Succinate, glycerophosphate and ascorbate as sources of cellular energy and as antiteratogens

Development ◽  
1970 ◽  
Vol 24 (1) ◽  
pp. 187-202
Author(s):  
Walter Landauer ◽  
Dinah Sopher
Keyword(s):  
Respiratory Chain ◽  
Energy Production ◽  
High Energy ◽  
Teratogenic Effects ◽  
Cellular Energy ◽  
Specific Affinity ◽  
Mitochondrial Energy Production ◽  
Experimental Findings ◽  
Induced Defects

Our experimental findings show that succinate and ascorbate greatly reduce the teratogenic effects of 3-acetylpyridine, 6-aminonicotinamide and sulfanilamide. Glycerophosphate led to similar alleviating results when used in combination with 3-acetylpyridine and 6-aminonicotinamide, but not with sulfanilamide. With certain other teratogens the high-energy intermediates failed to alleviate; in some instances (acetazolamide, insulin) they even led to potentiation of teratogen-induced defects. The results of our experiments demonstrate clearly that high-energy intermediates, by being fed into the respiratory chain of the mitochondria, can alleviate incidence and degree of expression of malformations produced by specific teratogens. In concert with earlier evidence on the nature of antiteratogenic compounds it can further be concluded that the particular teratogens in question exert their effects by interference with mitochondrial energy production in the tissues for which they have specific affinity.

scholarly journals Nitric oxide and platelet energy metabolism.

2004 ◽  
Vol 51 (3) ◽  
pp. 789-803 ◽  
Author(s):  
Marian Tomasiak ◽  
Halina Stelmach ◽  
Tomasz Rusak ◽  
Jolanta Wysocka
Keyword(s):  
Nitric Oxide ◽  
Cytochrome Oxidase ◽  
Respiratory Chain ◽  
Energy Production ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Antimycin A ◽  
No Donors ◽  
Mitochondrial Energy Production ◽  
Induced Aggregation ◽  
Platelet Secretion

This study was undertaken to determine whether nitric oxide (NO) can affect platelet responses through the inhibition of energy production. It was found that NO donors: S-nitroso-N-acetylpenicyllamine, SNAP, (5-50 microM) and sodium nitroprusside, SNP, (5-100 microM) inhibited collagen- and ADP-induced aggregation of porcine platelets. The corresponding IC50 values for SNAP and SNP varied from 5 to 30 microM and from 9 to 75 microM, respectively. Collagen- and thrombin-induced platelet secretion was inhibited by SNAP (IC50 = 50 microM) and by SNP (IC50 = 100 microM). SNAP (20-100 microM), SNP (10-200 microM) and collagen (20 microg/ml) stimulated glycolysis in intact platelets. The degree of glycolysis stimulation exerted by NO donors was similar to that produced by respiratory chain inhibitors (cyanide and antimycin A) or uncouplers (2,4-dinitrophenol). Neither the NO donors nor the respiratory chain blockers affected glycolysis in platelet homogenate. SNAP (20-100 microM) and SNP (50-200 microM) inhibited oxygen consumption by platelets. The effect of SNP and SNAP on glycolysis and respiration was not reduced by 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one, a selective inhibitor of NO-stimulated guanylate cyclase. SNAP (5-100 microM) and SNP (10-300 microM) inhibited the activity of platelet cytochrome oxidase and had no effect on NADH:ubiquinone oxidoreductase and succinate dehydrogenase. Blocking of the mitochondrial energy production by antimycin A slightly affected collagen-evoked aggregation and strongly inhibited platelet secretion. The results indicate that: 1) in porcine platelets NO is able to diminish mitochondrial energy production through the inhibition of cytochrome oxidase, 2) the inhibitory effect of NO on platelet secretion (but not aggregation) can be attributed to the reduction of mitochondrial energy production.

scholarly journals Mitochondrial energy dysfunction induces remodeling of the cardiac mitochondrial protein acylome

2021 ◽  
Author(s):  
Jessica N. Peoples ◽  
Nasab Ghazal ◽  
Duc M. Duong ◽  
Katherine R. Hardin ◽  
Nicholas T. Seyfried ◽  
...  
Keyword(s):  
Energy Production ◽  
Mitochondrial Protein ◽  
Atp Synthesis ◽  
High Energy ◽  
Heart Tissue ◽  
Mitochondrial Proteins ◽  
Isocitrate Dehydrogenase 2 ◽  
Mitochondrial Energy Production ◽  
Signaling Organelles

