The uncoupling of respiration in plant mitochondria: keeping reactive oxygen and nitrogen species under control

2020 ◽  
Author(s):  
Vasily N Popov ◽  
Mikhail Y Syromyatnikov ◽  
Alisdair R Fernie ◽  
Subhra Chakraborty ◽  
Kapuganti Jagadis Gupta ◽  
...  
Keyword(s):  
Mitochondrial Respiration ◽  
Uncoupling Protein ◽  
Plant Mitochondria ◽  
Reactive Oxygen ◽  
Stress Factors ◽  
Atp Production ◽  
Alternative Pathways ◽  
Mitochondrial Functions ◽  
Far From Equilibrium

Abstract Plant mitochondrial respiration involves the operation of various alternative pathways. These pathways participate, both directly and indirectly, in the maintenance of mitochondrial functions though they do not contribute to energy production, being uncoupled from the generation of an electrochemical gradient across the mitochondrial membrane and thus from ATP production. Recent findings suggest that uncoupled respiration is involved in reactive oxygen species (ROS) and nitric oxide (NO) scavenging, regulation, and homeostasis. Here we discuss specific roles and possible functions of uncoupled mitochondrial respiration in ROS and NO metabolism. The mechanisms of expression and regulation of the NDA-, NDB- and NDC-type non-coupled NADH and NADPH dehydrogenases, the alternative oxidase (AOX), and the uncoupling protein (UCP) are examined in relation to their involvement in the establishment of the stable far-from-equilibrium state of plant metabolism. The role of uncoupled respiration in controlling the levels of ROS and NO as well as inducing signaling events is considered. Secondary functions of uncoupled respiration include its role in protection from stress factors and roles in biosynthesis and catabolism. It is concluded that uncoupled mitochondrial respiration plays an important role in providing rapid adaptation of plants to changing environmental factors via regulation of ROS and NO.

scholarly journals The role of Asprosin in patients with dilated cardiomyopathy

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Ming-Shien Wen ◽  
Chao-Yung Wang ◽  
Jih-Kai Yeh ◽  
Chun-Chi Chen ◽  
Ming-Lung Tsai ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Mitochondrial Respiration ◽  
Cardiovascular Events ◽  
Molecular Mechanisms ◽  
Major Adverse Cardiovascular Events ◽  
Study Cohort ◽  
Protective Mechanisms ◽  
Mitochondrial Functions ◽  
And Function

Abstract Background Asprosin is a novel fasting glucogenic adipokine discovered in 2016. Asprosin induces rapid glucose releases from the liver. However, its molecular mechanisms and function are still unclear. Adaptation of energy substrates from fatty acid to glucose is recently considered a novel therapeutic target in heart failure treatment. We hypothesized that the asprosin is able to modulate cardiac mitochondrial functions and has important prognostic implications in dilated cardiomyopathy (DCM) patients. Methods We prospectively enrolled 50 patients (86% male, mean age 55 ± 13 years) with DCM and followed their 5-year major adverse cardiovascular events from 2012 to 2017. Comparing with healthy individuals, DCM patients had higher asprosin levels (191.2 versus 79.7 ng/mL, P < 0.01). Results During the 5-year follow-up in the study cohort, 16 (32.0%) patients experienced adverse cardiovascular events. Patients with lower asprosin levels (< 210 ng/mL) were associated with increased risks of adverse clinical outcomes with a hazard ratio of 7.94 (95% CI 1.88–33.50, P = 0.005) when compared patients with higher asprosin levels (≥ 210 ng/mL). Using cardiomyoblasts as a cellular model, we showed that asprosin prevented hypoxia-induced cell death and enhanced mitochondrial respiration and proton leak under hypoxia. Conclusions In patients with DCM, elevated plasma asprosin levels are associated with less adverse cardiovascular events in five years. The underlying protective mechanisms of asprosin may be linked to its functions relating to enhanced mitochondrial respiration under hypoxia.

scholarly journals Genetic Association in the Maintenance of the Mitochondrial Microenvironment and Sperm Capacity

