scholarly journals Oxidative Stress and Mitochondrial Dysfunction in Human Diseases: Pathophysiology, Predictive Biomarkers, Therapeutic

Biomolecules ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 1558
Author(s):  
Chia-Jung Li
Keyword(s):  
Oxidative Stress ◽  
Fatty Acid ◽  
Amino Acid ◽  
Citric Acid ◽  
Oxidative Phosphorylation ◽  
Citric Acid Cycle ◽  
Acid Metabolism ◽  
Predictive Biomarkers ◽  
Acid Cycle ◽  
Cellular Processes

Mitochondria are important sites for a variety of cellular processes, including amino acid and fatty acid metabolism, the citric acid cycle, nitrogen metabolism, and oxidative phosphorylation to produce ATP [...]

498-P: Resistance Exercise Rapidly Alters Citric Acid Cycle and Amino Acid Metabolism in Skeletal Muscle

Diabetes ◽  
2021 ◽  
Vol 70 (Supplement 1) ◽  
pp. 498-P
Author(s):  
MARK W. PATAKY ◽  
ARATHI PRABHA KUMAR ◽  
KATHERINE KLAUS ◽  
K. SREEKUMARAN NAIR
Keyword(s):  
Skeletal Muscle ◽  
Amino Acid ◽  
Citric Acid ◽  
Resistance Exercise ◽  
Amino Acid Metabolism ◽  
Citric Acid Cycle ◽  
Acid Metabolism ◽  
Acid Cycle

scholarly journals Blood metabolomics analysis identifies abnormalities in the citric acid cycle, urea cycle, and amino acid metabolism in bipolar disorder

BBA Clinical ◽  
2016 ◽  
Vol 5 ◽  
pp. 151-158 ◽  
Author(s):  
Noriko Yoshimi ◽  
Takashi Futamura ◽  
Keiji Kakumoto ◽  
Alireza M. Salehi ◽  
Carl M. Sellgren ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Amino Acid ◽  
Citric Acid ◽  
Amino Acid Metabolism ◽  
Citric Acid Cycle ◽  
Acid Metabolism ◽  
Urea Cycle ◽  
Acid Cycle ◽  
Metabolomics Analysis

scholarly journals Conversion of glutamate into aspartate in guinea-pig cerebral-cortex slices

1968 ◽  
Vol 107 (1) ◽  
pp. 109-111 ◽  
Author(s):  
Gerald Simon ◽  
M. M. Cohen ◽  
J. F. Berry
Keyword(s):  
Cerebral Cortex ◽  
Amino Acid ◽  
Citric Acid ◽  
Guinea Pig ◽  
Amino Acid Metabolism ◽  
Citric Acid Cycle ◽  
Acid Metabolism ◽  
Acid Cycle ◽  
Cortex Slices

1. When guinea-pig cerebral-cortex slices were incubated with [U−14C]glutamate as substrate, the specific radioactivities of the citric acid-cycle intermediates were lower than that of the aspartate isolated from the same vessels. 2. Aspartate was significantly labelled when [5−14C]glutamate was used as substrate and the aspartate contained almost no label when [1−14C]glutamate was present as substrate. 3. When specifically labelled glutamate was used as substrate, the label was found in the isolated aspartate in the position that would be predicted by citric acid-cycle mechanisms. 4. The results are consistent with the theory of ‘compartmentation’ of amino acid metabolism.

scholarly journals Hepatitis C Virus Downregulates Core Subunits of Oxidative Phosphorylation, Reminiscent of the Warburg Effect in Cancer Cells

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1410 ◽  
Author(s):  
Gerresheim ◽  
Roeb ◽  
Michel ◽  
Niepmann
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Citric Acid ◽  
Oxidative Phosphorylation ◽  
Cancer Cells ◽  
Warburg Effect ◽  
Citric Acid Cycle ◽  
Host Cells ◽  
Acid Cycle ◽  
The Warburg Effect

