scholarly journals S3.18 Redox state of quinone affects Acanthamoeba castellanii mitochondrial uncoupling protein activity through sensitivity to purine nucleotides

2008 ◽  
Vol 1777 ◽  
pp. S29
Author(s):  
Aleksandra Swida ◽  
Andrzej Woyda-Ploszczyca ◽  
Wieslawa Jarmuszkiewicz
Keyword(s):  
Redox State ◽  
Uncoupling Protein ◽  
Acanthamoeba Castellanii ◽  
Purine Nucleotides ◽  
Protein Activity ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein

Redox state of quinone affects sensitivity of Acanthamoeba castellanii mitochondrial uncoupling protein to purine nucleotides

2008 ◽  
Vol 413 (2) ◽  
pp. 359-367 ◽  
Author(s):  
Aleksandra Swida ◽  
Andrzej Woyda-Ploszczyca ◽  
Wieslawa Jarmuszkiewicz
Keyword(s):  
Respiratory Rate ◽  
Redox State ◽  
Uncoupling Protein ◽  
Acanthamoeba Castellanii ◽  
Inhibitory Effect ◽  
Proton Conductance ◽  
Purine Nucleotides ◽  
Protein Activity ◽  
Mitochondrial Uncoupling ◽  
Quinone Reduction

We studied FFA (free fatty acid)-induced uncoupling activity in Acanthamoeba castellanii mitochondria in the non-phosphorylating state. Either succinate or external NADH was used as a respiratory substrate to determine the proton conductance curves and the relationships between respiratory rate and the quinone reduction level. Our determinations of the membranous quinone reduction level in non-phosphorylating mitochondria show that activation of UCP (uncoupling protein) activity leads to a PN (purine nucleotide)-sensitive decrease in the quinone redox state. The gradual decrease in the rate of quinone-reducing pathways (using titration of dehydrogenase activities) progressively leads to a full inhibitory effect of GDP on LA (linoleic acid) induced proton conductance. This inhibition cannot be attributed to changes in the membrane potential. Indeed, the lack of GDP inhibitory effect observed when the decrease in respiratory rate is accompanied by an increase in the quinone reduction level (using titration of the quinol-oxidizing pathway) proves that the inhibition by nucleotides can be revealed only for a low quinone redox state. It must be underlined that, in A. castellanii non-phosphorylating mitochondria, the transition of the inhibitory effect of GDP on LA-induced UCP-mediated uncoupling is observed for the same range of quinone reduction levels (between 50% and 40%) as that observed previously for phosphorylating conditions. This observation, drawn from the two different metabolic states of mitochondria, indicates that quinone could affect UCP activity through sensitivity to PNs.

In Phosphorylating Acanthamoeba castellanii Mitochondria the Sensitivity of Uncoupling Protein Activity to GTP Depends on the Redox State of Quinone

2005 ◽  
Vol 37 (2) ◽  
pp. 97-107 ◽  
Author(s):  
Wieslawa Jarmuszkiewicz ◽  
Aleksandra Swida ◽  
Malgorzata Czarna ◽  
Nina Antos ◽  
Claudine M. Sluse-Goffart ◽  
...  
Keyword(s):  
Redox State ◽  
Uncoupling Protein ◽  
Acanthamoeba Castellanii ◽  
Protein Activity

Hydroxynonenal-stimulated activity of the uncoupling protein in Acanthamoeba castellanii mitochondria under phosphorylating conditions

2013 ◽  
Vol 394 (5) ◽  
pp. 649-658 ◽  
Author(s):  
Andrzej Woyda-Ploszczyca ◽  
Wieslawa Jarmuszkiewicz
Keyword(s):  
Respiratory Rate ◽  
Atp Synthase ◽  
Redox State ◽  
Uncoupling Protein ◽  
Acanthamoeba Castellanii ◽  
Complex Iii ◽  
Dependent Manner ◽  
Mitochondrial Uncoupling ◽  
Concentration Dependent Manner ◽  
Succinate Oxidation

