Vanillin and vanillic acid modulate antioxidant defense system via amelioration of metabolic complications linked to Fe2+-induced brain tissues damage
The therapeutic effect of phenolics on neurodegenerative diseases has been attributed to their potent antioxidant properties. In the present study, the neuroprotective activities of vanillin and vanillic acid were investigated in Fe 2+ - induced oxidative toxicity in brain tissues by investigating t...
Gespeichert in:
| Veröffentlicht in: | Metabolic brain disease 2020-06, Vol.35 (5), p.727-738 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 738 |
|---|---|
| container_issue | 5 |
| container_start_page | 727 |
| container_title | Metabolic brain disease |
| container_volume | 35 |
| creator | Salau, Veronica F. Erukainure, Ochuko L. Ibeji, Collins U. Olasehinde, Tosin A. Koorbanally, Neil A. Islam, Md. Shahidul |
| description | The therapeutic effect of phenolics on neurodegenerative diseases has been attributed to their potent antioxidant properties. In the present study, the neuroprotective activities of vanillin and vanillic acid were investigated in Fe
2+
- induced oxidative toxicity in brain tissues by investigating their therapeutic effects on oxidative imbalance, cholinergic and nucleotide-hydrolyzing enzymes activities, dysregulated metabolic pathways. Their cytotoxicity was investigated in hippocampal neuronal cell lines (HT22). The reduced glutathione level, SOD and catalase activities were ameliorated in tissues treated with the phenolics, with concomitant depletion of malondialdehyde and nitric oxide levels. They inhibited acetylcholinesterase and butyrylcholinesterase activities, while concomitantly elevated ATPase activity. Treatment with vanillin led to restoration of oxidative-depleted metabolites and reactivation of the pentose phosphate and purine metabolism pathways, with concomitant activation of pathways for histidine and selenoamino metabolisms. While vanillic acid restored and reactivated oxidative-depleted metabolites and pathways but did not activate any additional pathway. Both phenolics portrayed good binding affinity for catalase, with vanillic acid having the higher binding energy of −7.0 kcal/mol. Both phenolics were not cytotoxic on HT22 cells, and their toxicity class were predicted to be 4. Only vanillin was predicted to be permeable across the blood brain barrier (BBB). These results insinuate that vanillin and vanillic acid confer a neuroprotective effect on oxidative brain damage, when vanillin being the most potent. |
| doi_str_mv | 10.1007/s11011-020-00545-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2356595991</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2402241122</sourcerecordid><originalsourceid>FETCH-LOGICAL-c348t-dd1baf68967d081ddf8c89bc1b61fe8d725028ebfeaa64dcd7a99fa1071557a43</originalsourceid><addsrcrecordid>eNp9kcFqFjEUhYMo-Ft9AVcBN4KkJpnJJFlKsVoouFG34U5yU1Jnkt_JTPF_kT6vaUcQXLg6XO53zr1wCHkt-LngXL-vQnAhGJecca56xU5PyEEo3THdDeopOXBjFNO95c_Ji1pvOeedEvZA7r9DTtOUMoUc6N0-eAo-BTqXsE2wYlutqfxKoSkNGDFXpPVUV5zpXQIKM06pLNCgTEukM64wlocYX-Zj08dNpe3KDwx0LfQS5TuWcth8m8cF2vk11bphpQFmuMGX5FmEqeKrP3pGvl1-_HrxmV1_-XR18eGa-a43KwtBjBAHYwcduBEhROONHb0YBxHRBC0VlwbHiABDH3zQYG0EwbVQSkPfnZG3e-5xKT_b-dXNqXqcJshYtupkpwZllbWioW_-QW_LtuT2nZM9l7IXQspGyZ3yS6l1weiOS5phOTnB3UNVbq_KtarcY1Xu1EzdbqoNzje4_I3-j-s3166aug</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2402241122</pqid></control><display><type>article</type><title>Vanillin and vanillic acid modulate antioxidant defense system via amelioration of metabolic complications linked to Fe2+-induced brain tissues damage</title><source>SpringerLink Journals - AutoHoldings</source><creator>Salau, Veronica F. ; Erukainure, Ochuko L. ; Ibeji, Collins U. ; Olasehinde, Tosin A. ; Koorbanally, Neil A. ; Islam, Md. Shahidul</creator><creatorcontrib>Salau, Veronica F. ; Erukainure, Ochuko L. ; Ibeji, Collins U. ; Olasehinde, Tosin A. ; Koorbanally, Neil A. ; Islam, Md. Shahidul</creatorcontrib><description>The therapeutic effect of phenolics on neurodegenerative diseases has been attributed to their potent antioxidant properties. In the present study, the neuroprotective activities of vanillin and vanillic acid were investigated in Fe
2+
