Mechanisms of Ascorbyl Radical Formation in Human Platelet-Rich Plasma
Identifieur interne : 002842 ( Main/Exploration ); précédent : 002841; suivant : 002843Mechanisms of Ascorbyl Radical Formation in Human Platelet-Rich Plasma
Auteurs : Kou-Gi Shyu [Taïwan] ; Chao-Chien Chang [Taïwan] ; Yu-Chieh Yeh [Taïwan] ; Joen-Rong Sheu [Taïwan] ; Duen-Suey Chou [Taïwan]Source :
- BioMed Research International [ 2314-6133 ] ; 2014.
Abstract
Recently, many clinical reports have suggested that the ascorbyl free radical (Asc∙) can be treated as a noninvasive, reliable, real-time marker of oxidative stress, but its generation mechanisms in human blood have rarely been discussed. In this study, we used upstream substances, enzyme inhibitors, and free radical scavengers to delineate the mechanisms of Asc∙ formation in human platelet-rich plasma (PRP). Our results show that the doublet signal was detected in PRP samples by using electron spin resonance, and the hyperfine splitting of the doublet signal was
Url:
DOI: 10.1155/2014/614506
PubMed: 24696859
PubMed Central: 3947840
Affiliations:
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Wu-Hsing Street, Taipei 110, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Clinical Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation></author><author><name sortKey="Chang, Chao Chien" sort="Chang, Chao Chien" uniqKey="Chang C" first="Chao-Chien" last="Chang">Chao-Chien Chang</name><affiliation wicri:level="1"><nlm:aff id="I3">Department of Cardiology, Cathay General Hospital, 280 Jen Ai Road, Section 4, Taipei 106, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Cardiology, Cathay General Hospital, 280 Jen Ai Road, Section 4, Taipei 106</wicri:regionArea><wicri:noRegion>Taipei 106</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="I4">Graduate Institute of Medical Sciences, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan</nlm:aff><country 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250 Wu-Hsing Street, Taipei 110, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Medical Sciences, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="I5">Department of Pharmacology, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Pharmacology, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation></author><author><name sortKey="Chou, Duen Suey" sort="Chou, Duen Suey" uniqKey="Chou D" first="Duen-Suey" last="Chou">Duen-Suey Chou</name><affiliation wicri:level="1"><nlm:aff id="I5">Department of Pharmacology, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Pharmacology, Taipei Medical University, 250 Wu-Hsing Street, Taipei 110</wicri:regionArea><wicri:noRegion>Taipei 110</wicri:noRegion></affiliation></author></analytic><series><title level="j">BioMed Research International</title><idno type="ISSN">2314-6133</idno><idno type="eISSN">2314-6141</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Recently, many clinical reports have suggested that the ascorbyl free radical (Asc<sup>∙</sup>) can be treated as a noninvasive, reliable, real-time marker of oxidative stress, but its generation mechanisms in human blood have rarely been discussed. In this study, we used upstream substances, enzyme inhibitors, and free radical scavengers to delineate the mechanisms of Asc<sup>∙</sup> formation in human platelet-rich plasma (PRP). Our results show that the doublet signal was detected in PRP samples by using electron spin resonance, and the hyperfine splitting of the doublet signal was <italic>a</italic><sup>H</sup> = 1.88 gauss and <italic>g</italic>-factor = 2.00627, which was determined to be the Asc<sup>∙</sup>. We observed that the inhibitors of NADPH oxidase (NOX), cyclooxygenase (COX), lipoxygenase (LOX), cytochrome P450 (CYP450), mitochondria complex III, and nitric oxide synthase (NOS), but not xanthine oxidase, diminished the intensity of the Asc<sup>∙</sup> signal dose dependently. All enzyme inhibitors showed no obvious antioxidant activity during a Fenton reaction assay. In summary, the obtained data suggest that Asc<sup>∙</sup> formation is associated with NOX, COX, LOX, CYP450, eNOS, and mitochondria in human PRP.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Valko, M" uniqKey="Valko M">M Valko</name></author><author><name sortKey="Leibfritz, D" uniqKey="Leibfritz D">D Leibfritz</name></author><author><name sortKey="Moncol, J" uniqKey="Moncol J">J Moncol</name></author><author><name sortKey="Cronin, Mtd" uniqKey="Cronin M">MTD Cronin</name></author><author><name sortKey="Mazur, M" uniqKey="Mazur M">M Mazur</name></author><author><name sortKey="Telser, J" uniqKey="Telser J">J Telser</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rice Evans, C" uniqKey="Rice Evans C">C Rice-Evans</name></author><author><name sortKey="Miller, N" uniqKey="Miller N">N Miller</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kokic, An" 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sortKey="Radomski, Mw" uniqKey="Radomski M">MW Radomski</name></author><author><name sortKey="Palmer, Rmj" uniqKey="Palmer R">RMJ Palmer</name></author><author><name sortKey="Moncada, S" uniqKey="Moncada S">S Moncada</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Shyu, Kou Gi" sort="Shyu, Kou Gi" uniqKey="Shyu K" first="Kou-Gi" last="Shyu">Kou-Gi Shyu</name></noRegion><name sortKey="Chang, Chao Chien" sort="Chang, Chao Chien" uniqKey="Chang C" first="Chao-Chien" last="Chang">Chao-Chien Chang</name><name sortKey="Chang, Chao Chien" sort="Chang, Chao Chien" uniqKey="Chang C" first="Chao-Chien" last="Chang">Chao-Chien Chang</name><name sortKey="Chou, Duen Suey" sort="Chou, Duen Suey" uniqKey="Chou D" first="Duen-Suey" last="Chou">Duen-Suey Chou</name><name sortKey="Sheu, Joen Rong" sort="Sheu, Joen Rong" uniqKey="Sheu J" first="Joen-Rong" last="Sheu">Joen-Rong Sheu</name><name sortKey="Sheu, Joen Rong" sort="Sheu, Joen Rong" uniqKey="Sheu J" first="Joen-Rong" last="Sheu">Joen-Rong Sheu</name><name sortKey="Shyu, Kou Gi" sort="Shyu, Kou Gi" uniqKey="Shyu K" first="Kou-Gi" last="Shyu">Kou-Gi Shyu</name><name sortKey="Yeh, Yu Chieh" sort="Yeh, Yu Chieh" uniqKey="Yeh Y" first="Yu-Chieh" last="Yeh">Yu-Chieh Yeh</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:24696859" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a LymphedemaV1
| This area was generated with Dilib version V0.6.31. |  |