作者: M. Jacob , I. Bjarnason , S. Rafi , J. Wrigglesworth , R. J. Simpson
DOI: 10.1046/J.1365-2036.2001.01095.X
关键词: Oxidative phosphorylation 、 Mechanism of action 、 Dinitrophenol 、 Adenosine triphosphate 、 Toxicity 、 Indometacin 、 Internal medicine 、 Biology 、 Enzyme inhibitor 、 Endocrinology 、 Mitochondrion 、 Pharmacology (medical)
摘要: Background: A part of the mechanism gastrointestinal toxicity exhibited by non-steroidal anti-inflammatory drugs is believed to involve uncoupling mitochondrial oxidative phosphorylation. Most previous studies have used rat liver mitochondria. There little information on effects mitochondria from other species. Aim: To study effect indometacin isolated rats, mice and humans. Methods: We studied respiration adenosine triphosphate synthesis humans. Its were compared with those dinitrophenol, a classical uncoupler. Results: Indometacin uncoupled phosphorylation at low concentrations (P < 0.05) inhibited high (P < 0.01) in all three species. Adenosine was, however, more sensitive dinitrophenol or lower mouse human (P < 0.05). Conclusions: The current shows that acts as an inhibitory uncoupler It also demonstrates responses rat, are broadly similar.