Locomotor damage and brain oxidative stress induced by lead exposure are attenuated by gallic acid treatment
We investigated the antioxidant potential of gallic acid (GA), a natural compound found in vegetal sources, on the motor and oxidative damages induced by lead. Rats exposed to lead (50 mg/kg, i.p., once a day, 5 days) were treated with GA (13.5 mg/kg, p.o.) or EDTA (110 mg/kg, i.p.) daily, for 3 day...
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| Veröffentlicht in: | Toxicology letters 2011-05, Vol.203 (1), p.74-81 |
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| creator | Reckziegel, Patrícia Dias, Verônica Tironi Benvegnú, Dalila Boufleur, Nardeli Silva Barcelos, Raquel Cristine Segat, Hecson Jesser Pase, Camila Simonetti dos Santos, Clarissa Marques Moreira Flores, Érico Marlon Moraes Bürger, Marilise Escobar |
| description | We investigated the antioxidant potential of gallic acid (GA), a natural compound found in vegetal sources, on the motor and oxidative damages induced by lead. Rats exposed to lead (50
mg/kg, i.p., once a day, 5
days) were treated with GA (13.5
mg/kg, p.o.) or EDTA (110
mg/kg, i.p.) daily, for 3
days. Lead exposure decreased the locomotor and exploratory activities, reduced blood ALA-D activity, and increased brain catalase (CAT) activity without altering other antioxidant defenses. Brain oxidative stress (OS) estimated by lipid peroxidation (TBARS) and protein carbonyl were increased by lead. GA reversed the motor behavior parameters, the ALA-D activity, as well as the markers of OS changed by lead exposure. CAT activity remained high, possibly as a compensatory mechanism to eliminate hydroperoxides during lead poisoning. EDTA, a conventional chelating agent, was not beneficial on the lead-induced motor behavior and oxidative damages. Both GA (less) and EDTA (more) reduced the lead accumulation in brain tissue. Negative correlations were observed between the behavioral parameters and lipid peroxidation and the lead levels in brain tissue. In conclusion, GA may be an adjuvant in lead exposure, mainly by its antioxidant properties against the motor and oxidative damages resulting from such poisoning. |
| doi_str_mv | 10.1016/j.toxlet.2011.03.006 |
| format | Article |
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mg/kg, i.p., once a day, 5
days) were treated with GA (13.5
mg/kg, p.o.) or EDTA (110
mg/kg, i.p.) daily, for 3
days. Lead exposure decreased the locomotor and exploratory activities, reduced blood ALA-D activity, and increased brain catalase (CAT) activity without altering other antioxidant defenses. Brain oxidative stress (OS) estimated by lipid peroxidation (TBARS) and protein carbonyl were increased by lead. GA reversed the motor behavior parameters, the ALA-D activity, as well as the markers of OS changed by lead exposure. CAT activity remained high, possibly as a compensatory mechanism to eliminate hydroperoxides during lead poisoning. EDTA, a conventional chelating agent, was not beneficial on the lead-induced motor behavior and oxidative damages. Both GA (less) and EDTA (more) reduced the lead accumulation in brain tissue. Negative correlations were observed between the behavioral parameters and lipid peroxidation and the lead levels in brain tissue. In conclusion, GA may be an adjuvant in lead exposure, mainly by its antioxidant properties against the motor and oxidative damages resulting from such poisoning.</description><identifier>ISSN: 0378-4274</identifier><identifier>EISSN: 1879-3169</identifier><identifier>DOI: 10.1016/j.toxlet.2011.03.006</identifier><identifier>PMID: 21402136</identifier><identifier>CODEN: TOLED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Animals ; Antioxidant ; Antioxidants ; Antioxidants - pharmacology ; Behavior, Animal - drug effects ; Biological and medical sciences ; Brain ; Brain - drug effects ; Brain - metabolism ; Catalase - metabolism ; Chelating agent ; Chelating Agents - pharmacology ; Chemical and industrial products toxicology. Toxic occupational diseases ; Damage ; Disease Models, Animal ; Edetic Acid - pharmacology ; EDTA ; Exploratory Behavior - drug effects ; Gallic acid ; Gallic Acid - pharmacology ; Genetic algorithms ; Lead ; Lead Poisoning, Nervous System - metabolism ; Lead Poisoning, Nervous System - physiopathology ; Lead Poisoning, Nervous System - prevention & control ; Lead Poisoning, Nervous System - psychology ; Lipid Peroxidation - drug effects ; Lipids ; Male ; Medical sciences ; Metals and various inorganic compounds ; Motor Activity - drug effects ; Motors ; Movement damages ; Nitrates ; Operating systems ; Oxidative stress ; Oxidative Stress - drug effects ; Porphobilinogen Synthase - metabolism ; Protein Carbonylation - drug effects ; Rats ; Rats, Wistar ; Toxicology</subject><ispartof>Toxicology letters, 2011-05, Vol.203 (1), p.74-81</ispartof><rights>2011 Elsevier Ireland Ltd</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-b5da9ce243a7068656734578e39e8f7114e39f7f0ddbfac107e17e10e96961283</citedby><cites>FETCH-LOGICAL-c456t-b5da9ce243a7068656734578e39e8f7114e39f7f0ddbfac107e17e10e96961283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.toxlet.2011.03.006$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24186736$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21402136$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reckziegel, Patrícia</creatorcontrib><creatorcontrib>Dias, Verônica Tironi</creatorcontrib><creatorcontrib>Benvegnú, Dalila</creatorcontrib><creatorcontrib>Boufleur, Nardeli</creatorcontrib><creatorcontrib>Silva Barcelos, Raquel Cristine</creatorcontrib><creatorcontrib>Segat, Hecson Jesser</creatorcontrib><creatorcontrib>Pase, Camila Simonetti</creatorcontrib><creatorcontrib>dos Santos, Clarissa Marques Moreira</creatorcontrib><creatorcontrib>Flores, Érico Marlon Moraes</creatorcontrib><creatorcontrib>Bürger, Marilise Escobar</creatorcontrib><title>Locomotor damage and brain oxidative stress induced by lead exposure are attenuated by gallic acid treatment</title><title>Toxicology letters</title><addtitle>Toxicol Lett</addtitle><description>We investigated the antioxidant potential of gallic acid (GA), a natural compound found in vegetal sources, on the motor and oxidative damages induced by lead. Rats exposed to lead (50
mg/kg, i.p., once a day, 5
days) were treated with GA (13.5
mg/kg, p.o.) or EDTA (110
mg/kg, i.p.) daily, for 3
days. Lead exposure decreased the locomotor and exploratory activities, reduced blood ALA-D activity, and increased brain catalase (CAT) activity without altering other antioxidant defenses. Brain oxidative stress (OS) estimated by lipid peroxidation (TBARS) and protein carbonyl were increased by lead. GA reversed the motor behavior parameters, the ALA-D activity, as well as the markers of OS changed by lead exposure. CAT activity remained high, possibly as a compensatory mechanism to eliminate hydroperoxides during lead poisoning. EDTA, a conventional chelating agent, was not beneficial on the lead-induced motor behavior and oxidative damages. Both GA (less) and EDTA (more) reduced the lead accumulation in brain tissue. Negative correlations were observed between the behavioral parameters and lipid peroxidation and the lead levels in brain tissue. In conclusion, GA may be an adjuvant in lead exposure, mainly by its antioxidant properties against the motor and oxidative damages resulting from such poisoning.</description><subject>Animals</subject><subject>Antioxidant</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Behavior, Animal - drug effects</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Catalase - metabolism</subject><subject>Chelating agent</subject><subject>Chelating Agents - pharmacology</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Damage</subject><subject>Disease Models, Animal</subject><subject>Edetic Acid - pharmacology</subject><subject>EDTA</subject><subject>Exploratory Behavior - drug effects</subject><subject>Gallic acid</subject><subject>Gallic Acid - pharmacology</subject><subject>Genetic algorithms</subject><subject>Lead</subject><subject>Lead Poisoning, Nervous System - metabolism</subject><subject>Lead Poisoning, Nervous System - physiopathology</subject><subject>Lead Poisoning, Nervous System - prevention & control</subject><subject>Lead Poisoning, Nervous System - psychology</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Lipids</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metals and various inorganic compounds</subject><subject>Motor Activity - drug effects</subject><subject>Motors</subject><subject>Movement damages</subject><subject>Nitrates</subject><subject>Operating systems</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Porphobilinogen Synthase - metabolism</subject><subject>Protein Carbonylation - drug effects</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Toxicology</subject><issn>0378-4274</issn><issn>1879-3169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFq3DAQhkVpSDZp3qAUXUp7sStZsmRfCiW0aWEhl_YsZqVx0GJbW0kOm7evFm_bW0CDBPP9o5n5CXnLWc0ZV5_2dQ7HEXPdMM5rJmrG1Cuy4Z3uK8FV_5psmNBdJRstr8h1SntWCKnaS3LVcMkaLtSGjNtgwxRyiNTBBI9IYXZ0F8HPNBy9g-yfkKYcMSXqZ7dYLOlnOiI4isdDSEssmlPkjPMCec0_wjh6S8F6R4sY8oRzfkMuBhgT3p7vG_Lr29efd9-r7cP9j7sv28rKVuVq1zroLTZSgGaqU63SQra6Q9FjN2jOZXkNemDO7QawnGnk5TDsVa9404kb8mGte4jh94Ipm8kni-MIM4YlmU6rpmn7XhXy44skV5oLKUoLBZUramNIKeJgDtFPEJ8NZ-bkiNmb1RFzcsQwYcq-i-zd-YdlN6H7J_prQQHenwFIFsYhwmx9-s9J3pX5T9znlcOyuSeP0STrcS5--Ig2Gxf8y538AU3UrAE</recordid><startdate>20110530</startdate><enddate>20110530</enddate><creator>Reckziegel, Patrícia</creator><creator>Dias, Verônica Tironi</creator><creator>Benvegnú, Dalila</creator><creator>Boufleur, Nardeli</creator><creator>Silva Barcelos, Raquel Cristine</creator><creator>Segat, Hecson Jesser</creator><creator>Pase, Camila Simonetti</creator><creator>dos Santos, Clarissa Marques Moreira</creator><creator>Flores, Érico Marlon Moraes</creator><creator>Bürger, Marilise Escobar</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</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>8FD</scope><scope>FR3</scope><scope>KR7</scope><scope>7ST</scope><scope>7U7</scope><scope>C1K</scope><scope>SOI</scope></search><sort><creationdate>20110530</creationdate><title>Locomotor damage and brain oxidative stress induced by lead exposure are attenuated by gallic acid treatment</title><author>Reckziegel, Patrícia ; Dias, Verônica Tironi ; Benvegnú, Dalila ; Boufleur, Nardeli ; Silva Barcelos, Raquel Cristine ; Segat, Hecson Jesser ; Pase, Camila Simonetti ; dos Santos, Clarissa Marques Moreira ; Flores, Érico Marlon Moraes ; Bürger, Marilise Escobar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-b5da9ce243a7068656734578e39e8f7114e39f7f0ddbfac107e17e10e96961283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Antioxidant</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Behavior, Animal - drug effects</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Catalase - metabolism</topic><topic>Chelating agent</topic><topic>Chelating Agents - pharmacology</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Damage</topic><topic>Disease Models, Animal</topic><topic>Edetic Acid - pharmacology</topic><topic>EDTA</topic><topic>Exploratory Behavior - drug effects</topic><topic>Gallic acid</topic><topic>Gallic Acid - pharmacology</topic><topic>Genetic algorithms</topic><topic>Lead</topic><topic>Lead Poisoning, Nervous System - metabolism</topic><topic>Lead Poisoning, Nervous System - physiopathology</topic><topic>Lead Poisoning, Nervous System - prevention & control</topic><topic>Lead Poisoning, Nervous System - psychology</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Lipids</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metals and various inorganic compounds</topic><topic>Motor Activity - drug effects</topic><topic>Motors</topic><topic>Movement damages</topic><topic>Nitrates</topic><topic>Operating systems</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Porphobilinogen Synthase - metabolism</topic><topic>Protein Carbonylation - drug effects</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Reckziegel, Patrícia</creatorcontrib><creatorcontrib>Dias, Verônica Tironi</creatorcontrib><creatorcontrib>Benvegnú, Dalila</creatorcontrib><creatorcontrib>Boufleur, Nardeli</creatorcontrib><creatorcontrib>Silva Barcelos, Raquel Cristine</creatorcontrib><creatorcontrib>Segat, Hecson