A study of the effects of indometacin on liver mitochondria from rats, mice and humans
A part of the mechanism of the gastrointestinal toxicity exhibited by non-steroidal anti-inflammatory drugs is believed to involve the uncoupling of mitochondrial oxidative phosphorylation. Most previous uncoupling studies have used rat liver mitochondria. There is little information on the effects...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Jacob, M. [verfasserIn] Bjarnason, I. [verfasserIn] Rafi, S. [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford UK: Blackwell Science Ltd ; 2001 |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2008 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Alimentary pharmacology & therapeutics - Oxford : Blackwell Science, 1987, 15(2001), 11, Seite 0 |
| Übergeordnetes Werk: |
volume:15 ; year:2001 ; number:11 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1046/j.1365-2036.2001.01095.x |
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NLEJ242209556 |
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| 245 | 1 | 0 | |a A study of the effects of indometacin on liver mitochondria from rats, mice and humans |
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| 520 | |a A part of the mechanism of the gastrointestinal toxicity exhibited by non-steroidal anti-inflammatory drugs is believed to involve the uncoupling of mitochondrial oxidative phosphorylation. Most previous uncoupling studies have used rat liver mitochondria. There is little information on the effects of the drugs on mitochondria from other species.<section xml:id="abs1-2"><title type="main">Aim:To study the effect of indometacin on isolated liver mitochondria from rats, mice and humans.<section xml:id="abs1-3"><title type="main">Methods:We studied the effects of indometacin on respiration and adenosine triphosphate synthesis by isolated liver mitochondria from rats, mice and humans. Its effects were compared with those of dinitrophenol, a classical uncoupler.<section xml:id="abs1-4"><title type="main">Results:Indometacin uncoupled oxidative phosphorylation at low concentrations (P < 0.05) and inhibited respiration at high concentrations (P < 0.01) in all three species. Adenosine triphosphate synthesis was, however, more sensitive to dinitrophenol or indometacin at lower concentrations in mouse and human compared to rat liver mitochondria (P < 0.05).<section xml:id="abs1-5"><title type="main">Conclusions:The current study shows that indometacin acts as an inhibitory uncoupler in human mitochondria. It also demonstrates that the responses of rat, mouse and human mitochondria to indometacin are broadly similar. | ||
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10.1046/j.1365-2036.2001.01095.x doi (DE-627)NLEJ242209556 DE-627 ger DE-627 rakwb Jacob, M. verfasserin aut A study of the effects of indometacin on liver mitochondria from rats, mice and humans Oxford UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A part of the mechanism of the gastrointestinal toxicity exhibited by non-steroidal anti-inflammatory drugs is believed to involve the uncoupling of mitochondrial oxidative phosphorylation. Most previous uncoupling studies have used rat liver mitochondria. There is little information on the effects of the drugs on mitochondria from other species.<section xml:id="abs1-2"><title type="main">Aim:To study the effect of indometacin on isolated liver mitochondria from rats, mice and humans.<section xml:id="abs1-3"><title type="main">Methods:We studied the effects of indometacin on respiration and adenosine triphosphate synthesis by isolated liver mitochondria from rats, mice and humans. Its effects were compared with those of dinitrophenol, a classical uncoupler.<section xml:id="abs1-4"><title type="main">Results:Indometacin uncoupled oxidative phosphorylation at low concentrations (P < 0.05) and inhibited respiration at high concentrations (P < 0.01) in all three species. Adenosine triphosphate synthesis was, however, more sensitive to dinitrophenol or indometacin at lower concentrations in mouse and human compared to rat liver mitochondria (P < 0.05).<section xml:id="abs1-5"><title type="main">Conclusions:The current study shows that indometacin acts as an inhibitory uncoupler in human mitochondria. It also demonstrates that the responses of rat, mouse and human mitochondria to indometacin are broadly similar. 2008 Blackwell Publishing Journal Backfiles 1879-2005 |2008|||||||||| Bjarnason, I. verfasserin aut Rafi, S. verfasserin aut Wrigglesworth, J. oth Simpson, R. J. oth In Alimentary pharmacology & therapeutics Oxford : Blackwell Science, 1987 15(2001), 11, Seite 0 Online-Ressource (DE-627)NLEJ243926529 (DE-600)2003094-0 1365-2036 nnns volume:15 year:2001 number:11 pages:0 http://dx.doi.org/10.1046/j.1365-2036.2001.01095.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 15 2001 11 0 |
