scholarly journals Evaluation of theIn VivoandIn VitroEffects of Fructose on Respiratory Chain Complexes in Tissues of Young Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Ernesto António Macongonde ◽  
Thais Ceresér Vilela ◽  
Giselli Scaini ◽  
Cinara Ludvig Gonçalves ◽  
Bruna Klippel Ferreira ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cerebral Cortex ◽  
Respiratory Chain ◽  
Biological Fluids ◽  
Control Group ◽  
Respiratory Chain Complexes ◽  
Mitochondrial Energy Metabolism ◽  
Chain Complexes ◽  
Aldolase B

Hereditary fructose intolerance (HFI) is an autosomal-recessive disorder characterized by fructose and fructose-1-phosphate accumulation in tissues and biological fluids of patients. This disease results from a deficiency of aldolase B, which metabolizes fructose in the liver, kidney, and small intestine. We here investigated the effect of acute fructose administration on the activities of mitochondrial respiratory chain complexes, succinate dehydrogenase (SDH), and malate dehydrogenase (MDH) in cerebral cortex, liver, kidney, and skeletal muscle of male 30-day-old Wistar rats. The rats received subcutaneous injection of sodium chloride (0.9%; control group) or fructose solution (5 μmol/g; treated group). One hour later, the animals were euthanized and the cerebral cortex, liver, kidney, and skeletal muscle were isolated and homogenized for the investigations. Acute fructose administration increased complex I-III activity in liver. On the other hand, decreased complexes II and II-III activities in skeletal muscle and MDH in kidney were found. Interestingly, none of these parameters were affectedin vitro. Our present data indicate that fructose administration elicits impairment of mitochondrial energy metabolism, which may contribute to the pathogenesis of the HFI patients.

scholarly journals Impairment of Electron Transfer Chain Induced by Acute Carnosine Administration in Skeletal Muscle of Young Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
José Roberto Macarini ◽  
Soliany Grassi Maravai ◽  
José Henrique Cararo ◽  
Nádia Webber Dimer ◽  
Cinara Ludvig Gonçalves ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electron Transfer ◽  
Creatine Kinase ◽  
Respiratory Chain ◽  
Atp Depletion ◽  
Neurological Dysfunction ◽  
Control Group ◽  
Mrna Levels ◽  
Respiratory Chain Complexes ◽  
Chain Complexes

Serum carnosinase deficiency is an inherited disorder that leads to an accumulation of carnosine in the brain tissue, cerebrospinal fluid, skeletal muscle, and other tissues of affected patients. Considering that high levels of carnosine are associated with neurological dysfunction and that the pathophysiological mechanisms involved in serum carnosinase deficiency remain poorly understood, we investigated thein vivoeffects of carnosine on bioenergetics parameters, namely, respiratory chain complexes (I–III, II, and II-III), malate dehydrogenase, succinate dehydrogenase, and creatine kinase activities and the expression of mitochondrial-specific transcription factors (NRF-1, PGC-1α, andTFAM) in skeletal muscle of young Wistar rats. We observed a significant decrease of complexes I–III and II activities in animals receiving carnosine acutely, as compared to control group. However, no significant alterations in respiratory chain complexes, citric acid cycle enzymes, and creatine kinase activities were found between rats receiving carnosine chronically and control group animals. As compared to control group, mRNA levels ofNRF-1, PGC-1α, andTFAMwere unchanged. The present findings indicate that electron transfer through the respiratory chain is impaired in skeletal muscle of rats receiving carnosine acutely. In case these findings are confirmed by further studies and ATP depletion is also observed, impairment of bioenergetics could be considered a putative mechanism responsible for the muscle damage observed in serum carnosinase-deficient patients.

In vitro effect of antipsychotics on brain energy metabolism parameters in the brain of rats

2013 ◽  
Vol 25 (1) ◽  
pp. 18-26 ◽  
Author(s):  
Giselli Scaini ◽  
Natália Rochi ◽  
Meline O. S. Morais ◽  
Débora D. Maggi ◽  
Bruna T. De-Nês ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Respiratory Chain ◽  
Antipsychotic Drugs ◽  
Reaction Medium ◽  
Respiratory Chain Complexes ◽  
Posterior Cortex ◽  
Chain Complexes ◽  
Vitro Effect ◽  
The Brain

