Antiepileptic Drugs and Their Dual Mechanism of Action on Carbonic Anhydrase
(1) Background: The benefit of using inhibitors of carbonic anhydrase (CA), such as acetazolamide, in the treatment of epilepsy has previously been described. (2) Methods: In this paper, the effect on CA of the most well-known antiepileptic drugs was studied in vitro and in vivo. The effects, after...
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| Veröffentlicht in: | Journal of clinical medicine 2022-05, Vol.11 (9), p.2614 |
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| creator | Magheru, Calin Magheru, Sorina Coltau, Marcela Hoza, Anica Moldovan, Corina Sachelarie, Liliana Gradinaru, Irina Hurjui, Loredana Liliana Marc, Felicia Farcas, Dorina Maria |
| description | (1) Background: The benefit of using inhibitors of carbonic anhydrase (CA), such as acetazolamide, in the treatment of epilepsy has previously been described. (2) Methods: In this paper, the effect on CA of the most well-known antiepileptic drugs was studied in vitro and in vivo. The effects, after chronic treatment, of carbamazepine, phenytoin, valproate, primidone, clonazepam, and ethosuximide were studied in vitro on purified CA, isozyme I (CA I) and CA, and isozyme II (CA II) activity and in vivo on epileptic erythrocyte CA I and CA II activity. (3) Results: In vitro results showed that all antiepileptic drugs reduced purified CA II activity according to dose-response relationships and slightly inhibited CA I activity. In vivo results showed that the chronic administration of antiseizure drugs induced a progressive reduction in erythrocyte CA II activity in all the groups studied. This study shows that CA II inhibition can be induced both in vitro and in vivo by major antiepileptic agents as it might be one of the effective mechanisms of these anticonvulsant drugs. (4) Conclusions: The decrease in CA II activity in epileptic patients after antiseizure treatment suggests the involvement of CA II in the pathogenesis of epilepsy. |
| doi_str_mv | 10.3390/jcm11092614 |
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(2) Methods: In this paper, the effect on CA of the most well-known antiepileptic drugs was studied in vitro and in vivo. The effects, after chronic treatment, of carbamazepine, phenytoin, valproate, primidone, clonazepam, and ethosuximide were studied in vitro on purified CA, isozyme I (CA I) and CA, and isozyme II (CA II) activity and in vivo on epileptic erythrocyte CA I and CA II activity. (3) Results: In vitro results showed that all antiepileptic drugs reduced purified CA II activity according to dose-response relationships and slightly inhibited CA I activity. In vivo results showed that the chronic administration of antiseizure drugs induced a progressive reduction in erythrocyte CA II activity in all the groups studied. This study shows that CA II inhibition can be induced both in vitro and in vivo by major antiepileptic agents as it might be one of the effective mechanisms of these anticonvulsant drugs. (4) Conclusions: The decrease in CA II activity in epileptic patients after antiseizure treatment suggests the involvement of CA II in the pathogenesis of epilepsy.</description><identifier>ISSN: 2077-0383</identifier><identifier>EISSN: 2077-0383</identifier><identifier>DOI: 10.3390/jcm11092614</identifier><identifier>PMID: 35566738</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acids ; Carbon dioxide ; Clinical medicine ; Consciousness ; Convulsions & seizures ; Drugs ; Electrocardiography ; Electroencephalography ; Epilepsy ; Hydration ; Metabolism ; Patients</subject><ispartof>Journal of clinical medicine, 2022-05, Vol.11 (9), p.2614</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c306t-c2e1eae5fc6de7fe2b0167c8f538ebea90f636f341e934dfe99bb7bce7abd2bc3</citedby><cites>FETCH-LOGICAL-c306t-c2e1eae5fc6de7fe2b0167c8f538ebea90f636f341e934dfe99bb7bce7abd2bc3</cites><orcidid>0000-0003-3803-9405 ; 0000-0001-7701-2307</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9105189/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9105189/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35566738$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Magheru, Calin</creatorcontrib><creatorcontrib>Magheru, Sorina</creatorcontrib><creatorcontrib>Coltau, Marcela</creatorcontrib><creatorcontrib>Hoza, Anica</creatorcontrib><creatorcontrib>Moldovan, Corina</creatorcontrib><creatorcontrib>Sachelarie, Liliana</creatorcontrib><creatorcontrib>Gradinaru, Irina</creatorcontrib><creatorcontrib>Hurjui, Loredana Liliana</creatorcontrib><creatorcontrib>Marc, Felicia</creatorcontrib><creatorcontrib>Farcas, Dorina Maria</creatorcontrib><title>Antiepileptic Drugs and Their Dual Mechanism of Action on Carbonic Anhydrase</title><title>Journal of clinical medicine</title><addtitle>J Clin Med</addtitle><description>(1) Background: The benefit of using inhibitors of carbonic anhydrase (CA), such as acetazolamide, in the treatment of epilepsy has previously been described. (2) Methods: In this paper, the effect on CA of the most well-known