High dose clopidogrel decreases mice liver mitochondrial respiration function in vitro

International Journal of Cardiology
Yee Kit TaiCraig S McLachlan

Abstract

The effects of clopidogrel on mitochondrial respiratory function have not been previously investigated. We show in vitro that isolated mice liver mitochondria treated with very high doses of clopidogrel 10 microg/ml significantly reduces pre-treatment mitochondrial respiratory state 3 (P<0.05) and state 4 respiration (P<0.01), while oxygen consumption in State 3 is prolonged. This suggests a compromise to mitochondrial oxidative phosphorylation following the addition of high dose clopidogrel. Because clopidogrel at human therapeutic doses 40 ng/ml did not affect isolated mitochondrial respiration, it is thus unlikely, in the absence of cellular bioaccumulation, that clinical doses of clopidogrel would affect mitochondrial bioenergetics in vivo.

References

Jun 1, 1986·Biochemical Pharmacology·S Abou-KhalilA A Yunis
Aug 22, 2006·International Journal of Cardiology·Zakaria A AlmsherqiSadik M Sharef
Feb 13, 2007·Brain Research Bulletin·Patryk KrzeminskiJolanta Brańska
Jun 2, 2007·Alimentary Pharmacology & Therapeutics·M SabatéJ-R Laporte

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Citations

Oct 22, 2014·Expert Opinion on Drug Metabolism & Toxicology·Josef Finsterer, Sinda Zarrouk-Mahjoub

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