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10.1046/j.1365-2036.2001.01095.x doi (DE-627)NLEJ242209556 DE-627 ger DE-627 rakwb Jacob, M. verfasserin aut A study of the effects of indometacin on liver mitochondria from rats, mice and humans Oxford UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A part of the mechanism of the gastrointestinal toxicity exhibited by non-steroidal anti-inflammatory drugs is believed to involve the uncoupling of mitochondrial oxidative phosphorylation. Most previous uncoupling studies have used rat liver mitochondria. There is little information on the effects of the drugs on mitochondria from other species.<section xml:id="abs1-2"><title type="main">Aim:To study the effect of indometacin on isolated liver mitochondria from rats, mice and humans.<section xml:id="abs1-3"><title type="main">Methods:We studied the effects of indometacin on respiration and adenosine triphosphate synthesis by isolated liver mitochondria from rats, mice and humans. Its effects were compared with those of dinitrophenol, a classical uncoupler.<section xml:id="abs1-4"><title type="main">Results:Indometacin uncoupled oxidative phosphorylation at low concentrations (P < 0.05) and inhibited respiration at high concentrations (P < 0.01) in all three species. Adenosine triphosphate synthesis was, however, more sensitive to dinitrophenol or indometacin at lower concentrations in mouse and human compared to rat liver mitochondria (P < 0.05).<section xml:id="abs1-5"><title type="main">Conclusions:The current study shows that indometacin acts as an inhibitory uncoupler in human mitochondria. It also demonstrates that the responses of rat, mouse and human mitochondria to indometacin are broadly similar. 2008 Blackwell Publishing Journal Backfiles 1879-2005 |2008|||||||||| Bjarnason, I. verfasserin aut Rafi, S. verfasserin aut Wrigglesworth, J. oth Simpson, R. J. oth In Alimentary pharmacology & therapeutics Oxford : Blackwell Science, 1987 15(2001), 11, Seite 0 Online-Ressource (DE-627)NLEJ243926529 (DE-600)2003094-0 1365-2036 nnns volume:15 year:2001 number:11 pages:0 http://dx.doi.org/10.1046/j.1365-2036.2001.01095.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 15 2001 11 0 |
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10.1046/j.1365-2036.2001.01095.x doi (DE-627)NLEJ242209556 DE-627 ger DE-627 rakwb Jacob, M. verfasserin aut A study of the effects of indometacin on liver mitochondria from rats, mice and humans Oxford UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A part of the mechanism of the gastrointestinal toxicity exhibited by non-steroidal anti-inflammatory drugs is believed to involve the uncoupling of mitochondrial oxidative phosphorylation. Most previous uncoupling studies have used rat liver mitochondria. There is little information on the effects of the drugs on mitochondria from other species.<section xml:id="abs1-2"><title type="main">Aim:To study the effect of indometacin on isolated liver mitochondria from rats, mice and humans.<section xml:id="abs1-3"><title type="main">Methods:We studied the effects of indometacin on respiration and adenosine triphosphate synthesis by isolated liver mitochondria from rats, mice and humans. Its effects were compared with those of dinitrophenol, a classical uncoupler.<section xml:id="abs1-4"><title type="main">Results:Indometacin uncoupled oxidative phosphorylation at low concentrations (P < 0.05) and inhibited respiration at high concentrations (P < 0.01) in all three species. Adenosine triphosphate synthesis was, however, more sensitive to dinitrophenol or indometacin at lower concentrations in mouse and human compared to rat liver mitochondria (P < 0.05).<section xml:id="abs1-5"><title type="main">Conclusions:The current study shows that indometacin acts as an inhibitory uncoupler in human mitochondria. It also demonstrates that the responses of rat, mouse and human mitochondria to indometacin are broadly similar. 2008 Blackwell Publishing Journal Backfiles 1879-2005 |2008|||||||||| Bjarnason, I. verfasserin aut Rafi, S. verfasserin aut Wrigglesworth, J. oth Simpson, R. J. oth In Alimentary pharmacology & therapeutics Oxford : Blackwell Science, 1987 15(2001), 11, Seite 0 Online-Ressource (DE-627)NLEJ243926529 (DE-600)2003094-0 1365-2036 nnns volume:15 year:2001 number:11 pages:0 http://dx.doi.org/10.1046/j.1365-2036.2001.01095.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 15 2001 11 0 |