ABSTRACTMitochondria are increasingly recognized as signaling organelles because, under conditions of stress, mitochondria can trigger various signaling pathways to coordinate the cell’s response. The specific pathway(s) engaged by mitochondria in response to defects in mitochondrial energy production in vivo and in high-energy tissues like the heart are not fully understood. Here, we investigated cardiac pathways activated in response to mitochondrial energy dysfunction by studying mice with cardiomyocyte-specific loss of the mitochondrial phosphate carrier (SLC25A3), an established model that develops cardiomyopathy as a result of defective mitochondrial ATP synthesis. In heart tissue from these mice, mitochondrial energy dysfunction induced a striking pattern of acylome remodeling, with significantly increased post-translational acetylation and malonylation. Mass spectrometry-based proteomics further revealed that energy dysfunction-induced remodeling of the acetylome and malonylome preferentially impacts mitochondrial proteins. Acetylation and malonylation modified a highly interconnected interactome of mitochondrial proteins, and both modifications were present on the enzyme isocitrate dehydrogenase 2 (IDH2). Intriguingly, IDH2 activity was enhanced in SLC25A3-deleted mitochondria, and further study of IDH2 sites targeted by both acetylation and malonylation revealed that these modifications can have site-specific and distinct functional effects. Finally, we uncovered a novel crosstalk between the two modifications, whereby mitochondrial energy dysfunction-induced acetylation of sirtuin 5 (SIRT5), inhibited its function. Because SIRT5 is a mitochondrial deacylase with demalonylase activity, this finding suggests that acetylation can modulate the malonylome. Together, our results position acylations as an arm of the mitochondrial response to energy dysfunction and suggest a mechanism by which focal disruption to the mitochondrial energy production machinery can have an expanded impact on global mitochondrial function.

Assessing desalination as a sustainable alternative using a multiple criteria decision support model

2008 ◽  
Vol 3 (3) ◽  
Author(s):  
M. B. Fernandes ◽  
M. C. Almeida ◽  
A. G. Henriques
Keyword(s):  
Decision Support ◽  
Energy Production ◽  
Fossil Fuels ◽  
Cost Benefit Analysis ◽  
Cost Benefit ◽  
High Energy ◽  
Economic Benefits ◽  
Multiple Criteria ◽  
Water Production ◽  
Decision Support Model

Desalination technologies provide an alternative for potable water production, having significant potential for application where fresh water scarcity exists. Potential benefits have to be balanced with other factors, such as high costs, high energy consumption, and significant environmental impacts, for the understanding of real risks and gains of desalination within the context of integrated water resources management. Multiple factors can be considered when analysing the viability of a desalination project but often a limited approach is used. The complexity in the analysis lies in finding the alternatives that obey to multiple objectives (e.g. reduced environmental impact, social acceptance, less cost associated). In this paper, development of a methodology based on multiple criteria decision support system for the evaluation and ranking the potential of desalination technologies is described and applied to a Portuguese case study. Relevant factors to the selection of desalination technologies were identified using SWOT analysis and the MACBETH (Measuring Attractiveness by a Categorical Based Evaluation Technique) approach was applied. Technical alternatives considered include reverse osmosis and multi-effect desalination (MED), together with energy production by fossil fuels or solar energy. Production of water by conventional approaches was also considered. Results, for non-economic benefits, show higher score for MED solar but, in the cost-benefit analysis, conventional methods of water production have higher ranking since costs of renewable energies are not yet competitive. However, even if not preferred in economic terms, desalination is ranked significantly above the conventional approaches for non-economic criteria.

scholarly journals A vércukorértékek nem feltétlenül jellemzik megfelelően a sejtanyagcsere-állapotot

2017 ◽  
Vol 158 (11) ◽  
pp. 409-417
Author(s):  
Kornél Simon ◽  
István Wittmann
Keyword(s):  
Diabetes Mellitus ◽  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Energy Production ◽  
Cellular Metabolism ◽  
Transport Parameter ◽  
Metabolic State ◽  
Cellular Energy ◽  
Acute And Chronic Stress

