The role of glutamine synthetase in energy production and glutamine metabolism during oxidative stress

The hepatitis C virus (HCV) infection produces several pathological effects in host organism through a wide number of molecular/metabolic pathways. Today it is worldwide accepted that oxidative stress actively participates in HCV pathology, even if the antioxidant therapies adopted until now were scarcely effective. HCV causes oxidative stress by a variety of processes, such as activation of prooxidant enzymes, weakening of antioxidant defenses, organelle damage, and metals unbalance. A focal point, in HCV-related oxidative stress onset, is the mitochondrial failure. These organelles, known to be the “power plants” of cells, have a central role in energy production, metabolism, and metals homeostasis, mainly copper and iron. Furthermore, mitochondria are direct viral targets, because many HCV proteins associate with them. They are the main intracellular free radicals producers and targets. Mitochondrial dysfunctions play a key role in the metal imbalance. This event, today overlooked, is involved in oxidative stress exacerbation and may play a role in HCV life cycle. In this review, we summarize the role of mitochondria and metals in HCV-related oxidative stress, highlighting the need to consider their deregulation in the HCV-related liver damage and in the antiviral management of patients.

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Glutamine metabolism of small intestinal mucosa—role of glutamine synthetase and amidotransferase pathways

Clinical Nutrition ◽

10.1016/0261-5614(93)90192-7 ◽

1993 ◽

Vol 12 ◽

pp. 11

Author(s):

M. Plauth ◽

R. Reuter ◽

A. Raible ◽

D. Vieillard-Baron ◽

M. Gregor

Keyword(s):

Glutamine Synthetase ◽

Intestinal Mucosa ◽

Glutamine Metabolism ◽

Small Intestinal Mucosa ◽

Small Intestinal

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Mitochondria, oxidative stress and the petite phenotype in Saccharomyces cerevisiae

Microbiology Australia ◽

10.1071/ma10082 ◽

2010 ◽

Vol 31 (2) ◽

pp. 82

Author(s):

Anita Ayer ◽

Ian W Dawes ◽

Gabriel G Perrone

Keyword(s):

Oxidative Stress ◽

Energy Production ◽

Acid Synthesis ◽

Nuclear Space ◽

Amino Acid Synthesis ◽

Iron Sulfur Cluster ◽

Iron Sulfur ◽

Eukaryotic Organisms ◽

State Concentration

Oxidative stress has long been recognised as biologically important and is increasingly implicated in a variety of phenomena, such as mutation, carcinogenesis, degenerative and other diseases, inflammation, ageing, and development. The role of the mitochondrion in oxidative stress and the production of reactive oxygen species (ROS) and other radical species is well-established, with mitochondria providing a fascinating area of study within the oxidative stress field. Mitochondria are essential organelles for the viability of all eukaryotic organisms. While mitochondria perform important processes associated with oxidative phosphorylation and energy production, and numerous other metabolic processes, such as iron sulfur cluster biogenesis, lipid and amino acid synthesis, they also appear to be the largest intracellular source of ROS in aerobic cells. The steady state concentration of O2 in the mitochondrial matrix is five- to tenfold higher than in the cytosol or nuclear space according to one estimation. Therefore, mitochondrial macromolecules such as mitochondrial DNA are particularly susceptible to oxidative damage.

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The Role of Mitochondria in Cardiovascular Diseases

Biology ◽

10.3390/biology9060137 ◽

2020 ◽

Vol 9 (6) ◽

pp. 137 ◽

Cited By ~ 2

Author(s):

Anastasia V. Poznyak ◽

Ekaterina A. Ivanova ◽

Igor A. Sobenin ◽

Shaw-Fang Yet ◽

Alexander N. Orekhov

Keyword(s):

