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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Effects of Hydrogen Sulfide-releasing <sc>l</sc>-DOPA Derivatives on Glial Activation</title><author><name sortKey="Lee, Moonhee" sort="Lee, Moonhee" uniqKey="Lee M" first="Moonhee" last="Lee">Moonhee Lee</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Tazzari, Valerio" sort="Tazzari, Valerio" uniqKey="Tazzari V" first="Valerio" last="Tazzari">Valerio Tazzari</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Giustarini, Daniela" sort="Giustarini, Daniela" uniqKey="Giustarini D" first="Daniela" last="Giustarini">Daniela Giustarini</name><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author><author><name sortKey="Rossi, Ranieri" sort="Rossi, Ranieri" uniqKey="Rossi R" first="Ranieri" last="Rossi">Ranieri Rossi</name><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author><author><name sortKey="Sparatore, Anna" sort="Sparatore, Anna" uniqKey="Sparatore A" first="Anna" last="Sparatore">Anna Sparatore</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Del Soldato, Piero" sort="Del Soldato, Piero" uniqKey="Del Soldato P" first="Piero" last="Del Soldato">Piero Del Soldato</name><affiliation><nlm:aff id="aff4">CTG Pharma, Viale Gran Sasso 17, 20131 Milano, Italy</nlm:aff></affiliation></author><author><name sortKey="Mcgeer, Edith" sort="Mcgeer, Edith" uniqKey="Mcgeer E" first="Edith" last="Mcgeer">Edith Mcgeer</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">20368333</idno><idno type="pmc">2878495</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878495</idno><idno type="RBID">PMC:2878495</idno><idno type="doi">10.1074/jbc.M110.115261</idno><date when="2010">2010</date><idno type="wicri:Area/Pmc/Corpus">000550</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000550</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Effects of Hydrogen Sulfide-releasing <sc>l</sc>-DOPA Derivatives on Glial Activation</title><author><name sortKey="Lee, Moonhee" sort="Lee, Moonhee" uniqKey="Lee M" first="Moonhee" last="Lee">Moonhee Lee</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Tazzari, Valerio" sort="Tazzari, Valerio" uniqKey="Tazzari V" first="Valerio" last="Tazzari">Valerio Tazzari</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Giustarini, Daniela" sort="Giustarini, Daniela" uniqKey="Giustarini D" first="Daniela" last="Giustarini">Daniela Giustarini</name><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author><author><name sortKey="Rossi, Ranieri" sort="Rossi, Ranieri" uniqKey="Rossi R" first="Ranieri" last="Rossi">Ranieri Rossi</name><affiliation><nlm:aff id="aff3"></nlm:aff></affiliation></author><author><name sortKey="Sparatore, Anna" sort="Sparatore, Anna" uniqKey="Sparatore A" first="Anna" last="Sparatore">Anna Sparatore</name><affiliation><nlm:aff id="aff2"></nlm:aff></affiliation></author><author><name sortKey="Del Soldato, Piero" sort="Del Soldato, Piero" uniqKey="Del Soldato P" first="Piero" last="Del Soldato">Piero Del Soldato</name><affiliation><nlm:aff id="aff4">CTG Pharma, Viale Gran Sasso 17, 20131 Milano, Italy</nlm:aff></affiliation></author><author><name sortKey="Mcgeer, Edith" sort="Mcgeer, Edith" uniqKey="Mcgeer E" first="Edith" last="Mcgeer">Edith Mcgeer</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">The Journal of Biological Chemistry</title><idno type="ISSN">0021-9258</idno><idno type="eISSN">1083-351X</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The main lesion in Parkinson disease (PD) is loss of substantia nigra dopaminergic neurons. Levodopa (<sc>l</sc>-DOPA) is the most widely used therapy, but it does not arrest disease progression. Some possible contributing factors to the continuing neuronal loss are oxidative stress, including oxidation of <sc>l</sc>-DOPA, and neurotoxins generated by locally activated microglia and astrocytes. A possible