Abstract: In clinical recommendations the normalized blood glucose level is declared as the main target in therapy of diabetes mellitus, i.e. the achievement of euglycemia is the main therapeutic goal. This approach suggests, that the normal blood glucose value is the marker of the normal carbohydrate metabolism (eumetabolism), and vice versa: hyperglycemia is associated with abnormal metabolism (dysmetabolism). However the question arises, whether identical blood glucose values do reflect the same intracellular biochemical mechanisms? On the basis of data published in the literature authors try to answer these questions by studying the relations between the short/longterm blood glucose level and the cellular metabolism in different clinical settings characterized by divergent pathophysiological parameters. The correlations between blood glucose level and cellular metabolism in development of micro-, and macroangiopathy, in the breakthrough phenomenon, as well as during administration of metabolic promoters, the discrepancies of relation between blood glucose values and cellular metabolism in type 1, and type 2 diabetes mellitus, furthermore association between blood glucose value and myocardial metabolism in acute and chronic stress were analyzed. Authors conclude, that the actual blood glucose values reveal the actual cellular metabolism in a very variable manner: neither euglycemia does mandatorily indicate eumetabolism (balance of cellular energy production), nor hyperglycemia is necessarily a marker of abnormal metabolic state (dept of cellular energy production). Moreover, at the same actual blood glucose level both the metabolic efficacy of the same organ may sharply vary, and the intracellular biochemical machinery could also be very different. In case of the very same longterm blood glucose level the metabolic state of the different organs could be very variable: some organs show an energetically balanced metabolism, while others produce a significant deficit. These inconsistencies between blood glucose level and cellular metabolism can be explained by the fact, that blood glucose value is a transport parameter, reflecting the actual steady state of glucose transport from the carbohydrate pools into the blood, and that from the blood into the tissues. Without knowing the speed of these transports of opposite direction, the blood glucose value per se can not reveal the quantitative and qualitative characteristics of cellular metabolism. Orv. Hetil., 2017, 158(11), 409–417.

Loss of the mitochondrial phosphate carrier SLC25A3 induces remodeling of the cardiac mitochondrial protein acylome

2021 ◽  
Author(s):  
Jessica N. Peoples ◽  
Nasab Ghazal ◽  
Duc M. Duong ◽  
Katherine R. Hardin ◽  
Janet R. Manning ◽  
...  
Keyword(s):  
Energy Production ◽  
Mitochondrial Protein ◽  
Atp Synthesis ◽  
High Energy ◽  
Mitochondrial Proteins ◽  
Isocitrate Dehydrogenase 2 ◽  
Signaling Organelles ◽  
Specific Pathway ◽  
Phosphate Carrier

Mitochondria are recognized as signaling organelles because, under stress, mitochondria can trigger various signaling pathways to coordinate the cell's response. The specific pathway(s) engaged by mitochondria in response to mitochondrial energy defects in vivo and in high-energy tissues like the heart are not fully understood. Here, we investigated cardiac pathways activated in response to mitochondrial energy dysfunction by studying mice with cardiomyocyte-specific loss of the mitochondrial phosphate carrier (SLC25A3), an established model that develops cardiomyopathy as a result of defective mitochondrial ATP synthesis. Mitochondrial energy dysfunction induced a striking pattern of acylome remodeling, with significantly increased post-translational acetylation and malonylation. Mass spectrometry-based proteomics further revealed that energy dysfunction-induced remodeling of the acetylome and malonylome preferentially impacts mitochondrial proteins. Acetylation and malonylation modified a highly interconnected interactome of mitochondrial proteins, and both modifications were present on the enzyme isocitrate dehydrogenase 2 (IDH2). Intriguingly, IDH2 activity was enhanced in SLC25A3-deleted mitochondria, and further study of IDH2 sites targeted by both acetylation and malonylation revealed that these modifications can have site-specific and distinct functional effects. Finally, we uncovered a novel crosstalk between the two modifications, whereby mitochondrial energy dysfunction-induced acetylation of sirtuin 5 (SIRT5), inhibited its function. Because SIRT5 is a mitochondrial deacylase with demalonylase activity, this finding suggests that acetylation can modulate the malonylome. Together, our results position acylations as an arm of the mitochondrial response to energy dysfunction and suggest a mechanism by which focal disruption to the energy production machinery can have an expanded impact on global mitochondrial function.

scholarly journals Lower Mitochondrial Energy Production of the Thigh Muscles in Patients With Low‐Normal Ankle‐Brachial Index