- induced oxidative toxicity in brain tissues by investigating their therapeutic effects on oxidative imbalance, cholinergic and nucleotide-hydrolyzing enzymes activities, dysregulated metabolic pathways. Their cytotoxicity was investigated in hippocampal neuronal cell lines (HT22). The reduced glutathione level, SOD and catalase activities were ameliorated in tissues treated with the phenolics, with concomitant depletion of malondialdehyde and nitric oxide levels. They inhibited acetylcholinesterase and butyrylcholinesterase activities, while concomitantly elevated ATPase activity. Treatment with vanillin led to restoration of oxidative-depleted metabolites and reactivation of the pentose phosphate and purine metabolism pathways, with concomitant activation of pathways for histidine and selenoamino metabolisms. While vanillic acid restored and reactivated oxidative-depleted metabolites and pathways but did not activate any additional pathway. Both phenolics portrayed good binding affinity for catalase, with vanillic acid having the higher binding energy of −7.0 kcal/mol. Both phenolics were not cytotoxic on HT22 cells, and their toxicity class were predicted to be 4. Only vanillin was predicted to be permeable across the blood brain barrier (BBB). These results insinuate that vanillin and vanillic acid confer a neuroprotective effect on oxidative brain damage, when vanillin being the most potent.</description><identifier>ISSN: 0885-7490</identifier><identifier>EISSN: 1573-7365</identifier><identifier>DOI: 10.1007/s11011-020-00545-y</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acetylcholinesterase ; Acids ; Activation ; Adenosine triphosphatase ; Antioxidants ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Blood-brain barrier ; Brain damage ; Brain injury ; Catalase ; Cell lines ; Cholinergics ; Complications ; Cytotoxicity ; Depletion ; Glutathione ; Hippocampus ; Histidine ; Iron ; Malondialdehyde ; Metabolic Diseases ; Metabolic pathways ; Metabolism ; Metabolites ; Neurodegenerative diseases ; Neurology ; Neuroprotection ; Neurosciences ; Nitric oxide ; Nucleotides ; Oncology ; Original Article ; Pentose ; Pentose phosphate pathway ; Phenols ; Restoration ; Tissues ; Toxicity ; Vanillic acid ; Vanillin</subject><ispartof>Metabolic brain disease, 2020-06, Vol.35 (5), p.727-738</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c348t-dd1baf68967d081ddf8c89bc1b61fe8d725028ebfeaa64dcd7a99fa1071557a43</citedby><cites>FETCH-LOGICAL-c348t-dd1baf68967d081ddf8c89bc1b61fe8d725028ebfeaa64dcd7a99fa1071557a43</cites><orcidid>0000-0003-0489-338X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11011-020-00545-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11011-020-00545-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27907,27908,41471,42540,51302</link.rule.ids></links><search><creatorcontrib>Salau, Veronica F.</creatorcontrib><creatorcontrib>Erukainure, Ochuko L.</creatorcontrib><creatorcontrib>Ibeji, Collins U.</creatorcontrib><creatorcontrib>Olasehinde, Tosin A.</creatorcontrib><creatorcontrib>Koorbanally, Neil A.</creatorcontrib><creatorcontrib>Islam, Md. Shahidul</creatorcontrib><title>Vanillin and vanillic acid modulate antioxidant defense system via amelioration of metabolic complications linked to Fe2+-induced brain tissues damage</title><title>Metabolic brain disease</title><addtitle>Metab Brain Dis</addtitle><description>The therapeutic effect of phenolics on neurodegenerative diseases has been attributed to their potent antioxidant properties. In the present study, the neuroprotective activities of vanillin and vanillic acid were investigated in Fe
2+
- induced oxidative toxicity in brain tissues by investigating their therapeutic effects on oxidative imbalance, cholinergic and nucleotide-hydrolyzing enzymes activities, dysregulated metabolic pathways. Their cytotoxicity was investigated in hippocampal neuronal cell lines (HT22). The reduced glutathione level, SOD and catalase activities were ameliorated in tissues treated with the phenolics, with concomitant depletion of malondialdehyde and nitric oxide levels. They inhibited acetylcholinesterase and butyrylcholinesterase activities, while concomitantly elevated ATPase activity. Treatment with vanillin led to restoration of oxidative-depleted metabolites and reactivation of the pentose phosphate and purine metabolism pathways, with concomitant activation of pathways for histidine and selenoamino metabolisms. While vanillic acid restored and reactivated oxidative-depleted metabolites and pathways but did not activate any additional pathway. Both phenolics portrayed good binding affinity for catalase, with vanillic acid having the higher binding energy of −7.0 kcal/mol. Both phenolics were not cytotoxic on HT22 cells, and their toxicity class were predicted to be 4. Only vanillin was predicted to be permeable across the blood brain barrier (BBB). These results insinuate that vanillin and vanillic acid confer a neuroprotective effect on oxidative brain damage, when vanillin being the most potent.