Oxidative Stress ◽

Cardiovascular Diseases ◽

Mitochondrial Dysfunction ◽

Energy Production ◽

Cardiovascular Disorders ◽

Intensive Study ◽

Potential Therapeutic Target ◽

Cell Dysfunction ◽

Mtdna Mutations

The role of mitochondria in cardiovascular diseases is receiving ever growing attention. As a central player in the regulation of cellular metabolism and a powerful controller of cellular fate, mitochondria appear to comprise an interesting potential therapeutic target. With the development of DNA sequencing methods, mutations in mitochondrial DNA (mtDNA) became a subject of intensive study, since many directly lead to mitochondrial dysfunction, oxidative stress, deficient energy production and, as a result, cell dysfunction and death. Many mtDNA mutations were found to be associated with chronic human diseases, including cardiovascular disorders. In particular, 17 mtDNA mutations were reported to be associated with ischemic heart disease in humans. In this review, we discuss the involvement of mitochondrial dysfunction in the pathogenesis of atherosclerosis and describe the mtDNA mutations identified so far that are associated with atherosclerosis and its risk factors.

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The Role of Oxidative Stress in Metals Toxicity; Mitochondrial Dysfunction as a Key Player

Galen Medical Journal ◽

10.31661/gmj.v3i1.100 ◽

2014 ◽

Vol 3 (1) ◽

pp. 2-13

Author(s):

Akram Ranjbar ◽

Hassan Ghasemi ◽

Farshad Rostampour‎

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Energy Production ◽

Reactive Oxygen ◽

Atp Synthesis ◽

Ros Generation ◽

Oxygen Species ◽

Cellular Oxygen ◽

A Site

Metals can cause oxidative stress by increasing the formation of reactive oxygen species (ROS), which make antioxidants incapable of defiance against growing amounts of free radicals. Metal toxicity is related to their oxidative state and reactivity with other compounds. However, several reports about metals have been published in the recent years. Mitochondria, as a site of cellular oxygen consumption and energy production, can be a target for metals toxicity. Dysfunction of Mitochondrial oxidative phosphorylation led to the production of some metals toxicities metals through alteration in the activities of I, II, III, IV and V complexes and disruption of mitochondrial membrane. Reductions of adenosine triphosphate (ATP) synthesis or induction of its hydrolysis can impair the cellular energy production. In the present review study, the researchers have criticized reviews and some evidence about the oxidative stress as a mechanism of toxicity of metals. The metals disrupt cellular and antioxidant defense, reactive oxygen species (ROS) generation, and promote oxidative damage. The oxidative injuries induced by metals can be restored by use of antioxidants such as chelators, vitamin E and C, herbal medicine, and through increasing the antioxidants level. However, to elucidate many aspect of mechanism toxicity of metals, further studies are yet to be carried out.

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Mitochondrial matrix calcium ions regulate energy production in myocardium: A cytochemical study

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100134429 ◽

1990 ◽

Vol 48 (2) ◽

pp. 166-167

Author(s):

W.A. Jacob ◽

R. Hertsens ◽

A. Van Bogaert ◽

M. De Smet

Keyword(s):

Energy Metabolism ◽

Calcium Ions ◽

Energy Production ◽

Regulation Of Respiration ◽

Free Calcium ◽

Mitochondrial Matrix ◽

Cytochemical Study ◽

Nmr Techniques

In the past most studies of the control of energy metabolism focus on the role of the phosphorylation potential ATP/ADP.Pi on the regulation of respiration. Studies using NMR techniques have demonstrated that the concentrations of these compounds for oxidation phosphorylation do not change appreciably throughout the cardiac cycle and during increases in cardiac work. Hence regulation of energy production by calcium ions, present in the mitochondrial matrix, has been the object of a number of recent studies.Three exclusively intramitochondnal dehydrogenases are key enzymes for the regulation of oxidative metabolism. They are activated by calcium ions in the low micromolar range. Since, however, earlier estimates of the intramitochondnal calcium, based on equilibrium thermodynamic considerations, were in the millimolar range, a physiological correlation was not evident. The introduction of calcium-sensitive probes fura-2 and indo-1 made monitoring of free calcium during changing energy metabolism possible. These studies were performed on isolated mitochondria and extrapolation to the in vivo situation is more or less speculative.

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