antiepileptic drugs was studied in vitro and in vivo. The effects, after chronic treatment, of carbamazepine, phenytoin, valproate, primidone, clonazepam, and ethosuximide were studied in vitro on purified CA, isozyme I (CA I) and CA, and isozyme II (CA II) activity and in vivo on epileptic erythrocyte CA I and CA II activity. (3) Results: In vitro results showed that all antiepileptic drugs reduced purified CA II activity according to dose-response relationships and slightly inhibited CA I activity. In vivo results showed that the chronic administration of antiseizure drugs induced a progressive reduction in erythrocyte CA II activity in all the groups studied. This study shows that CA II inhibition can be induced both in vitro and in vivo by major antiepileptic agents as it might be one of the effective mechanisms of these anticonvulsant drugs. (4) Conclusions: The decrease in CA II activity in epileptic patients after antiseizure treatment suggests the involvement of CA II in the pathogenesis of epilepsy.</description><subject>Acids</subject><subject>Carbon dioxide</subject><subject>Clinical medicine</subject><subject>Consciousness</subject><subject>Convulsions & seizures</subject><subject>Drugs</subject><subject>Electrocardiography</subject><subject>Electroencephalography</subject><subject>Epilepsy</subject><subject>Hydration</subject><subject>Metabolism</subject><subject>Patients</subject><issn>2077-0383</issn><issn>2077-0383</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNpVkE1LAzEQhoMottSevMuCR6nmo5tkL0Jp_YKKl3oOSXbSprTZNdkV-u9daS11GJiBeead4UXomuB7xgr8sLZbQnBBORmfoT7FQowwk-z8pO-hYUpr3IWUY0rEJeqxPOdcMNlH80loPNR-A3XjbTaL7TJlOpTZYgU-ZrNWb7J3sCsdfNpmlcsmtvFVyLqc6miq0C1NwmpXRp3gCl04vUkwPNQB-nx-WkxfR_OPl7fpZD6yDPNmZCkQ0JA7y0sQDqjBhAsrXc4kGNAFdpxxx8YECjYuHRSFMcJYENqU1Fg2QI973bo1WygthCbqjaqj3-q4U5X26v8k-JVaVt-qIDgnsugEbg8CsfpqITVqXbUxdD8ryjnDVFApO-puT9lYpRTBHS8QrH7dVyfud_TN6VNH9s9r9gMZ04Gh</recordid><startdate>20220506</startdate><enddate>20220506</enddate><creator>Magheru, Calin</creator><creator>Magheru, Sorina</creator><creator>Coltau, Marcela</creator><creator>Hoza, Anica</creator><creator>Moldovan, Corina</creator><creator>Sachelarie, Liliana</creator><creator>Gradinaru, Irina</creator><creator>Hurjui, Loredana Liliana</creator><creator>Marc, Felicia</creator><creator>Farcas, Dorina Maria</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-3803-9405</orcidid><orcidid>https://orcid.org/0000-0001-7701-2307</orcidid></search><sort><creationdate>20220506</creationdate><title>Antiepileptic Drugs and Their Dual Mechanism of Action on Carbonic Anhydrase</title><author>Magheru, Calin ; Magheru, Sorina ; Coltau, Marcela ; Hoza, Anica ; Moldovan, Corina ; Sachelarie, Liliana ; Gradinaru, Irina ; Hurjui, Loredana Liliana ; Marc, Felicia ; Farcas, Dorina Maria</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c306t-c2e1eae5fc6de7fe2b0167c8f538ebea90f636f341e934dfe99bb7bce7abd2bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Acids</topic><topic>Carbon dioxide</topic><topic>Clinical medicine</topic><topic>Consciousness</topic><topic>Convulsions & seizures</topic><topic>Drugs</topic><topic>Electrocardiography</topic><topic>Electroencephalography</topic><topic>Epilepsy</topic><topic>Hydration</topic><topic>Metabolism</topic><topic>Patients</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Magheru, Calin</creatorcontrib><creatorcontrib>Magheru, Sorina</creatorcontrib><creatorcontrib>Coltau, Marcela</creatorcontrib><creatorcontrib>Hoza, Anica</creatorcontrib><creatorcontrib>Moldovan, Corina</creatorcontrib><creatorcontrib>Sachelarie, Liliana</creatorcontrib><creatorcontrib>Gradinaru, Irina</creatorcontrib><creatorcontrib>Hurjui, Loredana Liliana</creatorcontrib><creatorcontrib>Marc, Felicia</creatorcontrib><creatorcontrib>Farcas, Dorina Maria</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of clinical medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Magheru, Calin</au><au>Magheru, Sorina</au><au>Coltau, Marcela</au><au>Hoza, Anica</au><au>Moldovan, Corina</au><au>Sachelarie, Liliana</au><au>Gradinaru, Irina</au><au>Hurjui, Loredana Liliana</au><au>Marc, Felicia</au><au>Farcas, Dorina Maria</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antiepileptic Drugs and Their Dual Mechanism of Action on Carbonic Anhydrase</atitle><jtitle>Journal of clinical medicine</jtitle><addtitle>J Clin Med</addtitle><date>2022-05-06</date><risdate>2022</risdate><volume>11</volume><issue>9</issue><spage>2614</spage><pages>2614-</pages><issn>2077-0383</issn><eissn>2077-0383</eissn><abstract>(1) Background: The benefit of using inhibitors of carbonic anhydrase (CA), such as acetazolamide, in the treatment of epilepsy has previously been described. 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| subjects | Acids Carbon dioxide Clinical medicine Consciousness Convulsions & seizures Drugs Electrocardiography Electroencephalography Epilepsy Hydration Metabolism Patients |
| title | Antiepileptic Drugs and Their Dual Mechanism of Action on Carbonic Anhydrase |
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