLC.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3536-dc3f577e76c4563d00427ed7aee4bda4f8d6eb6d9e8c28aa5852e36e37070b3</citedby><cites>FETCH-LOGICAL-c3536-dc3f577e76c4563d00427ed7aee4bda4f8d6eb6d9e8c28aa5852e36e37070b3</cites><orcidid>0000-0001-5678-5773</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjbt.23036$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjbt.23036$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35289026$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yadav, Bharti</creatorcontrib><creatorcontrib>Vishwakarma, Veena</creatorcontrib><creatorcontrib>Kumar, Sunil</creatorcontrib><creatorcontrib>Aggarwal, Neeraj K.</creatorcontrib><creatorcontrib>Gupta, Ranjan</creatorcontrib><creatorcontrib>Yadav, Anita</creatorcontrib><title>Ameliorative role of naringenin against lead‐induced genetic damage and oxidative stress in cultured human lymphocytes</title><title>Journal of biochemical and molecular toxicology</title><addtitle>J Biochem Mol Toxicol</addtitle><description>Lead (Pb) is a ubiquitous toxic heavy metal that is known to induce damage to major macromolecules (lipids, proteins, and nucleic acids) by enhancing the level of reactive oxygen species (ROS). Naringenin, a predominant flavonoid primarily found in citrus fruits has attained increasing attention due to its various pharmacological properties. Thus, the present investigation aimed to explore the ameliorative role of naringenin against Pb‐induced toxicity in human peripheral blood lymphocytes (PBLs) under in vitro conditions. For this purpose, PBLs were exposed to Pb (350 µg/ml) alone as well in combination with naringenin (10 and 30 µg/ml). Sister chromatid exchange (SCE) and alkaline comet assay were used as genotoxic indices to evaluate the genotoxic and antigenotoxic activity of Pb and naringenin, respectively. Lipid peroxidation (LPO), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) assays were used as oxidative damage markers. The results revealed that Pb induced a significant (p < 0.05) increase in genetic and oxidative damage as compared with the untreated sample whereas the treatment of cells along with naringenin (10 and 30 µg/ml) and Pb (350 µg/ml) caused a significant reduction in genetic damage and elevation in SOD, GPx, and CAT activities and GSH level, accompanied by a significant reduction in LPO level as compared with Pb alone treated sample. So, the present investigation revealed that naringenin might be used as a protective agent against Pb‐induced toxicity due to its antigenotoxic and antioxidative properties.</description><subject>antioxidant</subject><subject>Antioxidants - metabolism</subject><subject>Antioxidants - pharmacology</subject><subject>Bioassays</subject><subject>Catalase</subject><subject>Catalase - metabolism</subject><subject>Chromosome aberrations</subject><subject>Citrus fruits</subject><subject>Comet assay</subject><subject>Damage</subject><subject>Flavanones</subject><subject>Flavonoids</subject><subject>Genotoxicity</subject><subject>Glutathione</subject><subject>Glutathione - metabolism</subject><subject>Glutathione peroxidase</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>Heavy metals</subject><subject>Humans</subject><subject>Lead</subject><subject>Lead - toxicity</subject><subject>Lipid Peroxidation</subject><subject>Lipids</subject><subject>Lymphocytes</subject><subject>Lymphocytes - metabolism</subject><subject>Macromolecules</subject><subject>Naringenin</subject><subject>Nucleic acids</subject><subject>Oxidative Stress</subject><subject>Peripheral blood</subject><subject>Peroxidase</subject><subject>Peroxidation</subject><subject>Reactive oxygen species</subject><subject>Sister chromatid exchange</subject><subject>Superoxide dismutase</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Toxicity</subject><issn>1095-6670</issn><issn>1099-0461</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10bFu1TAUBmALgWgpDLwAssQCQ9oTO7aTsVRAqSox0D1y7JNbXzn2xU5K78Yj8Iw8CW5TOiAx-Uj-_OvIPyGvaziuAdjJdpiPGQcun5DDGrqugkbWT-9nUUmp4IC8yHkLAKJT4jk54IK1HTB5SG5PJ_QuJj27G6QpeqRxpEEnFzYYXKB6o13IM_Wo7e-fv1ywi0FLyyXOzlCrJ71BqoOl8dbZNSbPCXOm5bVZ_Lyk4q-XSQfq99PuOpr9jPkleTZqn_HVw3lEvn36eHV2Xl1-_fzl7PSyMlxwWVnDR6EUKmkaIbkFaJhCqzRiM1jdjK2VOEjbYWtYq7VoBUMukStQMPAj8m5N3aX4fcE895PLBr3XAeOSeyZ5x5hinSr07T90G5cUym5FKSmA1YwX9X5VJsWcE479LrlJp31fQ39XRl_K6O_LKPbNQ-IyTGgf5d_fL-BkBT-cx_3_k_qLD1dr5B-qRZZS</recordid><startdate>202206</startdate><enddate>202206</enddate><creator>Yadav, Bharti</creator><creator>Vishwakarma, Veena</creator><creator>Kumar, Sunil</creator><creator>Aggarwal, Neeraj K.