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|Title:||Uncoupling of oxidative phosphorylation by curcumin: Implication of its cellular mechanism of action|
|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|
|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.|
|Source Title:||Biochemical and Biophysical Research Communications|
|Appears in Collections:||Staff Publications|
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