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10.1046/j.1365-2036.2001.01095.x doi (DE-627)NLEJ242209556 DE-627 ger DE-627 rakwb Jacob, M. verfasserin aut A study of the effects of indometacin on liver mitochondria from rats, mice and humans Oxford UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A part of the mechanism of the gastrointestinal toxicity exhibited by non-steroidal anti-inflammatory drugs is believed to involve the uncoupling of mitochondrial oxidative phosphorylation. Most previous uncoupling studies have used rat liver mitochondria. There is little information on the effects of the drugs on mitochondria from other species.<section xml:id="abs1-2"><title type="main">Aim:To study the effect of indometacin on isolated liver mitochondria from rats, mice and humans.<section xml:id="abs1-3"><title type="main">Methods:We studied the effects of indometacin on respiration and adenosine triphosphate synthesis by isolated liver mitochondria from rats, mice and humans. Its effects were compared with those of dinitrophenol, a classical uncoupler.<section xml:id="abs1-4"><title type="main">Results:Indometacin uncoupled oxidative phosphorylation at low concentrations (P < 0.05) and inhibited respiration at high concentrations (P < 0.01) in all three species. Adenosine triphosphate synthesis was, however, more sensitive to dinitrophenol or indometacin at lower concentrations in mouse and human compared to rat liver mitochondria (P < 0.05).<section xml:id="abs1-5"><title type="main">Conclusions:The current study shows that indometacin acts as an inhibitory uncoupler in human mitochondria. It also demonstrates that the responses of rat, mouse and human mitochondria to indometacin are broadly similar. 2008 Blackwell Publishing Journal Backfiles 1879-2005 |2008|||||||||| Bjarnason, I. verfasserin aut Rafi, S. verfasserin aut Wrigglesworth, J. oth Simpson, R. J. oth In Alimentary pharmacology & therapeutics Oxford : Blackwell Science, 1987 15(2001), 11, Seite 0 Online-Ressource (DE-627)NLEJ243926529 (DE-600)2003094-0 1365-2036 nnns volume:15 year:2001 number:11 pages:0 http://dx.doi.org/10.1046/j.1365-2036.2001.01095.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 15 2001 11 0 |
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10.1046/j.1365-2036.2001.01095.x doi (DE-627)NLEJ242209556 DE-627 ger DE-627 rakwb Jacob, M. verfasserin aut A study of the effects of indometacin on liver mitochondria from rats, mice and humans Oxford UK Blackwell Science Ltd 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier A part of the mechanism of the gastrointestinal toxicity exhibited by non-steroidal anti-inflammatory drugs is believed to involve the uncoupling of mitochondrial oxidative phosphorylation. Most previous uncoupling studies have used rat liver mitochondria. There is little information on the effects of the drugs on mitochondria from other species.<section xml:id="abs1-2"><title type="main">Aim:To study the effect of indometacin on isolated liver mitochondria from rats, mice and humans.<section xml:id="abs1-3"><title type="main">Methods:We studied the effects of indometacin on respiration and adenosine triphosphate synthesis by isolated liver mitochondria from rats, mice and humans. Its effects were compared with those of dinitrophenol, a classical uncoupler.<section xml:id="abs1-4"><title type="main">Results:Indometacin uncoupled oxidative phosphorylation at low concentrations (P < 0.05) and inhibited respiration at high concentrations (P < 0.01) in all three species. Adenosine triphosphate synthesis was, however, more sensitive to dinitrophenol or indometacin at lower concentrations in mouse and human compared to rat liver mitochondria (P < 0.05).<section xml:id="abs1-5"><title type="main">Conclusions:The current study shows that indometacin acts as an inhibitory uncoupler in human mitochondria. It also demonstrates that the responses of rat, mouse and human mitochondria to indometacin are broadly similar. 2008 Blackwell Publishing Journal Backfiles 1879-2005 |2008|||||||||| Bjarnason, I. verfasserin aut Rafi, S. verfasserin aut Wrigglesworth, J. oth Simpson, R. J. oth In Alimentary pharmacology & therapeutics Oxford : Blackwell Science, 1987 15(2001), 11, Seite 0 Online-Ressource (DE-627)NLEJ243926529 (DE-600)2003094-0 1365-2036 nnns volume:15 year:2001 number:11 pages:0 http://dx.doi.org/10.1046/j.1365-2036.2001.01095.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 15 2001 11 0 |