</creator><creator>Gupta, Ranjan</creator><creator>Yadav, Anita</creator><general>Wiley Subscription Services, Inc</general><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>7QO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-5678-5773</orcidid></search><sort><creationdate>202206</creationdate><title>Ameliorative role of naringenin against lead‐induced genetic damage and oxidative stress in cultured human lymphocytes</title><author>Yadav, Bharti ; Vishwakarma, Veena ; Kumar, Sunil ; Aggarwal, Neeraj K. ; Gupta, Ranjan ; Yadav, Anita</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3536-dc3f577e76c4563d00427ed7aee4bda4f8d6eb6d9e8c28aa5852e36e37070b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>antioxidant</topic><topic>Antioxidants - metabolism</topic><topic>Antioxidants - pharmacology</topic><topic>Bioassays</topic><topic>Catalase</topic><topic>Catalase - metabolism</topic><topic>Chromosome aberrations</topic><topic>Citrus fruits</topic><topic>Comet assay</topic><topic>Damage</topic><topic>Flavanones</topic><topic>Flavonoids</topic><topic>Genotoxicity</topic><topic>Glutathione</topic><topic>Glutathione - metabolism</topic><topic>Glutathione peroxidase</topic><topic>Glutathione Peroxidase - metabolism</topic><topic>Heavy metals</topic><topic>Humans</topic><topic>Lead</topic><topic>Lead - toxicity</topic><topic>Lipid Peroxidation</topic><topic>Lipids</topic><topic>Lymphocytes</topic><topic>Lymphocytes - metabolism</topic><topic>Macromolecules</topic><topic>Naringenin</topic><topic>Nucleic acids</topic><topic>Oxidative Stress</topic><topic>Peripheral blood</topic><topic>Peroxidase</topic><topic>Peroxidation</topic><topic>Reactive oxygen species</topic><topic>Sister chromatid exchange</topic><topic>Superoxide dismutase</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yadav, Bharti</creatorcontrib><creatorcontrib>Vishwakarma, Veena</creatorcontrib><creatorcontrib>Kumar, Sunil</creatorcontrib><creatorcontrib>Aggarwal, Neeraj K.</creatorcontrib><creatorcontrib>Gupta, Ranjan</creatorcontrib><creatorcontrib>Yadav, Anita</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of biochemical and molecular toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yadav, Bharti</au><au>Vishwakarma, Veena</au><au>Kumar, Sunil</au><au>Aggarwal, Neeraj K.</au><au>Gupta, Ranjan</au><au>Yadav, Anita</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ameliorative role of naringenin against lead‐induced genetic damage and oxidative stress in cultured human lymphocytes</atitle><jtitle>Journal of biochemical and molecular toxicology</jtitle><addtitle>J Biochem Mol Toxicol</addtitle><date>2022-06</date><risdate>2022</risdate><volume>36</volume><issue>6</issue><spage>e23036</spage><epage>n/a</epage><pages>e23036-n/a</pages><issn>1095-6670</issn><eissn>1099-0461</eissn><abstract>Lead (Pb) is a ubiquitous toxic heavy metal that is known to induce damage to major macromolecules (lipids, proteins, and nucleic acids) by enhancing the level of reactive oxygen species (ROS). Naringenin, a predominant flavonoid primarily found in citrus fruits has attained increasing attention due to its various pharmacological properties. Thus, the present investigation aimed to explore the ameliorative role of naringenin against Pb‐induced toxicity in human peripheral blood lymphocytes (PBLs) under in vitro conditions. For this purpose, PBLs were exposed to Pb (350 µg/ml) alone as well in combination with naringenin (10 and 30 µg/ml). Sister chromatid exchange (SCE) and alkaline comet assay were used as genotoxic indices to evaluate the genotoxic and antigenotoxic activity of Pb and naringenin, respectively. Lipid peroxidation (LPO), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) assays were used as oxidative damage markers. The results revealed that Pb induced a significant (p < 0.05) increase in genetic and oxidative damage as compared with the untreated sample whereas the treatment of cells along with naringenin (10 and 30 µg/ml) and Pb (350 µg/ml) caused a significant reduction in genetic damage and elevation in SOD, GPx, and CAT activities and GSH level, accompanied by a significant reduction in LPO level as compared with Pb alone treated sample. So, the present investigation revealed that naringenin might be used as a protective agent against Pb‐induced toxicity due to its antigenotoxic and antioxidative properties.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>35289026</pmid><doi>10.1002/jbt.23036</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0001-5678-5773</orcidid></addata></record> |
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| subjects | antioxidant Antioxidants - metabolism Antioxidants - pharmacology Bioassays Catalase Catalase - metabolism Chromosome aberrations Citrus fruits Comet assay Damage Flavanones Flavonoids Genotoxicity Glutathione Glutathione - metabolism Glutathione peroxidase Glutathione Peroxidase - metabolism Heavy metals Humans Lead Lead - toxicity Lipid Peroxidation Lipids Lymphocytes Lymphocytes - metabolism Macromolecules Naringenin Nucleic acids Oxidative Stress Peripheral blood Peroxidase Peroxidation Reactive oxygen species Sister chromatid exchange Superoxide dismutase Superoxide Dismutase - metabolism Toxicity |
| title | Ameliorative role of naringenin against lead‐induced genetic damage and oxidative stress in cultured human lymphocytes |
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