Abstract The influence of 4-hydroxy-2-nonenal (HNE), a lipid peroxidation end product, on the activity of the amoeba Acanthamoeba castellanii uncoupling protein (AcUCP) in isolated phosphorylating mitochondria was studied. Under phosphorylating conditions, exogenously added HNE induced GTP-sensitive AcUCP-mediated mitochondrial uncoupling. The HNE-induced proton leak decreased the yield of oxidative phosphorylation in an HNE concentration-dependent manner. The present study describes how the contributions of ATP synthase and HNE-induced AcUCP in phosphorylating respiration vary when the rate of succinate oxidation is decreased by limiting succinate uptake or inhibiting complex III activity within the range of a constant membrane potential. In phosphorylating mitochondria, at a given HNE concentration (100 μm), the efficiency of AcUCP in mitochondrial uncoupling increased as the respiratory rate decreased because the AcUCP contribution remained constant while the ATP synthase contribution decreased with the respiratory rate. HNE-induced uncoupling can be inhibited by GTP only when ubiquinone is sufficiently oxidized, indicating that in phosphorylating A. castellanii mitochondria, the sensitivity of AcUCP activity to GTP depends on the redox state of the membranous ubiquinone.

scholarly journals Effects of Mitochondrial Uncoupling Protein 2 Inhibition by Genipin in Human Cumulus Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Hongshan Ge ◽  
Fan Zhang ◽  
Dan Shan ◽  
Hua Chen ◽  
Xiaona Wang ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Uncoupling Protein ◽  
Physiological Role ◽  
Cumulus Cells ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Cultural Medium ◽  
Cellular Autophagy ◽  
Significant Difference ◽  
Active Caspase

UCP2 plays a physiological role by regulating mitochondrial biogenesis, maintaining energy balance, ROS elimination, and regulating cellular autophagy in numerous tissues. But the exact roles of UCP2 in cumulus cells are still not clear. Genipin, a special UCP2 inhibitor, was added into the cultural medium to explore the roles of UCP2 in human cumulus cells. There were no significant differences in ATP and mitochondrial membrane potential levels in cumulus cells from UCP2 inhibiting groups as compared with the control. The levels of ROS and Mn-SOD were markedly elevated after UCP2 inhibited Genipin. However, the ratio of reduced GSH to GSSG significantly declined after treatment with Genipin. UCP2 inhibition by Genipin also resulted in obvious increase in the active caspase-3, which accompanied the decline of caspase-3 mRNA. The level of progesterone in culture medium declined obviously after Genipin treatment. But there was no significant difference in estradiol concentrations. This study indicated that UCP2 is expressed in human cumulus cells and plays important roles on mediate ROS production, apoptotic process, and steroidogenesis, suggesting UCP2 may be involved in regulation of follicle development and oocyte maturation and quality.

scholarly journals Mitochondrial Hormesis in PancreaticβCells: Does Uncoupling Protein 2 Play a Role?

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Ning Li ◽  
Suzana Stojanovski ◽  
Pierre Maechler
Keyword(s):  
Stress Responses ◽  
Defense Mechanisms ◽  
Defense Mechanism ◽  
Cell Function ◽  
Uncoupling Protein ◽  
Glucose Sensing ◽  
Mitochondrial Uncoupling ◽  
Mitochondrial Uncoupling Protein ◽  
Cellular Stresses ◽  
Excessive Nutrients

In pancreaticβcells, mitochondrial metabolism translates glucose sensing into signals regulating insulin secretion. Chronic exposure ofβcells to excessive nutrients, namely, glucolipotoxicity, impairsβ-cell function. This is associated with elevated ROS production from overstimulated mitochondria. Mitochondria are not only the major source of cellular ROS, they are also the primary target of ROS attacks. The mitochondrial uncoupling protein UCP2, even though its uncoupling properties are debated, has been associated with protective functions against ROS toxicity. Hormesis, an adaptive response to cellular stresses, might contribute to the protection againstβ-cell death, possibly limiting the development of type 2 diabetes. Mitochondrial hormesis, or mitohormesis, is a defense mechanism observed in ROS-induced stress-responses by mitochondria. Inβcells, mitochondrial damages induced by sublethal exogenous H2O2can induce secondary repair and defense mechanisms. In this context, UCP2 is a marker of mitohormesis, being upregulated following stress conditions. When overexpressed in nonstressed naïve cells, UCP2 confers resistance to oxidative stress. Whether treatment with mitohormetic inducers is sufficient to restore or ameliorate secretory function ofβcells remains to be determined.

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