ObjectiveTypical and atypical antipsychotic drugs have been shown to have different clinical, biochemical and behavioural profiles. It is well described that impairment of metabolism, especially in the mitochondria, leads to oxidative stress and neuronal death and has been implicated in the pathogenesis of a number of diseases in the brain. In this context, we investigated the in vitro effect of antipsychotic drugs on energy metabolism parameters in the brain of rats.MethodsClozapine (0.1, 0.5 and 1.0 mg/ml), olanzapine (0.1, 0.5 and 1.0 mg/ml) and aripiprazole (0.05, 0.15 and 0.3 mg/ml) were suspended in buffer and added to the reaction medium containing rat tissue homogenates and the respiratory chain complexes, succinate dehydrogenase and creatine kinase (CK) activities were evaluated.ResultsOur results showed that olanzapine and aripriprazole increased the activities of respiratory chain complexes. On the other hand, complex IV activity was inhibited by clozapine, olanzapine and aripriprazole. CK activity was increased by clozapine at 0.5 and 1.0 mg/ml in prefrontal cortex, cerebellum, striatum, hippocampus and posterior cortex of rats. Moreover, olanzapine and aripiprazole did not affect CK activity.ConclusionIn this context, if the hypothesis that metabolism impairment is involved in the pathophysiology of neuropsychiatric disorders is correct and these results also occur in vivo, we suggest that olanzapine may reverse a possible diminution of metabolism.

scholarly journals The Novel Arylamidine T-2307 Selectively Disrupts Yeast Mitochondrial Function by Inhibiting Respiratory Chain Complexes

2019 ◽  
Vol 63 (8) ◽  
Author(s):  
Kohei Yamashita ◽  
Taiga Miyazaki ◽  
Yoshiko Fukuda ◽  
Junichi Mitsuyama ◽  
Tomomi Saijo ◽  
...  
Keyword(s):  
Respiratory Chain ◽  
Mitochondrial Function ◽  
Yeast Cells ◽  
Dependent Manner ◽  
The Novel ◽  
Respiratory Chain Complexes ◽  
Content Type ◽  
Chain Complexes

ABSTRACT The novel arylamidine T-2307 exhibits broad-spectrum in vitro and in vivo antifungal activities against clinically significant pathogens. Previous studies have shown that T-2307 accumulates in yeast cells via a specific polyamine transporter and disrupts yeast mitochondrial membrane potential. Further, it has little effect on rat liver mitochondrial function. The mechanism by which T-2307 disrupts yeast mitochondrial function is poorly understood, and its elucidation may provide important information for developing novel antifungal agents. This study aimed to determine how T-2307 promotes yeast mitochondrial dysfunction and to investigate the selectivity of this mechanism between fungi and mammals. T-2307 inhibited the respiration of yeast whole cells and isolated yeast mitochondria in a dose-dependent manner. The similarity of the effects of T-2307 and respiratory chain inhibitors on mitochondrial respiration prompted us to investigate the effect of T-2307 on mitochondrial respiratory chain complexes. T-2307 particularly inhibited respiratory chain complexes III and IV not only in Saccharomyces cerevisiae but also in Candida albicans, indicating that T-2307 acts against pathogenic fungi in a manner similar to that of yeast. Conversely, T-2307 showed little effect on bovine respiratory chain complexes. Additionally, we demonstrated that the inhibition of respiratory chain complexes by T-2307 resulted in a decrease in the intracellular ATP levels in yeast cells. These results indicate that inhibition of respiratory chain complexes III and IV is a key factor for selective disruption of yeast mitochondrial function and antifungal activity.

scholarly journals Skeletal muscle metabolism in sea-acclimatized king penguins. II. Improved efficiency of mitochondrial bioenergetics

2020 ◽  
Vol 223 (21) ◽  
pp. jeb233684
Author(s):  
Damien Roussel ◽  
Vincent Marmillot ◽  
Pierre-Axel Monternier ◽  
Aurore Bourguignon ◽  
Gaëlle Toullec ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Respiratory Chain ◽  
Citrate Synthase ◽  
Coupling Efficiency ◽  
Chain Complex ◽  
Atp Synthesis ◽  
Respiratory Chain Complexes ◽  
Marine Habitat ◽  
Muscle Mitochondria