Jesser</creatorcontrib><creatorcontrib>Pase, Camila Simonetti</creatorcontrib><creatorcontrib>dos Santos, Clarissa Marques Moreira</creatorcontrib><creatorcontrib>Flores, Érico Marlon Moraes</creatorcontrib><creatorcontrib>Bürger, Marilise Escobar</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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Civil Engineering Abstracts</collection><collection>Environment Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Environment Abstracts</collection><jtitle>Toxicology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Reckziegel, Patrícia</au><au>Dias, Verônica Tironi</au><au>Benvegnú, Dalila</au><au>Boufleur, Nardeli</au><au>Silva Barcelos, Raquel Cristine</au><au>Segat, Hecson Jesser</au><au>Pase, Camila Simonetti</au><au>dos Santos, Clarissa Marques Moreira</au><au>Flores, Érico Marlon Moraes</au><au>Bürger, Marilise Escobar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Locomotor damage and brain oxidative stress induced by lead exposure are attenuated by gallic acid treatment</atitle><jtitle>Toxicology letters</jtitle><addtitle>Toxicol Lett</addtitle><date>2011-05-30</date><risdate>2011</risdate><volume>203</volume><issue>1</issue><spage>74</spage><epage>81</epage><pages>74-81</pages><issn>0378-4274</issn><eissn>1879-3169</eissn><coden>TOLED5</coden><abstract>We investigated the antioxidant potential of gallic acid (GA), a natural compound found in vegetal sources, on the motor and oxidative damages induced by lead. Rats exposed to lead (50
mg/kg, i.p., once a day, 5
days) were treated with GA (13.5
mg/kg, p.o.) or EDTA (110
mg/kg, i.p.) daily, for 3
days. Lead exposure decreased the locomotor and exploratory activities, reduced blood ALA-D activity, and increased brain catalase (CAT) activity without altering other antioxidant defenses. Brain oxidative stress (OS) estimated by lipid peroxidation (TBARS) and protein carbonyl were increased by lead. GA reversed the motor behavior parameters, the ALA-D activity, as well as the markers of OS changed by lead exposure. CAT activity remained high, possibly as a compensatory mechanism to eliminate hydroperoxides during lead poisoning. EDTA, a conventional chelating agent, was not beneficial on the lead-induced motor behavior and oxidative damages. Both GA (less) and EDTA (more) reduced the lead accumulation in brain tissue. Negative correlations were observed between the behavioral parameters and lipid peroxidation and the lead levels in brain tissue. In conclusion, GA may be an adjuvant in lead exposure, mainly by its antioxidant properties against the motor and oxidative damages resulting from such poisoning.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>21402136</pmid><doi>10.1016/j.toxlet.2011.03.006</doi><tpages>8</tpages></addata></record> |
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| ispartof | Toxicology letters, 2011-05, Vol.203 (1), p.74-81 |
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| subjects | Animals Antioxidant Antioxidants Antioxidants - pharmacology Behavior, Animal - drug effects Biological and medical sciences Brain Brain - drug effects Brain - metabolism Catalase - metabolism Chelating agent Chelating Agents - pharmacology Chemical and industrial products toxicology. Toxic occupational diseases Damage Disease Models, Animal Edetic Acid - pharmacology EDTA Exploratory Behavior - drug effects Gallic acid Gallic Acid - pharmacology Genetic algorithms Lead Lead Poisoning, Nervous System - metabolism Lead Poisoning, Nervous System - physiopathology Lead Poisoning, Nervous System - prevention & control Lead Poisoning, Nervous System - psychology Lipid Peroxidation - drug effects Lipids Male Medical sciences Metals and various inorganic compounds Motor Activity - drug effects Motors Movement damages Nitrates Operating systems Oxidative stress Oxidative Stress - drug effects Porphobilinogen Synthase - metabolism Protein Carbonylation - drug effects Rats Rats, Wistar Toxicology |
| title | Locomotor damage and brain oxidative stress induced by lead exposure are attenuated by gallic acid treatment |
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