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Hwang I. S. Thomas ◽  
Ying-Shiuan Chen ◽  
Ching-Han Hung ◽  
Dilip Bhargava Sreerangaraja Urs ◽  
Tien-Ling Liao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Sperm Motility ◽  
Manganese Superoxide Dismutase ◽  
Uncoupling Protein ◽  
Reactive Oxygen ◽  
Human Sperm ◽  
Oxygen Species ◽  
Genotype Frequencies ◽  
The Impact

Sperm motility is one of the major determinants of male fertility. Since sperm need a great deal of energy to support their fast movement by active metabolism, they are thus extremely vulnerable to oxidative damage by the reactive oxygen species (ROS) and other free radicals generated as byproducts in the electron transport chain. The present study is aimed at understanding the impact of a mitochondrial oxidizing/reducing microenvironment in the etiopathology of male infertility. We detected the mitochondrial DNA (mtDNA) 4,977 bp deletion in human sperm. We examined the gene mutation of ATP synthase 6 (ATPase6 m.T8993G) in ATP generation, the gene polymorphisms of uncoupling protein 2 (UCP2, G-866A) in the uncoupling of oxidative phosphorylation, the role of genes such as manganese superoxide dismutase (MnSOD, C47T) and catalase (CAT, C-262T) in the scavenging system in neutralizing reactive oxygen species, and the role of human 8-oxoguanine DNA glycosylase (hOGG1, C1245G) in 8-hydroxy-2 ′ -deoxyguanosine (8-OHdG) repair. We found that the sperm with higher motility were found to have a higher mitochondrial membrane potential and mitochondrial bioenergetics. The genotype frequencies of UCP2 G-866A, MnSOD C47T, and CAT C-262T were found to be significantly different among the fertile subjects, the infertile subjects with more than 50% motility, and the infertile subjects with less than 50% motility. A higher prevalence of the mtDNA 4,977 bp deletion was found in the subjects with impaired sperm motility and fertility. Furthermore, we found that there were significant differences between the occurrences of the mtDNA 4,977 bp deletion and MnSOD (C47T) and hOGG1 (C1245G). In conclusion, the maintenance of the mitochondrial redox microenvironment and genome integrity is an important issue in sperm motility and fertility.

scholarly journals Mitochondrial localization of SESN2

2019 ◽  
Author(s):  
Irina E. Kovaleva ◽  
Artem V. Tokarchuk ◽  
Andrei O. Zeltukhin ◽  
Grigoriy Safronov ◽  
Aleksandra G. Evstafieva ◽  
...  
Keyword(s):  
Protein Complex ◽  
Inhibitory Effect ◽  
Small Gtpase ◽  
Stress Factors ◽  
Mitochondrial Localization ◽  
Mitochondrial Functions ◽  
Ros Accumulation ◽  
Evolutionarily Conserved ◽  
Established Role

SESN2 is a member of evolutionarily conserved sestrin protein family found in most of Metazoa species. SESN2 is transcriptionally activated by many stress factors including metabolic derangements, oxidants and DNA-damage. As a result, SESN2 controls ROS accumulation, metabolism and cell viability. The best known function of SESN2 is the regulation of mechanistic target of rapamycin complex 1 kinase (mTORC1) that plays the central role in the stimulation of cell growth and suppression of autophagy. SESN2 inhibits mTORC1 activity through interaction with the GATOR2 protein complex that suppresses an inhibitory effect of GATOR2 on the GATOR1 protein complex. GATOR1 inhibits mTORC1 through its GAP activity toward the small GTPase RagA/B which in complex with RagC/D proteins stimulate mTORC1 translocation to the lysosomes where this kinase is activated by small GTPase Rheb. Despite the well-established role of SESN2 in mTORC1 inhibition, the other SESN2 activities are not well characterised. We recently showed that SESN2 can control mitochondrial function and cell death via mTORC1-independent mechanisms and these activities might be explained by direct effects of SESN2 on mitochondria. In this work we examined mitochondrial localization of SESN2 and demonstrated that SESN2 is located on mitochondria and can be directly involved in the regulation of mitochondrial functions.