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A study of the effects of indometacin on liver mitochondria from rats, mice and humans |
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A part of the mechanism of the gastrointestinal toxicity exhibited by non-steroidal anti-inflammatory drugs is believed to involve the uncoupling of mitochondrial oxidative phosphorylation. Most previous uncoupling studies have used rat liver mitochondria. There is little information on the effects of the drugs on mitochondria from other species.<section xml:id="abs1-2"><title type="main">Aim:To study the effect of indometacin on isolated liver mitochondria from rats, mice and humans.<section xml:id="abs1-3"><title type="main">Methods:We studied the effects of indometacin on respiration and adenosine triphosphate synthesis by isolated liver mitochondria from rats, mice and humans. Its effects were compared with those of dinitrophenol, a classical uncoupler.<section xml:id="abs1-4"><title type="main">Results:Indometacin uncoupled oxidative phosphorylation at low concentrations (P < 0.05) and inhibited respiration at high concentrations (P < 0.01) in all three species. Adenosine triphosphate synthesis was, however, more sensitive to dinitrophenol or indometacin at lower concentrations in mouse and human compared to rat liver mitochondria (P < 0.05).<section xml:id="abs1-5"><title type="main">Conclusions:The current study shows that indometacin acts as an inhibitory uncoupler in human mitochondria. It also demonstrates that the responses of rat, mouse and human mitochondria to indometacin are broadly similar. |
| abstractGer |
A part of the mechanism of the gastrointestinal toxicity exhibited by non-steroidal anti-inflammatory drugs is believed to involve the uncoupling of mitochondrial oxidative phosphorylation. Most previous uncoupling studies have used rat liver mitochondria. There is little information on the effects of the drugs on mitochondria from other species.<section xml:id="abs1-2"><title type="main">Aim:To study the effect of indometacin on isolated liver mitochondria from rats, mice and humans.<section xml:id="abs1-3"><title type="main">Methods:We studied the effects of indometacin on respiration and adenosine triphosphate synthesis by isolated liver mitochondria from rats, mice and humans. Its effects were compared with those of dinitrophenol, a classical uncoupler.<section xml:id="abs1-4"><title type="main">Results:Indometacin uncoupled oxidative phosphorylation at low concentrations (P < 0.05) and inhibited respiration at high concentrations (P < 0.01) in all three species. Adenosine triphosphate synthesis was, however, more sensitive to dinitrophenol or indometacin at lower concentrations in mouse and human compared to rat liver mitochondria (P < 0.05).<section xml:id="abs1-5"><title type="main">Conclusions:The current study shows that indometacin acts as an inhibitory uncoupler in human mitochondria. It also demonstrates that the responses of rat, mouse and human mitochondria to indometacin are broadly similar. |
| abstract_unstemmed |
A part of the mechanism of the gastrointestinal toxicity exhibited by non-steroidal anti-inflammatory drugs is believed to involve the uncoupling of mitochondrial oxidative phosphorylation. Most previous uncoupling studies have used rat liver mitochondria. There is little information on the effects of the drugs on mitochondria from other species.<section xml:id="abs1-2"><title type="main">Aim:To study the effect of indometacin on isolated liver mitochondria from rats, mice and humans.<section xml:id="abs1-3"><title type="main">Methods:We studied the effects of indometacin on respiration and adenosine triphosphate synthesis by isolated liver mitochondria from rats, mice and humans. Its effects were compared with those of dinitrophenol, a classical uncoupler.<section xml:id="abs1-4"><title type="main">Results:Indometacin uncoupled oxidative phosphorylation at low concentrations (P < 0.05) and inhibited respiration at high concentrations (P < 0.01) in all three species. Adenosine triphosphate synthesis was, however, more sensitive to dinitrophenol or indometacin at lower concentrations in mouse and human compared to rat liver mitochondria (P < 0.05).<section xml:id="abs1-5"><title type="main">Conclusions:The current study shows that indometacin acts as an inhibitory uncoupler in human mitochondria. It also demonstrates that the responses of rat, mouse and human mitochondria to indometacin are broadly similar. |
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