</description><subject>Acetylcholinesterase</subject><subject>Acids</subject><subject>Activation</subject><subject>Adenosine triphosphatase</subject><subject>Antioxidants</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood-brain barrier</subject><subject>Brain damage</subject><subject>Brain injury</subject><subject>Catalase</subject><subject>Cell lines</subject><subject>Cholinergics</subject><subject>Complications</subject><subject>Cytotoxicity</subject><subject>Depletion</subject><subject>Glutathione</subject><subject>Hippocampus</subject><subject>Histidine</subject><subject>Iron</subject><subject>Malondialdehyde</subject><subject>Metabolic Diseases</subject><subject>Metabolic pathways</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neurosciences</subject><subject>Nitric oxide</subject><subject>Nucleotides</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Pentose</subject><subject>Pentose phosphate pathway</subject><subject>Phenols</subject><subject>Restoration</subject><subject>Tissues</subject><subject>Toxicity</subject><subject>Vanillic acid</subject><subject>Vanillin</subject><issn>0885-7490</issn><issn>1573-7365</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kcFqFjEUhYMo-Ft9AVcBN4KkJpnJJFlKsVoouFG34U5yU1Jnkt_JTPF_kT6vaUcQXLg6XO53zr1wCHkt-LngXL-vQnAhGJecca56xU5PyEEo3THdDeopOXBjFNO95c_Ji1pvOeedEvZA7r9DTtOUMoUc6N0-eAo-BTqXsE2wYlutqfxKoSkNGDFXpPVUV5zpXQIKM06pLNCgTEukM64wlocYX-Zj08dNpe3KDwx0LfQS5TuWcth8m8cF2vk11bphpQFmuMGX5FmEqeKrP3pGvl1-_HrxmV1_-XR18eGa-a43KwtBjBAHYwcduBEhROONHb0YBxHRBC0VlwbHiABDH3zQYG0EwbVQSkPfnZG3e-5xKT_b-dXNqXqcJshYtupkpwZllbWioW_-QW_LtuT2nZM9l7IXQspGyZ3yS6l1weiOS5phOTnB3UNVbq_KtarcY1Xu1EzdbqoNzje4_I3-j-s3166aug</recordid><startdate>20200601</startdate><enddate>20200601</enddate><creator>Salau, Veronica F.</creator><creator>Erukainure, Ochuko L.</creator><creator>Ibeji, Collins U.</creator><creator>Olasehinde, Tosin A.</creator><creator>Koorbanally, Neil A.</creator><creator>Islam, Md. Shahidul</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0489-338X</orcidid></search><sort><creationdate>20200601</creationdate><title>Vanillin and vanillic acid modulate antioxidant defense system via amelioration of metabolic complications linked to Fe2+-induced brain tissues damage</title><author>Salau, Veronica F. ; Erukainure, Ochuko L. ; Ibeji, Collins U. ; Olasehinde, Tosin A. ; Koorbanally, Neil A. ; Islam, Md. Shahidul</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c348t-dd1baf68967d081ddf8c89bc1b61fe8d725028ebfeaa64dcd7a99fa1071557a43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acetylcholinesterase</topic><topic>Acids</topic><topic>Activation</topic><topic>Adenosine triphosphatase</topic><topic>Antioxidants</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood-brain barrier</topic><topic>Brain damage</topic><topic>Brain injury</topic><topic>Catalase</topic><topic>Cell lines</topic><topic>Cholinergics</topic><topic>Complications</topic><topic>Cytotoxicity</topic><topic>Depletion</topic><topic>Glutathione</topic><topic>Hippocampus</topic><topic>Histidine</topic><topic>Iron</topic><topic>Malondialdehyde</topic><topic>Metabolic Diseases</topic><topic>Metabolic pathways</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neurosciences</topic><topic>Nitric oxide</topic><topic>Nucleotides</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Pentose</topic><topic>Pentose phosphate pathway</topic><topic>Phenols</topic><topic>Restoration</topic><topic>Tissues</topic><topic>Toxicity</topic><topic>Vanillic acid</topic><topic>Vanillin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Salau, Veronica F.</creatorcontrib><creatorcontrib>Erukainure, Ochuko L.</creatorcontrib><creatorcontrib>Ibeji, Collins U.</creatorcontrib><creatorcontrib>Olasehinde, Tosin A.</creatorcontrib><creatorcontrib>Koorbanally, Neil A.