Cystamine metabolism and brain transport properties: clinical implications for neurodegenerative diseases
Identifieur interne : 000376 ( PascalFrancis/Checkpoint ); précédent : 000375; suivant : 000377Cystamine metabolism and brain transport properties: clinical implications for neurodegenerative diseases
Auteurs : Mélanie Bousquet [Canada] ; Claire Gibrat [Canada] ; Mélissa Ouellet [Canada] ; Claude Rouillard [Canada] ; Frédéric Calon [Canada] ; Francesca Cicchetti [Canada]Source :
- Journal of neurochemistry [ 0022-3042 ] ; 2010.
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Abstract
Cystamine has shown significant neuroprotective properties in preclinical studies of Parkinson's disease (PD) and Hunting-ton's disease (HD). Cysteamine, its FDA-approved reduced form, is scheduled to be tested for clinical efficacy in HD patients. Here, we studied the key cystamine metabolites, namely cysteamine, hypotaurine and taurine, as well as cysteine, in order to identify which one is more distinctively responsible for the neuroprotective action of cystamine. After a single administration of cystamine (10, 50 or 200 mg/kg), naive mice were perfused with phosphate-buffered saline (PBS) at 1, 3, 12, 24 or 48 h post-injection and brain and plasma samples were analyzed by two distinct HPLC methods. Although plasma levels remained under the detection threshold, significant increases in cysteamine brain levels were detected with the 50 and 200 mg/kg doses in mice perfused 1 and 3 h following cystamine injection. To further assess cysteamine as the candidate molecule for pre-clinical and clinical trials in PD, we evaluated its capacity to cross the blood brain barrier. Using an in situ cerebral perfusion technique, we determined that the brain transport coefficient (Clup) of cysteamine (259 μM) was 0.15 ± 0.02 μL/g/s and was increased up to 0.34 ± 0.07 μL/g/s when co-perfused in the presence of cysteine. Taken together, these results strongly suggest that cysteamine is the neuroactive metabolite of cystamine and may further support its therapeutic use in neurodegenerative diseases, particularly in HD and PD.
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aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Québec, Québec</wicri:noRegion></affiliation></author><author><name sortKey="Calon, Frederic" sort="Calon, Frederic" uniqKey="Calon F" first="Frédéric" last="Calon">Frédéric Calon</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Centre de Recherche du CHUL (CHUQ), Axe Neurosciences</s1><s2>Québec, Québec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Québec, Québec</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Faculté de Pharmacie, Université Laval</s1><s2>Québec, Québec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Québec, Québec</wicri:noRegion></affiliation></author><author><name sortKey="Cicchetti, Francesca" sort="Cicchetti, Francesca" uniqKey="Cicchetti F" first="Francesca" last="Cicchetti">Francesca Cicchetti</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Centre de Recherche du CHUL (CHUQ), Axe Neurosciences</s1><s2>Québec, Québec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Québec, Québec</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Département de Psychiatrie et Neurosciences, Université Laval</s1><s2>Québec, Québec</s2><s3>CAN</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Québec, Québec</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Biological transport</term><term>Blood brain barrier</term><term>Clinical test</term><term>Cysteine</term><term>Detection threshold</term><term>Encephalon</term><term>Metabolism</term><term>Metabolite</term><term>Mouse</term><term>Parkinson disease</term><term>Perfusion</term><term>Phosphates</term><term>Taurine</term><term>Threshold detection</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Métabolisme</term><term>Encéphale</term><term>Transport biologique</term><term>Test clinique</term><term>Métabolite</term><term>Taurine</term><term>Cystéine</term><term>Phosphate</term><term>Maladie de Parkinson</term><term>Seuil détection</term><term>Détection seuil</term><term>Barrière hématoencéphalique</term><term>Perfusion</term><term>Souris</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Phosphate</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cystamine has shown significant neuroprotective properties in preclinical studies of Parkinson's disease (PD) and Hunting-ton's disease (HD). Cysteamine, its FDA-approved reduced form, is scheduled to be tested for clinical efficacy in HD patients. Here, we studied the key cystamine metabolites, namely cysteamine, hypotaurine and taurine, as well as cysteine, in order to identify which one is more distinctively responsible for the neuroprotective action of cystamine. After a single administration of cystamine (10, 50 or 200 mg/kg), naive mice were perfused with phosphate-buffered saline (PBS) at 1, 3, 12, 24 or 48 h post-injection and brain and plasma samples were analyzed by two distinct HPLC methods. Although plasma levels remained under the detection threshold, significant increases in cysteamine brain levels were detected with the 50 and 200 mg/kg doses in mice perfused 1 and 3 h following cystamine injection. To further assess cysteamine as the candidate molecule for pre-clinical and clinical trials in PD, we evaluated its capacity to cross the blood brain barrier. Using an in situ cerebral perfusion technique, we determined that the brain transport coefficient (Clup) of cysteamine (259 μM) was 0.15 ± 0.02 μL/g/s and was increased up to 0.34 ± 0.07 μL/g/s when co-perfused in the presence of cysteine. Taken together, these results strongly suggest that cysteamine is the neuroactive metabolite of cystamine and may further support its therapeutic use in neurodegenerative diseases, particularly in HD and PD.