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Chlorogenic acids inhibit glutamate dehydrogenase and decrease intracellular ATP levels in cultures of chick embryo retina cells
[Display omitted] Chlorogenic acids (CGAs) are a group of phenolic compounds found in worldwide consumed beverages such as coffee and green tea. They are synthesized from an esterification reaction between cinnamic acids, including caffeic (CFA), ferulic and p-coumaric acids with quinic acid (QA), f...
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Published in: | Biochemical pharmacology 2018-09, Vol.155, p.393-402 |
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creator | Domith, Ivan Duarte-Silva, Aline T. Garcia, Carlos Gustavo Calaza, Karin da Costa Paes-de-Carvalho, Roberto Cossenza, Marcelo |
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Chlorogenic acids (CGAs) are a group of phenolic compounds found in worldwide consumed beverages such as coffee and green tea. They are synthesized from an esterification reaction between cinnamic acids, including caffeic (CFA), ferulic and p-coumaric acids with quinic acid (QA), forming several mono- and di-esterified isomers. The most prevalent and studied compounds are 3-O-caffeoylquinic acid (3-CQA), 4-O-caffeoylquinic acid (4-CQA) and 5-O-caffeoylquinic acid (5-CQA), widely described as having antioxidant and cell protection effects. CGAs can also modulate glutamate release from microglia by a mechanism involving a decrease of reactive oxygen species (ROS). Increased energy metabolism is highly associated with enhancement of ROS production and cellular damage. Glutamate can also be used as an energy source by glutamate dehydrogenase (GDH) enzyme, providing α-ketoglutarate to the tricarboxylic acid (TCA) cycle for ATP synthesis. High GDH activity is associated with some disorders, such as schizophrenia and hyperinsulinemia/hyperammonemia syndrome. In line with this, our objective was to investigate the effect of CGAs on GDH activity. We show that CGAs and CFA inhibits GDH activity in dose-dependent manner, reaching complete inhibition at high concentration with IC50 of 52 μM for 3-CQA and 158.2 μM for CFA. Using live imaging confocal microscopy and microplate reader, we observed that 3-CQA and CFA can be transported into neuronal cells by an Na+-dependent mechanism. Moreover, neuronal cells treated with CGAs presented lower intracellular ATP levels. Overall, these data suggest that CGAs have therapeutic potential for treatment of disorders associated with high GDH activity. |
doi_str_mv | 10.1016/j.bcp.2018.07.023 |
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Chlorogenic acids (CGAs) are a group of phenolic compounds found in worldwide consumed beverages such as coffee and green tea. They are synthesized from an esterification reaction between cinnamic acids, including caffeic (CFA), ferulic and p-coumaric acids with quinic acid (QA), forming several mono- and di-esterified isomers. The most prevalent and studied compounds are 3-O-caffeoylquinic acid (3-CQA), 4-O-caffeoylquinic acid (4-CQA) and 5-O-caffeoylquinic acid (5-CQA), widely described as having antioxidant and cell protection effects. CGAs can also modulate glutamate release from microglia by a mechanism involving a decrease of reactive oxygen species (ROS). Increased energy metabolism is highly associated with enhancement of ROS production and cellular damage. Glutamate can also be used as an energy source by glutamate dehydrogenase (GDH) enzyme, providing α-ketoglutarate to the tricarboxylic acid (TCA) cycle for ATP synthesis. High GDH activity is associated with some disorders, such as schizophrenia and hyperinsulinemia/hyperammonemia syndrome. In line with this, our objective was to investigate the effect of CGAs on GDH activity. We show that CGAs and CFA inhibits GDH activity in dose-dependent manner, reaching complete inhibition at high concentration with IC50 of 52 μM for 3-CQA and 158.2 μM for CFA. Using live imaging confocal microscopy and microplate reader, we observed that 3-CQA and CFA can be transported into neuronal cells by an Na+-dependent mechanism. Moreover, neuronal cells treated with CGAs presented lower intracellular ATP levels. Overall, these data suggest that CGAs have therapeutic potential for treatment of disorders associated with high GDH activity.</description><identifier>ISSN: 0006-2952</identifier><identifier>EISSN: 1873-2968</identifier><identifier>DOI: 10.1016/j.bcp.2018.07.023</identifier><identifier>PMID: 30031809</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Adenosine Triphosphate - antagonists & inhibitors ; Adenosine Triphosphate - metabolism ; Animals ; Caffeic acid ; Cells, Cultured ; Chick Embryo ; Chlorogenic Acid - pharmacology ; Dose-Response Relationship, Drug ; Fluorescence uptake ; Glutamate Dehydrogenase - antagonists & inhibitors ; Glutamate Dehydrogenase - metabolism ; Intracellular Fluid - drug effects ; Intracellular Fluid - metabolism ; Neuronal and glial metabolism ; Quinic acid ; Retina - cytology ; Retina - drug effects ; Retina - metabolism</subject><ispartof>Biochemical pharmacology, 2018-09, Vol.155, p.393-402</ispartof><rights>2018 Elsevier Inc.