scholarly journals ‘Green’ …yet wasting energy?: Mitochondrial respiration in plants

2006 ◽  
Vol 28 (4) ◽  
pp. 13-16
Author(s):  
Anthony L. Moore ◽  
Mary S. Albury ◽  
Paul G. Crichton
Keyword(s):  
Plant Growth ◽  
Mitochondrial Respiration ◽  
Alternative Oxidase ◽  
Plant Mitochondria ◽  
Carboxylate Group ◽  
Defence Mechanism ◽  
Alternative Pathways ◽  
Warm Environment ◽  
Inner Surface ◽  
Iron Carboxylate

Plant mitochondria are characterized by the presence of both phosphorylating (cytochrome) and non-phosphorylating (alternative) pathways, the activity of which directly affects the efficiency of mitochondrial energy conservation. The cyanide-insensitive AOX (alternative oxidase) is located on the inner surface of the inner membrane, results in the oxidation of ubiquinol and the net reduction of oxygen to water, is non-protonmotive and is considered to be one of the newest members of the di-iron carboxylate group of proteins. In thermogenic tissues it plays a key role in pollination and the maintenance of a warm environment for the flower, whereas in non-thermogenic tissues functions include acting as an energy overflow, part of the oxygen defence mechanism and maintaining plant growth homoeostasis.

Regulation of insulin secretion by uncoupling protein

2006 ◽  
Vol 34 (5) ◽  
pp. 802-805 ◽  
Author(s):  
C.B. Chan ◽  
N. Kashemsant
Keyword(s):  
Insulin Secretion ◽  
Fatty Acid ◽  
Uncoupling Protein ◽  
Physiological Role ◽  
Atp Production ◽  
Ucp2 Expression ◽  
Increased Sensitivity ◽  
Glucose Stimulated Insulin Secretion

UCPs (uncoupling proteins) can regulate cellular ATP production by uncoupling oxidative phosphorylation. UCP2 is expressed in islet β-cells and its induction reduces glucose-stimulated insulin secretion. Under physiological conditions, superoxide, formed as a by-product of respiration, activates UCP2. This leads to reduced ATP production, which impairs closure of the ATP-dependent K+ channels to prevent insulin secretion. It is suggested that the physiological role of UCP2 is to prevent excessive superoxide generation through a feedback loop. UCP2 induction may also alter fatty acid metabolism by altering NAD/NADH or by facilitating cycling of fatty acid anions. Recently, UCP2 has been proposed to keep insulin secretion low during starvation, a function under the control of the transcription co-repressor, surtuin-1, which has been shown to bind to the UCP2 promoter. Pathological UCP2 expression or activation may suppress glucose-stimulated insulin secretion to the extent that diabetes onset is hastened. In ob/ob mice, induction of UCP2 at age 5 weeks precedes development of insulin secretion defects and hyperglycaemia. Activating protein kinase A-dependent pathways can normalize insulin secretion in UCP2-overexpressing islets. Conversely, lowering UCP2 expression may promote increased insulin secretion. UCP2 knockout mice were protected from the diabetogenic effects of a high-fat diet and their islets exhibited increased sensitivity to glucose and elevated ATP/ADP. These results support a role for UCP2 as a gene contributing to the pathogenesis of Type 2 diabetes.

scholarly journals Developmental shift to mitochondrial respiration for energetic support of sustained transmission during maturation at the calyx of Held

2021 ◽  
Author(s):  
Brendan J Lujan ◽  
Mahendra Singh ◽  
Abhyudai Singh ◽  
Robert B Renden
Keyword(s):  
Mitochondrial Respiration ◽  
High Frequency ◽  
Synaptic Activity ◽  
Calyx Of Held ◽  
Atp Production ◽  
Vesicle Recycling ◽  
Developmental Shift ◽  
Synaptic Maturation ◽  
Fuel Source