method of reducing these factors is to produce <sc>l</sc>-DOPA hybrid compounds that have antioxidant and antiinflammatory properties. Here we demonstrate the properties of four such <sc>l</sc>-DOPA hybrids based on coupling <sc>l</sc>-DOPA to four different hydrogen sulfide-donating compounds. The donors themselves were shown to be capable of conversion by isolated mitochondria to H<sub>2</sub>S or equivalent SH<sup>−</sup> ions. This capability was confirmed by <italic>in vivo</italic> results, showing a large increase in intracerebral dopamine and glutathione after iv administration in rats. When human microglia, astrocytes, and SH-SY5Y neuroblastoma cells were treated with these donating agents, they all accumulated H<sub>2</sub>S intracellularly as did their derivatives coupled to <sc>l</sc>-DOPA. The donating agents and the <sc>l</sc>-DOPA hybrids reduced the release of tumor necrosis factor-α, interleukin-6, and nitric oxide from stimulated microglia, astrocytes as well as the THP-1 and U373 cell lines. They also demonstrated a neuroprotective effect by reducing the toxicity of supernatants from these stimulated cells to SH-SY5Y cells. <sc>l</sc>-DOPA itself was without effect in any of these assays. The H<sub>2</sub>S-releasing <sc>l</sc>-DOPA hybrid molecules also inhibited MAO B activity. They may be useful for the treatment of PD because of their significant antiinflammatory, antioxidant, and neuroprotective properties.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Biol Chem</journal-id><journal-id journal-id-type="hwp">jbc</journal-id><journal-id journal-id-type="pmc">jbc</journal-id><journal-id journal-id-type="publisher-id">JBC</journal-id><journal-title-group><journal-title>The Journal of Biological Chemistry</journal-title></journal-title-group><issn pub-type="ppub">0021-9258</issn><issn pub-type="epub">1083-351X</issn><publisher><publisher-name>American Society for Biochemistry and Molecular Biology</publisher-name><publisher-loc>9650 Rockville Pike, Bethesda, MD 20814, U.S.A.</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">20368333</article-id><article-id pub-id-type="pmc">2878495</article-id><article-id pub-id-type="publisher-id">M110.115261</article-id><article-id pub-id-type="doi">10.1074/jbc.M110.115261</article-id><article-categories><subj-group subj-group-type="heading"><subject>Molecular Bases of Disease</subject></subj-group></article-categories><title-group><article-title>Effects of Hydrogen Sulfide-releasing <sc>l</sc>-DOPA Derivatives on Glial Activation</article-title><subtitle>POTENTIAL FOR TREATING PARKINSON DISEASE<xref ref-type="fn" rid="FN1">*</xref><xref ref-type="fn" rid="FN2"><sup><inline-graphic xlink:href="sbox.jpg"></inline-graphic></sup></xref></subtitle></title-group><contrib-group><contrib contrib-type="author"><name><surname>Lee</surname><given-names>Moonhee</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>Tazzari</surname><given-names>Valerio</given-names></name><xref ref-type="aff" rid="aff2"><sup>§</sup></xref></contrib><contrib contrib-type="author"><name><surname>Giustarini</surname><given-names>Daniela</given-names></name><xref ref-type="aff" rid="aff3"><sup>¶</sup></xref></contrib><contrib contrib-type="author"><name><surname>Rossi</surname><given-names>Ranieri</given-names></name><xref ref-type="aff" rid="aff3"><sup>¶</sup></xref></contrib><contrib contrib-type="author"><name><surname>Sparatore</surname><given-names>Anna</given-names></name><xref ref-type="aff" rid="aff2"><sup>§</sup></xref></contrib><contrib contrib-type="author"><name><surname>Del Soldato</surname><given-names>Piero</given-names></name><xref ref-type="aff" rid="aff4"><sup>‖</sup></xref></contrib><contrib contrib-type="author"><name><surname>McGeer</surname><given-names>Edith</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref></contrib><contrib contrib-type="author"><name><surname>McGeer</surname><given-names>Patrick L.