ABSTRACTAt fledging, juvenile king penguins (Aptenodytes patagonicus) must overcome the tremendous energetic constraints imposed by their marine habitat, including during sustained extensive swimming activity and deep dives in cold seawater. Both endurance swimming and skeletal muscle thermogenesis require high mitochondrial respiratory capacity while the submerged part of dive cycles repeatedly and greatly reduces oxygen availability, imposing a need for solutions to conserve oxygen. The aim of the present study was to determine in vitro whether skeletal muscle mitochondria become more ‘thermogenic’ to sustain heat production or more ‘economical’ to conserve oxygen in sea-acclimatized immature penguins (hereafter ‘immatures’) compared with terrestrial juveniles. Rates of mitochondrial oxidative phosphorylation were measured in permeabilized fibers and mitochondria from the pectoralis muscle. Mitochondrial ATP synthesis and coupling efficiency were measured in isolated muscle mitochondria. The mitochondrial activities of respiratory chain complexes and citrate synthase were also assessed. The results showed that respiration, ATP synthesis and respiratory chain complex activities in pectoralis muscles were increased by sea acclimatization. Furthermore, muscle mitochondria were on average 30–45% more energy efficient in sea-acclimatized immatures than in pre-fledging juveniles, depending on the respiratory substrate used (pyruvate, palmitoylcarnitine). Hence sea acclimatization favors the development of economical management of oxygen, decreasing the oxygen needed to produce a given amount of ATP. This mitochondrial phenotype may improve dive performance during the early marine life of king penguins, by extending their aerobic dive limit.

scholarly journals In Vitro Mitochondrial Toxicity of Metacavir, a New Nucleoside Reverse Transcriptase Inhibitor for Treatment of Hepatitis B Virus

2010 ◽  
Vol 54 (11) ◽  
pp. 4887-4892 ◽  
Author(s):  
Pinghu Zhang ◽  
Luyong Zhang ◽  
Zhenzhou Jiang ◽  
Tao Wang ◽  
Hongkui Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Respiratory Chain ◽  
Enzyme Activities ◽  
Mitochondrial Toxicity ◽  
Respiratory Chain Complexes ◽  
Chain Complexes ◽  
B Virus

ABSTRACT Therapy with nucleoside reverse transcriptase inhibitors (NRTIs) can be associated with mitochondrial toxicity. In vitro studies have been used to predict the predisposition for and characterize the mechanisms causing mitochondrial toxicity. Metacavir (PNA) is a novel synthetic nucleoside analog for oral administration with potent and specific antiviral activity against hepatitis B virus (HBV). We assessed the potential for mitochondrial toxicity of PNA in long-term cultures of HepG2 hepatoma cells by measuring mitochondrial function (through lactate secretion), levels of mitochondrial DNA (mtDNA), and the activities of respiratory-chain complexes I to IV. Exposure of HepG2 cells to PNA at concentrations up to 50 μM for 15 days resulted in no deleterious effect on cell proliferation, levels of lactate or mtDNA, or enzyme activities of respiratory-chain complexes I to IV. In contrast, dideoxycytosine at 10 μM and zidovudine at 50 μM have significant effects on cell proliferation, levels of lactate and mtDNA, and enzyme activities of respiratory-chain complexes I to IV. However, PNA at a supratherapeutic concentration of 250 μM could result in significant alterations in the levels of mtDNA and the activities of respiratory-chain complex enzymes, revealing evidence of the potential mitochondrial toxicity of PNA. In summary, these in vitro results indicate that the potential for PNA to interfere with mitochondrial functions is low.

A fast method for high resolution oxymetry study of skeletal muscle mitochondrial respiratory chain complexes

2017 ◽  
Vol 528 ◽  
pp. 57-62 ◽  
Author(s):  
Jean-Claude Vienne ◽  
Catherine Cimetta ◽  
Marie Dubois ◽  
Thibault Duburcq ◽  
Raphaël Favory ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Resolution ◽  
Respiratory Chain ◽  
Mitochondrial Respiratory Chain ◽  
Fast Method ◽  
Respiratory Chain Complexes ◽  
Chain Complexes ◽  
Mitochondrial Respiratory

Acute Carnosine Administration Increases Respiratory Chain Complexes and Citric Acid Cycle Enzyme Activities in Cerebral Cortex of Young Rats

2015 ◽  
Vol 53 (8) ◽  
pp. 5582-5590 ◽  
Author(s):  
Levy W. Macedo ◽  
José H. Cararo ◽  
Soliany G. Maravai ◽  
Cinara L. Gonçalves ◽  
Giovanna M. T. Oliveira ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Citric Acid ◽  
Respiratory Chain ◽  
Enzyme Activities ◽  
Citric Acid Cycle ◽  
Respiratory Chain Complexes ◽  
Acid Cycle ◽  
Cycle Enzyme ◽  
Young Rats ◽  
Chain Complexes
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