High dose Clopidogrel decreases mice liver mitochondrial respiration function in vitro

Yee Kit Tai, Yuh Meng Clement Cheong, Zakaria A. Almsherqi, Shu Hui Chia, Yuru Deng, Craig S. McLachlan

Research output: Contribution to journalArticle

3 Citations (Scopus)

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 μg/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.

Original languageEnglish
Pages (from-to)250-252
Number of pages3
JournalInternational Journal of Cardiology
Volume133
Issue number2
DOIs
Publication statusPublished - 3 Apr 2009
Externally publishedYes

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Keywords

  • Bioenergetics
  • Clopidogrel
  • Liver
  • Mice
  • Mitochondria
  • P2Y12

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