</given-names></name><xref ref-type="aff" rid="aff1"><sup>‡</sup></xref><xref ref-type="corresp" rid="cor1"><sup>1</sup></xref></contrib><aff id="aff1">From the<label>‡</label>Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada,</aff><aff id="aff2">the<label>§</label>Dipartimento di Scienze Farmaceutiche Pietro Pratesi, Università degli Studi di Milano, Via Mangiagalli 25, 20133, Milano, Italy,</aff><aff id="aff3">the<label>¶</label>Department of Evolutionary Biology, Laboratory of Pharmacology and Toxicology, University of Siena, via A. Moro 4, I-53100, Siena, Italy, and</aff><aff id="aff4"><label>‖</label>CTG Pharma, Viale Gran Sasso 17, 20131 Milano, Italy</aff></contrib-group><author-notes><corresp id="cor1"><label>1</label> To whom correspondence should be addressed: <addr-line>Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada.</addr-line> Tel.: <phone>604-822-7377</phone>; Fax: <fax>604-822-7086</fax>; E-mail: <email>mcgeerpl@interchange.ubc.ca</email>.</corresp></author-notes><pub-date pub-type="ppub"><day>4</day><month>6</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>5</day><month>4</month><year>2010</year></pub-date><volume>285</volume><issue>23</issue><fpage>17318</fpage><lpage>17328</lpage><history><date date-type="received"><day>17</day><month>2</month><year>2010</year></date><date date-type="rev-recd"><day>26</day><month>3</month><year>2010</year></date></history><permissions><copyright-statement>© 2010 by The American Society for Biochemistry and Molecular Biology, Inc.</copyright-statement></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zbc02310017318.pdf"></self-uri><abstract><p>The main lesion in Parkinson disease (PD) is loss of substantia nigra dopaminergic neurons. Levodopa (<sc>l</sc>-DOPA) is the most widely used therapy, but it does not arrest disease progression. Some possible contributing factors to the continuing neuronal loss are oxidative stress, including oxidation of <sc>l</sc>-DOPA, and neurotoxins generated by locally activated microglia and astrocytes. A possible method of reducing these factors is to produce <sc>l</sc>-DOPA hybrid compounds that have antioxidant and antiinflammatory properties. Here we demonstrate the properties of four such <sc>l</sc>-DOPA hybrids based on coupling <sc>l</sc>-DOPA to four different hydrogen sulfide-donating compounds. The donors themselves were shown to be capable of conversion by isolated mitochondria to H<sub>2</sub>S or equivalent SH<sup>−</sup> ions. This capability was confirmed by <italic>in vivo</italic> results, showing a large increase in intracerebral dopamine and glutathione after iv administration in rats. When human microglia, astrocytes, and SH-SY5Y neuroblastoma cells were treated with these donating agents, they all accumulated H<sub>2</sub>S intracellularly as did their derivatives coupled to <sc>l</sc>-DOPA. The donating agents and the <sc>l</sc>-DOPA hybrids reduced the release of tumor necrosis factor-α, interleukin-6, and nitric oxide from stimulated microglia, astrocytes as well as the THP-1 and U373 cell lines. They also demonstrated a neuroprotective effect by reducing the toxicity of supernatants from these stimulated cells to SH-SY5Y cells. <sc>l</sc>-DOPA itself was without effect in any of these assays. The H<sub>2</sub>S-releasing <sc>l</sc>-DOPA hybrid molecules also inhibited MAO B activity. They may be useful for the treatment of PD because of their significant antiinflammatory, antioxidant, and neuroprotective properties.</p></abstract><kwd-group><kwd>Cytokine</kwd><kwd>Neurodegeneration</kwd><kwd>Neurological Diseases</kwd><kwd>Nitric Oxide</kwd><kwd>Parkinsons Disease</kwd><kwd>GSH</kwd><kwd>Astroglia</kwd><kwd>Microglia</kwd><kwd>Monoamine Oxidase</kwd><kwd>Neuroinflammation</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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