2017 ◽  
Vol 6 (9) ◽  
Author(s):  
Majd AlGhatrif ◽  
Ariel Zane ◽  
Matt Oberdier ◽  
Marco Canepa ◽  
Stephanie Studenski ◽  
...  
Keyword(s):  
Energy Production ◽  
Ankle Brachial Index ◽  
Thigh Muscles ◽  
Mitochondrial Energy Production

Effect of mangiferin on mitochondrial energy production in experimentally induced myocardial infarcted rats

2006 ◽  
Vol 44 (6) ◽  
pp. 519-525 ◽  
Author(s):  
S. Prabhu ◽  
Mallika Jainu ◽  
K.E. Sabitha ◽  
C.S. Shyamala Devi
Keyword(s):  
Energy Production ◽  
Mitochondrial Energy Production ◽  
Experimentally Induced

Nuclear Structure and High-Energy Production Processes

1975 ◽  
Vol 34 (10) ◽  
pp. 622-624 ◽  
Author(s):  
P. J. Camillo ◽  
Paul M. Fishbane ◽  
J. S. Trefil
Keyword(s):  
Nuclear Structure ◽  
Energy Production ◽  
High Energy ◽  
Production Processes

Amorphous CdO‐In 2 O 3 Electrode for Perovskite‐based Bifacial and Tandem Photovoltaic Technologies with High Energy Production

Solar RRL ◽  
2021 ◽  
Author(s):  
Yuanhang Cheng ◽  
Zixin Zeng ◽  
Tianyuan Liu ◽  
Ying Wang ◽  
Carlos D. Rodríguez-Gallegos ◽  
...  
Keyword(s):  
Energy Production ◽  
High Energy ◽  
Photovoltaic Technologies

scholarly journals Methylpiperidinopyrazole Attenuates Estrogen-Induced Mitochondrial Energy Production and Subsequent Osteoblast Maturation via an Estrogen Receptor Alpha-Dependent Mechanism

Molecules ◽  
2020 ◽  
Vol 25 (12) ◽  
pp. 2876
Author(s):  
Poh-Shiow Yeh ◽  
Jui-Tai Chen ◽  
Yih-Giun Cherng ◽  
Shun-Tai Yang ◽  
Yu-Ting Tai ◽  
...  
Keyword(s):  
Energy Production ◽  
Estrogen Receptor Alpha ◽  
Type I Collagen ◽  
Atp Synthesis ◽  
Neonatal Rat ◽  
Type I ◽  
Collagen Mrna ◽  
Adenosine Phosphate ◽  
Mitochondrial Energy Production ◽  
Osteoblast Maturation

An estrogen deficiency is the main cause of osteoporosis in postmenopausal women. In bone remodeling, estrogen receptors (ERs) can mediate estrogen-transducing signals. Methylpiperidinopyrazole (MPP) is a highly specific antagonist of ER-alpha (ERα). This study was designed to evaluate the effects of MPP on estrogen-induced energy production, subsequent osteoblast maturation, and the possible mechanisms. Exposure of primary osteoblasts isolated from neonatal rat calvarias to MPP did not affect cell morphology or survival. Estradiol can induce translocation of ERα into mitochondria from the cytoplasm. Interestingly, pretreatment of rat calvarial osteoblasts with MPP lowered estrogen-induced ERα translocation. Sequentially, estrogen-triggered expressions of mitochondrial energy production-linked cytochrome c oxidase (COX) I and COX II messenger (m)RNAs were inhibited following pretreatment with MPP. Consequently, MPP caused decreases in estrogen-triggered augmentation of the activities of mitochondrial respiratory complex enzymes and levels of cellular adenosine phosphate (ATP). During progression of osteoblast maturation, estrogen induced bone morphogenetic protein (BMP)-6 and type I collagen mRNA expressions, but MPP treatment inhibited such induction. Consequently, estrogen-induced osteoblast activation and mineralization were attenuated after exposure to MPP. Taken together, MPP suppressed estrogen-induced osteoblast maturation through decreasing chromosomal osteogenesis-related BMP-6 and type I collagen mRNA expressions and mitochondrial ATP synthesis due to inhibiting energy production-linked COX I and II mRNA expressions. MPP can appropriately be applied to evaluate estrogen-involved bioenergetics and osteoblast maturation.

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