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-3042</s0></fA01><fA02 i1="01"><s0>JONRA9</s0></fA02><fA03 i2="1"><s0>J. neurochem.</s0></fA03><fA05><s2>114</s2></fA05><fA06><s2>6</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Cystamine metabolism and brain transport properties: clinical implications for neurodegenerative diseases</s1></fA08><fA11 i1="01" i2="1"><s1>BOUSQUET (Mélanie)</s1></fA11><fA11 i1="02" i2="1"><s1>GIBRAT (Claire)</s1></fA11><fA11 i1="03" i2="1"><s1>OUELLET (Mélissa)</s1></fA11><fA11 i1="04" i2="1"><s1>ROUILLARD (Claude)</s1></fA11><fA11 i1="05" i2="1"><s1>CALON (Frédéric)</s1></fA11><fA11 i1="06" i2="1"><s1>CICCHETTI (Francesca)</s1></fA11><fA14 i1="01"><s1>Centre de Recherche du CHUL (CHUQ), Axe Neurosciences</s1><s2>Québec, Québec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="02"><s1>Département de Psychiatrie et Neurosciences, Université Laval</s1><s2>Québec, Québec</s2><s3>CAN</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="03"><s1>Faculté de Pharmacie, Université Laval</s1><s2>Québec, Québec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></fA14><fA20><s1>1651-1658</s1></fA20><fA21><s1>2010</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>4037</s2><s5>354000192648950110</s5></fA43><fA44><s0>0000</s0><s1>© 2010 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.1/4</s0></fA45><fA47 i1="01" i2="1"><s0>10-0434654</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of neurochemistry</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>Cystamine has shown significant neuroprotective properties in preclinical studies of Parkinson's disease (PD) and Hunting-ton's disease (HD). Cysteamine, its FDA-approved reduced form, is scheduled to be tested for clinical efficacy in HD patients. Here, we studied the key cystamine metabolites, namely cysteamine, hypotaurine and taurine, as well as cysteine, in order to identify which one is more distinctively responsible for the neuroprotective action of cystamine. After a single administration of cystamine (10, 50 or 200 mg/kg), naive mice were perfused with phosphate-buffered saline (PBS) at 1, 3, 12, 24 or 48 h post-injection and brain and plasma samples were analyzed by two distinct HPLC methods. Although plasma levels remained under the detection threshold, significant increases in cysteamine brain levels were detected with the 50 and 200 mg/kg doses in mice perfused 1 and 3 h following cystamine injection. To further assess cysteamine as the candidate molecule for pre-clinical and clinical trials in PD, we evaluated its capacity to cross the blood brain barrier. Using an in situ cerebral perfusion technique, we determined that the brain transport coefficient (Clup) of cysteamine (259 μM) was 0.15 ± 0.02 μL/g/s and was increased up to 0.34 ± 0.07 μL/g/s when co-perfused in the presence of cysteine. Taken together, these results strongly suggest that cysteamine is the neuroactive metabolite of cystamine and may further support its therapeutic use in neurodegenerative diseases, particularly in HD and PD.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC02 i1="02" i2="X"><s0>002B17A01</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Métabolisme</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Metabolism</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Metabolismo</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Encéphale</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Encephalon</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Encéfalo</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Transport biologique</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Biological transport</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Transporte biológico</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Test 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l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fN21><s1>284</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard></inist><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Bousquet, Melanie" sort="Bousquet, Melanie" uniqKey="Bousquet M" first="Mélanie" last="Bousquet">Mélanie Bousquet</name></noRegion><name sortKey="Bousquet, Melanie" sort="Bousquet, Melanie" uniqKey="Bousquet M" first="Mélanie" last="Bousquet">Mélanie Bousquet</name><name sortKey="Calon, Frederic" sort="Calon, Frederic" uniqKey="Calon F" first="Frédéric" last="Calon">Frédéric Calon</name><name sortKey="Calon, Frederic" sort="Calon, Frederic" uniqKey="Calon F" first="Frédéric" last="Calon">Frédéric Calon</name><name sortKey="Cicchetti, Francesca" sort="Cicchetti, Francesca" uniqKey="Cicchetti F" first="Francesca" last="Cicchetti">Francesca Cicchetti</name><name sortKey="Cicchetti, Francesca" sort="Cicchetti, Francesca" uniqKey="Cicchetti F" first="Francesca" last="Cicchetti">Francesca Cicchetti</name><name sortKey="Gibrat, Claire" sort="Gibrat, Claire" uniqKey="Gibrat C" first="Claire" last="Gibrat">Claire Gibrat</name><name sortKey="Ouellet, Melissa" sort="Ouellet, Melissa" uniqKey="Ouellet M" first="Mélissa" last="Ouellet">Mélissa Ouellet</name><name sortKey="Ouellet, Melissa" sort="Ouellet, Melissa" uniqKey="Ouellet M" first="Mélissa" last="Ouellet">Mélissa Ouellet</name><name sortKey="Rouillard, Claude" sort="Rouillard, Claude" uniqKey="Rouillard C" first="Claude" last="Rouillard">Claude Rouillard</name><name sortKey="Rouillard, Claude" sort="Rouillard, Claude" uniqKey="Rouillard C" first="Claude" last="Rouillard">Claude Rouillard</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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