</rights><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-19b616c164a92aa6fc0dda79912c2300803abc4738917cdcf9ac7324859ed5943</citedby><cites>FETCH-LOGICAL-c396t-19b616c164a92aa6fc0dda79912c2300803abc4738917cdcf9ac7324859ed5943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27900,27901</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30031809$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Domith, Ivan</creatorcontrib><creatorcontrib>Duarte-Silva, Aline T.</creatorcontrib><creatorcontrib>Garcia, Carlos Gustavo</creatorcontrib><creatorcontrib>Calaza, Karin da Costa</creatorcontrib><creatorcontrib>Paes-de-Carvalho, Roberto</creatorcontrib><creatorcontrib>Cossenza, Marcelo</creatorcontrib><title>Chlorogenic acids inhibit glutamate dehydrogenase and decrease intracellular ATP levels in cultures of chick embryo retina cells</title><title>Biochemical pharmacology</title><addtitle>Biochem Pharmacol</addtitle><description>[Display omitted]
Chlorogenic acids (CGAs) are a group of phenolic compounds found in worldwide consumed beverages such as coffee and green tea. They are synthesized from an esterification reaction between cinnamic acids, including caffeic (CFA), ferulic and p-coumaric acids with quinic acid (QA), forming several mono- and di-esterified isomers. The most prevalent and studied compounds are 3-O-caffeoylquinic acid (3-CQA), 4-O-caffeoylquinic acid (4-CQA) and 5-O-caffeoylquinic acid (5-CQA), widely described as having antioxidant and cell protection effects. CGAs can also modulate glutamate release from microglia by a mechanism involving a decrease of reactive oxygen species (ROS). Increased energy metabolism is highly associated with enhancement of ROS production and cellular damage. Glutamate can also be used as an energy source by glutamate dehydrogenase (GDH) enzyme, providing α-ketoglutarate to the tricarboxylic acid (TCA) cycle for ATP synthesis. High GDH activity is associated with some disorders, such as schizophrenia and hyperinsulinemia/hyperammonemia syndrome. In line with this, our objective was to investigate the effect of CGAs on GDH activity. We show that CGAs and CFA inhibits GDH activity in dose-dependent manner, reaching complete inhibition at high concentration with IC50 of 52 μM for 3-CQA and 158.2 μM for CFA. Using live imaging confocal microscopy and microplate reader, we observed that 3-CQA and CFA can be transported into neuronal cells by an Na+-dependent mechanism. Moreover, neuronal cells treated with CGAs presented lower intracellular ATP levels. Overall, these data suggest that CGAs have therapeutic potential for treatment of disorders associated with high GDH activity.</description><subject>Adenosine Triphosphate - antagonists & inhibitors</subject><subject>Adenosine Triphosphate - metabolism</subject><subject>Animals</subject><subject>Caffeic acid</subject><subject>Cells, Cultured</subject><subject>Chick Embryo</subject><subject>Chlorogenic Acid - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fluorescence uptake</subject><subject>Glutamate Dehydrogenase - antagonists & inhibitors</subject><subject>Glutamate Dehydrogenase - metabolism</subject><subject>Intracellular Fluid - drug effects</subject><subject>Intracellular Fluid - metabolism</subject><subject>Neuronal and glial metabolism</subject><subject>Quinic acid</subject><subject>Retina - cytology</subject><subject>Retina - drug effects</subject><subject>Retina - metabolism</subject><issn>0006-2952</issn><issn>1873-2968</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp9kM1u1DAUhS1ERYeWB2CDvGQzwT-JE4tVNeJPqkQX7dpyrm86HpxksJ1Ks-PRcZjCkpV9re8cXX-EvOWs4oyrD4eqh2MlGO8q1lZMyBdkw7tWboVW3UuyYYypcm_EJXmd0mEdO8VfkUvJmOQd0xvya7cPc5wfcfJALXiXqJ_2vveZPoYl29FmpA73J_cHsgmpnVx5gYjr4KccLWAIS7CR3tzf0YBPGNYWCkvIS8RE54HC3sMPimMfTzONmP1k6RpL1-RisCHhm-fzijx8_nS_-7q9_f7l2-7mdgtSq7zluldcAVe11cJaNQBzzrZacwGifKdj0vZQt7LTvAUHg7bQSlF3jUbX6Fpekffn3mOcfy6Yshl9WjewE85LMoK1NReyaWRB-RmFOKcUcTDH6EcbT4Yzs4o3B1PEm1W8Ya0p4kvm3XP90o_o_iX-mi7AxzNQ5OCTx2gSeJwAnY8I2bjZ_6f-N4kqlTU</recordid><startdate>201809</startdate><enddate>201809</enddate><creator>Domith, Ivan</creator><creator>Duarte-Silva, Aline T.