Respiratory Chain and Energy Metabolism of Corynebacterium glutamicum

2020 ◽  
pp. 61-85
Author(s):  
Naoya Kataoka ◽  
Minenosuke Matsutani ◽  
Kazunobu Matsushita
Keyword(s):  
Energy Metabolism ◽  
Corynebacterium Glutamicum ◽  
Respiratory Chain

scholarly journals Role of Natural Antioxidants on Neuroprotection and Neuroinflammation

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 608
Author(s):  
Domenico Nuzzo
Keyword(s):  
Reactive Oxygen Species ◽  
Energy Metabolism ◽  
Respiratory Chain ◽  
Reactive Oxygen ◽  
Natural Antioxidants ◽  
Oxygen Species

All cells continuously generate reactive oxygen species (ROS) through the respiratory chain during the energy metabolism process [...]

Effects of maintenance electroshock on mitochondrial respiratory chain and creatine kinase activities in the rat brain

2012 ◽  
Vol 24 (5) ◽  
pp. 275-285
Author(s):  
Gislaine Z. Réus ◽  
Roberto B. Stringari ◽  
Gislaine T. Rezin ◽  
Daiana P. Pezente ◽  
Giselli Scaini ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Energy Metabolism ◽  
Rat Brain ◽  
Respiratory Chain ◽  
Brain Area ◽  
Mitochondrial Respiratory Chain ◽  
Respiratory Chain Complexes ◽  
Chain Complexes ◽  
Male Wistar Rats ◽  
Mitochondrial Respiratory

Réus GZ, Stringari RB, Rezin GT, Pezente DP, Scaini G, Maggi DD, De-Nês BT, Streck EL, Quevedo J, Feier G. Effects of maintenance electroshock on mitochondrial respiratory chain and creatine kinase activities in the rat brain.Objective: Electroconvulsive therapy is used efficacious treatment for a variety of complicated psychiatric disorders and evidences have indicated that energy metabolism impairment may be involved in pathophysiology and treatment of mood disorders. This work was performed to determine creatine kinase and mitochondrial respiratory chain activities at different times after the maintenance electroconvulsive shock (ECS).Methods: Male Wistar rats received a protocol mimicking therapeutic of maintenance or simulated ECS (sham) and were subsequently sacrificed immediately after, 48 h and 7 days after the last maintenance ECS. We measured creatine kinase and mitochondrial respiratory chain activities in the prefrontal cortex, hippocampus, cortex, cerebellum and striatum.Results: Our results showed that maintenance ECS alter respiratory chain complexes and creatine kinase activities in the rat brain, but these effects were related to brain area and time after the ECS, in which the animal were killed.Conclusion: Finally, these findings further support the hypothesis that alteration on the energy metabolism could be involved in the therapeutic or adverse effects of ECS.

Brain energy metabolism is increased by chronic administration of bupropion

2012 ◽  
Vol 24 (2) ◽  
pp. 115-121 ◽  
Author(s):  
Gabriela K. Ferreira ◽  
Gislaine T. Rezin ◽  
Mariane R. Cardoso ◽  
Cinara L. Gonçalves ◽  
Lislaine S. Borges ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Malate Dehydrogenase ◽  
Respiratory Chain ◽  
Citrate Synthase ◽  
Chronic Administration ◽  
Mitochondrial Respiratory Chain ◽  
Brain Energy Metabolism ◽  
Respiratory Chain Complexes ◽  
Chain Complexes ◽  
Brain Energy

Objectives: Based on the hypothesis that energy impairment may be involved in the pathophysiology of depression, we evaluated the activities of citrate synthase, malate dehydrogenase, succinate dehydrogenase (SDH), mitochondrial respiratory chain complexes I, II, II-III, IV and creatine kinase (CK) in the brain of rats submitted to chronic administration of bupropion.Methods: Animals received daily administration of bupropion dissolved in saline (10 mg/kg, intraperitoneal) at 1.0 ml/kg body weight. The rats received injections once a day for 14 days; control rats received an equivalent volume of saline. Twelve hours after the last administration, the rats were killed by decapitation and brain was rapidly removed and kept on an ice plate. The activities of the enzymes were measured in different brain areas.Results: We observed that the activities of citrate synthase and malate dehydrogenase, mithocondrial respiratory chain complexes I, II-III and IV and CK were not altered after chronic administration of bupropion. However, SDH activity was increased in the prefrontal cortex and cerebellum. In the hippocampus, cerebellum and striatum the activity of complex II was increased after chronic administration of bupropion.Conclusions: Our results demonstrated that bupropion increased some enzymes of brain energy metabolism. These findings are in accordance with other studies which showed that some antidepressants may improve energy metabolism. The present results reinforce the hypothesis that antidepressants modulate brain energy metabolism.