</creatorcontrib><creatorcontrib>Islam, Md. Shahidul</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</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>Environmental Sciences and Pollution Management</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 Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Metabolic brain disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Salau, Veronica F.</au><au>Erukainure, Ochuko L.</au><au>Ibeji, Collins U.</au><au>Olasehinde, Tosin A.</au><au>Koorbanally, Neil A.</au><au>Islam, Md. Shahidul</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vanillin and vanillic acid modulate antioxidant defense system via amelioration of metabolic complications linked to Fe2+-induced brain tissues damage</atitle><jtitle>Metabolic brain disease</jtitle><stitle>Metab Brain Dis</stitle><date>2020-06-01</date><risdate>2020</risdate><volume>35</volume><issue>5</issue><spage>727</spage><epage>738</epage><pages>727-738</pages><issn>0885-7490</issn><eissn>1573-7365</eissn><abstract>The therapeutic effect of phenolics on neurodegenerative diseases has been attributed to their potent antioxidant properties. In the present study, the neuroprotective activities of vanillin and vanillic acid were investigated in Fe
2+
- induced oxidative toxicity in brain tissues by investigating their therapeutic effects on oxidative imbalance, cholinergic and nucleotide-hydrolyzing enzymes activities, dysregulated metabolic pathways. Their cytotoxicity was investigated in hippocampal neuronal cell lines (HT22). The reduced glutathione level, SOD and catalase activities were ameliorated in tissues treated with the phenolics, with concomitant depletion of malondialdehyde and nitric oxide levels. They inhibited acetylcholinesterase and butyrylcholinesterase activities, while concomitantly elevated ATPase activity. Treatment with vanillin led to restoration of oxidative-depleted metabolites and reactivation of the pentose phosphate and purine metabolism pathways, with concomitant activation of pathways for histidine and selenoamino metabolisms. While vanillic acid restored and reactivated oxidative-depleted metabolites and pathways but did not activate any additional pathway. Both phenolics portrayed good binding affinity for catalase, with vanillic acid having the higher binding energy of −7.0 kcal/mol. Both phenolics were not cytotoxic on HT22 cells, and their toxicity class were predicted to be 4. Only vanillin was predicted to be permeable across the blood brain barrier (BBB). These results insinuate that vanillin and vanillic acid confer a neuroprotective effect on oxidative brain damage, when vanillin being the most potent.</abstract><cop>New York</cop><pub>Springer US</pub><doi>10.1007/s11011-020-00545-y</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-0489-338X</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0885-7490 |
| ispartof | Metabolic brain disease, 2020-06, Vol.35 (5), p.727-738 |
| issn | 0885-7490 1573-7365 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2356595991 |
| source | SpringerLink Journals - AutoHoldings |
| subjects | Acetylcholinesterase Acids Activation Adenosine triphosphatase Antioxidants Biochemistry Biomedical and Life Sciences Biomedicine Blood-brain barrier Brain damage Brain injury Catalase Cell lines Cholinergics Complications Cytotoxicity Depletion Glutathione Hippocampus Histidine Iron Malondialdehyde Metabolic Diseases Metabolic pathways Metabolism Metabolites Neurodegenerative diseases Neurology Neuroprotection Neurosciences Nitric oxide Nucleotides Oncology Original Article Pentose Pentose phosphate pathway Phenols Restoration Tissues Toxicity Vanillic acid Vanillin |
| title | Vanillin and vanillic acid modulate antioxidant defense system via amelioration of metabolic complications linked to Fe2+-induced brain tissues damage |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-17T08%3A23%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Vanillin%20and%20vanillic%20acid%20modulate%20antioxidant%20defense%20system%20via%20amelioration%20of%20metabolic%20complications%20linked%20to%20Fe2+-induced%20brain%20tissues%20damage&rft.jtitle=Metabolic%20brain%20disease&rft.au=Salau,%20Veronica%20F.&rft.date=2020-06-01&rft.volume=35&rft.issue=5&rft.spage=727&rft.epage=738&rft.pages=727-738&rft.issn=0885-7490&rft.eissn=1573-7365&rft_id=info:doi/10.1007/s11011-020-00545-y&rft_dat=%3Cproquest_cross%3E2402241122%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2402241122&rft_id=info:pmid/&rfr_iscdi=true |