Please use this identifier to cite or link to this item:
|dc.title||Uncoupling of oxidative phosphorylation by curcumin: Implication of its cellular mechanism of action|
|dc.identifier.citation||Lim, H.W., Lim, H.Y., Wong, K.P. (2009). Uncoupling of oxidative phosphorylation by curcumin: Implication of its cellular mechanism of action. Biochemical and Biophysical Research Communications 389 (1) : 187-192. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2009.08.121|
|dc.description.abstract||Curcumin is a phytochemical isolated from the rhizome of turmeric. Recent reports have shown curcumin to have antioxidant, anti-inflammatory and anti-tumor properties as well as affecting the 5′-AMP activated protein kinase (AMPK), mTOR and STAT-3 signaling pathways. We provide evidence that curcumin acts as an uncoupler. Well-established biochemical techniques were performed on isolated rat liver mitochondria in measuring oxygen consumption, F0F1-ATPase activity and ATP biosynthesis. Curcumin displays all the characteristics typical of classical uncouplers like fccP and 2,4-dinitrophenol. In addition, at concentrations higher than 50 μM, curcumin was found to inhibit mitochondrial respiration which is a characteristic feature of inhibitory uncouplers. As a protonophoric uncoupler and as an activator of F0F1-ATPase, curcumin causes a decrease in ATP biosynthesis in rat liver mitochondria. The resulting change in ATP:AMP could disrupt the phosphorylation status of the cell; this provides a possible mechanism for its activation of AMPK and its downstream mTOR and STAT-3 signaling. © 2009 Elsevier Inc. All rights reserved.|
|dc.description.sourcetitle||Biochemical and Biophysical Research Communications|
|Appears in Collections:||Staff Publications|
Show simple item record
Files in This Item:
There are no files associated with this item.
checked on May 28, 2020
WEB OF SCIENCETM
checked on May 19, 2020
checked on May 13, 2020
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.