scholarly journals Control of respiration and ATP synthesis in mammalian mitochondria and cells

1992 ◽  
Vol 284 (1) ◽  
pp. 1-13 ◽  
Author(s):  
G C Brown
Keyword(s):  
Energy Metabolism ◽  
Oxidative Phosphorylation ◽  
Respiratory Chain ◽  
Atp Synthase ◽  
Energy Charge ◽  
Atp Synthesis ◽  
Basic Mechanism ◽  
Proton Leak ◽  
Control Of Respiration ◽  
Phosphorylation Potential

We have seen that there is no simple answer to the question ‘what controls respiration?’ The answer varies with (a) the size of the system examined (mitochondria, cell or organ), (b) the conditions (rate of ATP use, level of hormonal stimulation), and (c) the particular organ examined. Of the various theories of control of respiration outlined in the introduction the ideas of Chance & Williams (1955, 1956) give the basic mechanism of how respiration is regulated. Increased ATP usage can cause increased respiration and ATP synthesis by mass action in all the main tissues. Superimposed on this basic mechanism is calcium control of matrix dehydrogenases (at least in heart and liver), and possibly also of the respiratory chain (at least in liver) and ATP synthase (at least in heart). In many tissues calcium also stimulates ATP usage directly; thus calcium may stimulate energy metabolism at (at least) four possible sites, the importance of each regulation varying with tissue. Regulation of multiple sites may occur (from a teleological point of view) because: (a) energy metabolism is branched and thus proportionate regulation of branches is required in order to maintain constant fluxes to branches (e.g. to proton leak or different ATP uses); and/or (b) control over fluxes is shared by a number of reactions, so that large increases in flux requires stimulation at multiple sites because each site has relatively little control. Control may be distributed throughout energy metabolism, possibly due to the necessity of minimizing cell protein levels (see Brown, 1991). The idea that energy metabolism is regulated by energy charge (as proposed by Atkinson, 1968, 1977) is misleading in mammals. Neither mitochondrial ATP synthesis nor cellular ATP usage is a unique function of energy charge as AMP is not a significant regulator (see for example Erecinska et al., 1977). The near-equilibrium hypothesis of Klingenberg (1961) and Erecinska & Wilson (1982) is partially correct in that oxidative phosphorylation is often close to equilibrium (apart from cytochrome oxidase) and as a consequence respiration and ATP synthesis are mainly regulated by (a) the phosphorylation potential, and (b) the NADH/NAD+ ratio. However, oxidative phosphorylation is not always close to equilibrium, at least in isolated mitochondria, and relative proximity to equilibrium does not prevent the respiratory chain, the proton leak, the ATP synthase and ANC having significant control over the fluxes. Thus in some conditions respiration rate correlates better with [ADP] than with phosphorylation potential, and may be relatively insensitive to mitochondrial NADH/NAD+ ratio.(ABSTRACT TRUNCATED AT 400 WORDS)

Impaired energy metabolism in septic hearts of baboons: diminished activities of complex I and complex II of the mitochondrial respiratory chain

Shock ◽  
1997 ◽  
Vol 7 (Supplement) ◽  
pp. 24
Author(s):  
Sonata Trumbeckaite ◽  
Kathrin Hertel ◽  
Gilles Durrieu ◽  
Frank Gellerich ◽  
Ursula Müller-Werdan ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Respiratory Chain ◽  
Complex I ◽  
Mitochondrial Respiratory Chain ◽  
Complex Ii ◽  
Impaired Energy Metabolism ◽  
Mitochondrial Respiratory

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.

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