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.
