Please use this identifier to cite or link to this item:
|Title:||High dose Clopidogrel decreases mice liver mitochondrial respiration function in vitro|
|Authors:||Tai, Y.K. |
|Source:||Tai, Y.K., Cheong, Y.M.C., Almsherqi, Z.A., Chia, S.H., Deng, Y., McLachlan, C.S. (2009). High dose Clopidogrel decreases mice liver mitochondrial respiration function in vitro. International Journal of Cardiology 133 (2) : 250-252. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ijcard.2007.10.022|
|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. © 2009.|
|Source Title:||International Journal of Cardiology|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Dec 7, 2017
WEB OF SCIENCETM
checked on Nov 29, 2017
checked on Dec 11, 2017
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.