A considerable amount of energy is expended following presynaptic activity to regenerate electrical polarization and maintain efficient release and recycling of neurotransmitter. Mitochondria are the major suppliers of neuronal energy, generating ATP via oxidative phosphorylation. However, the specific utilization of energy from cytosolic glycolysis rather than mitochondrial respiration at the presynaptic terminal during synaptic activity remains unclear and controversial. We use a synapse specialized for high frequency transmission in mice, the calyx of Held, to test the sources of energy utilized to maintain energy during short activity bursts (<1 sec) and sustained neurotransmission (30-150 sec). We dissect the role of presynaptic glycolysis versus mitochondrial respiration by acutely and selectively blocking these ATP-generating pathways in a synaptic preparation where mitochondria and synaptic vesicles are prolific, under near-physiological conditions. Surprisingly, if either glycolysis or mitochondrial ATP production is intact, transmission during repetitive short bursts of activity is not affected. In slices from young animals prior to the onset of hearing, where the synapse is not yet fully specialized, both glycolytic and mitochondrial ATP production are required to support sustained, high frequency neurotransmission. In mature synapses, sustained transmission relies exclusively on mitochondrial ATP production supported by bath lactate, but not glycolysis. At both ages, we observe that action potential propagation begins to fail prior to defects in synaptic vesicle recycling. Our data describe a specific metabolic profile to support high-frequency information transmission at the mature calyx of Held, shifting during postnatal synaptic maturation from glycolysis to rely on monocarboxylates as a fuel source.

Activation of pattern recognition receptors in brown adipocytes induces inflammation and suppresses uncoupling protein 1 expression and mitochondrial respiration

2014 ◽  
Vol 306 (10) ◽  
pp. C918-C930 ◽  
Author(s):  
Jiyoung Bae ◽  
Carolyn J. Ricciardi ◽  
Debora Esposito ◽  
Slavko Komarnytsky ◽  
Pan Hu ◽  
...  
Keyword(s):  
Pattern Recognition ◽  
Mitochondrial Respiration ◽  
Uncoupling Protein ◽  
Mapk Signaling ◽  
Pattern Recognition Receptors ◽  
Brown Adipocyte ◽  
Uncoupling Protein 1 ◽  
Brown Adipocytes ◽  
Brown Adipose

Pattern recognition receptors (PRR), Toll-like receptors (TLR), and nucleotide-oligomerization domain-containing proteins (NOD) play critical roles in mediating inflammation and modulating functions in white adipocytes in obesity. However, the role of PRR activation in brown adipocytes, which are recently found to be present in adult humans, has not been studied. Here we report that mRNA of TLR4, TLR2, NOD1, and NOD2 is upregulated, paralleled with upregulated mRNA of inflammatory cytokines and chemokines in the brown adipose tissue (BAT) of the obese mice. During brown adipocyte differentiation, mRNA and protein expression of NOD1 and TLR4, but not TLR2 and NOD2, is also increased. Activation of TLR4, TLR2, or NOD1 in brown adipocytes induces activation of NF-κB and MAPK signaling pathways, leading to inflammatory cytokine/chemokine mRNA expression and/or protein secretion. Moreover, activation of TLR4, TLR2, or NOD1 attenuates both basal and isoproterenol-induced uncoupling protein 1 (UCP-1) expression without affecting mitochondrial biogenesis and lipid accumulation in brown adipocytes. Cellular bioenergetics measurements confirm that attenuation of UCP-1 expression by PRR activation is accompanied by suppression of both basal and isoproterenol-stimulated oxygen consumption rates and isoproterenol-induced uncoupled respiration from proton leak; however, maximal respiration and ATP-coupled respiration are not changed. Further, the attenuation of UCP-1 by PRR activation appears to be mediated through downregulation of the UCP-1 promoter activities. Taken together, our results demonstrate the role of selected PRR activation in inducing inflammation and downregulation of UCP-1 expression and mitochondrial respiration in brown adipocytes. Our results uncover novel targets in BAT for obesity treatment and prevention.

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