</creator><creator>Garcia, Carlos Gustavo</creator><creator>Calaza, Karin da Costa</creator><creator>Paes-de-Carvalho, Roberto</creator><creator>Cossenza, Marcelo</creator><general>Elsevier 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>7X8</scope></search><sort><creationdate>201809</creationdate><title>Chlorogenic acids inhibit glutamate dehydrogenase and decrease intracellular ATP levels in cultures of chick embryo retina cells</title><author>Domith, Ivan ; Duarte-Silva, Aline T. ; Garcia, Carlos Gustavo ; Calaza, Karin da Costa ; Paes-de-Carvalho, Roberto ; Cossenza, Marcelo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-19b616c164a92aa6fc0dda79912c2300803abc4738917cdcf9ac7324859ed5943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adenosine Triphosphate - antagonists & inhibitors</topic><topic>Adenosine Triphosphate - metabolism</topic><topic>Animals</topic><topic>Caffeic acid</topic><topic>Cells, Cultured</topic><topic>Chick Embryo</topic><topic>Chlorogenic Acid - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fluorescence uptake</topic><topic>Glutamate Dehydrogenase - antagonists & inhibitors</topic><topic>Glutamate Dehydrogenase - metabolism</topic><topic>Intracellular Fluid - drug effects</topic><topic>Intracellular Fluid - metabolism</topic><topic>Neuronal and glial metabolism</topic><topic>Quinic acid</topic><topic>Retina - cytology</topic><topic>Retina - drug effects</topic><topic>Retina - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Domith, Ivan</creatorcontrib><creatorcontrib>Duarte-Silva, Aline T.</creatorcontrib><creatorcontrib>Garcia, Carlos Gustavo</creatorcontrib><creatorcontrib>Calaza, Karin da Costa</creatorcontrib><creatorcontrib>Paes-de-Carvalho, Roberto</creatorcontrib><creatorcontrib>Cossenza, Marcelo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Domith, Ivan</au><au>Duarte-Silva, Aline T.</au><au>Garcia, Carlos Gustavo</au><au>Calaza, Karin da Costa</au><au>Paes-de-Carvalho, Roberto</au><au>Cossenza, Marcelo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chlorogenic acids inhibit glutamate dehydrogenase and decrease intracellular ATP levels in cultures of chick embryo retina cells</atitle><jtitle>Biochemical pharmacology</jtitle><addtitle>Biochem Pharmacol</addtitle><date>2018-09</date><risdate>2018</risdate><volume>155</volume><spage>393</spage><epage>402</epage><pages>393-402</pages><issn>0006-2952</issn><eissn>1873-2968</eissn><abstract>[Display omitted]
Chlorogenic acids (CGAs) are a group of phenolic compounds found in worldwide consumed beverages such as coffee and green tea. They are synthesized from an esterification reaction between cinnamic acids, including caffeic (CFA), ferulic and p-coumaric acids with quinic acid (QA), forming several mono- and di-esterified isomers. The most prevalent and studied compounds are 3-O-caffeoylquinic acid (3-CQA), 4-O-caffeoylquinic acid (4-CQA) and 5-O-caffeoylquinic acid (5-CQA), widely described as having antioxidant and cell protection effects. CGAs can also modulate glutamate release from microglia by a mechanism involving a decrease of reactive oxygen species (ROS). Increased energy metabolism is highly associated with enhancement of ROS production and cellular damage. Glutamate can also be used as an energy source by glutamate dehydrogenase (GDH) enzyme, providing α-ketoglutarate to the tricarboxylic acid (TCA) cycle for ATP synthesis. High GDH activity is associated with some disorders, such as schizophrenia and hyperinsulinemia/hyperammonemia syndrome. In line with this, our objective was to investigate the effect of CGAs on GDH activity. We show that CGAs and CFA inhibits GDH activity in dose-dependent manner, reaching complete inhibition at high concentration with IC50 of 52 μM for 3-CQA and 158.2 μM for CFA. Using live imaging confocal microscopy and microplate reader, we observed that 3-CQA and CFA can be transported into neuronal cells by an Na+-dependent mechanism. Moreover, neuronal cells treated with CGAs presented lower intracellular ATP levels. Overall, these data suggest that CGAs have therapeutic potential for treatment of disorders associated with high GDH activity.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>30031809</pmid><doi>10.1016/j.bcp.2018.07.023</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adenosine Triphosphate - antagonists & inhibitors Adenosine Triphosphate - metabolism Animals Caffeic acid Cells, Cultured Chick Embryo Chlorogenic Acid - pharmacology Dose-Response Relationship, Drug Fluorescence uptake Glutamate Dehydrogenase - antagonists & inhibitors Glutamate Dehydrogenase - metabolism Intracellular Fluid - drug effects Intracellular Fluid - metabolism Neuronal and glial metabolism Quinic acid Retina - cytology Retina - drug effects Retina - metabolism |
title | Chlorogenic acids inhibit glutamate dehydrogenase and decrease intracellular ATP levels in cultures of chick embryo retina cells |
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