Hepatitis C Virus (HCV) mainly infects liver hepatocytes and replicates its single-stranded plus strand RNA genome exclusively in the cytoplasm. Viral proteins and RNA interfere with the host cell immune response, allowing the virus to continue replication. Therefore, in about 70% of cases, the viral infection cannot be cleared by the immune system, but a chronic infection is established, often resulting in liver fibrosis, cirrhosis and hepatocellular carcinoma (HCC). Induction of cancer in the host cells can be regarded to provide further advantages for ongoing virus replication. One adaptation in cancer cells is the enhancement of cellular carbohydrate flux in glycolysis with a reduction of the activity of the citric acid cycle and aerobic oxidative phosphorylation. To this end, HCV downregulates the expression of mitochondrial oxidative phosphorylation complex core subunits quite early after infection. This so-called aerobic glycolysis is known as the “Warburg Effect” and serves to provide more anabolic metabolites upstream of the citric acid cycle, such as amino acids, pentoses and NADPH for cancer cell growth. In addition, HCV deregulates signaling pathways like those of TNF-β and MAPK by direct and indirect mechanisms, which can lead to fibrosis and HCC.

scholarly journals Citrus Flavanones Affect Hepatic Fatty Acid Oxidation in Rats by Acting as Prooxidant Agents

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Rodrigo Polimeni Constantin ◽  
Gilson Soares do Nascimento ◽  
Renato Polimeni Constantin ◽  
Clairce Luzia Salgueiro ◽  
Adelar Bracht ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Citric Acid ◽  
Oxygen Uptake ◽  
Fatty Acid Oxidation ◽  
Citric Acid Cycle ◽  
Acid Oxidation ◽  
Acid Cycle ◽  
Hepatic Fatty Acid ◽  
Wide Range ◽  
Hepatic Fatty Acid Oxidation

Citrus flavonoids have a wide range of biological activities and positive health effects on mammalian cells because of their antioxidant properties. However, they also act as prooxidants and thus may interfere with metabolic pathways. The purpose of this work was to evaluate the effects of three citrus flavanones, hesperidin, hesperetin, and naringenin, on several parameters linked to fatty acid oxidation in mitochondria, peroxisomes, and perfused livers of rats. When exogenous octanoate was used as substrate, hesperetin and naringenin reduced the mitochondrial NADH/NAD+ratio and stimulated the citric acid cycle without significant changes on oxygen uptake or ketogenesis. When fatty acid oxidation from endogenous sources was evaluated, hesperetin and naringenin strongly reduced the mitochondrial NADH/NAD+ratio. They also inhibited both oxygen uptake and ketogenesis and stimulated the citric acid cycle. Hesperidin, on the other hand, had little to no effect on these parameters. These results confirm the hypothesis that citrus flavanones are able to induce a more oxidised state in liver cells, altering parameters related to hepatic fatty acid oxidation. The prooxidant effect is most likely a consequence of the ability of these substances to oxidise NADH upon production of phenoxyl radicals in the presence of peroxidases and hydrogen peroxide.

scholarly journals A Dysfunctional Tricarboxylic Acid Cycle Enhances Fitness of Staphylococcus epidermidis During β-Lactam Stress

mBio ◽  
2013 ◽  
Vol 4 (4) ◽  
Author(s):  
Vinai Chittezham Thomas ◽  
Lauren C. Kinkead ◽  
Ashley Janssen ◽  
Carolyn R. Schaeffer ◽  
Keith M. Woods ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Citric Acid ◽  
Cell Surface ◽  
Staphylococcus Epidermidis ◽  
Citric Acid Cycle ◽  
Tricarboxylic Acid Cycle ◽  
Tca Cycle ◽  
Tricarboxylic Acid ◽  
Content Type ◽  
Acid Cycle

ABSTRACT A recent controversial hypothesis suggested that the bactericidal action of antibiotics is due to the generation of endogenous reactive oxygen species (ROS), a process requiring the citric acid cycle (tricarboxylic acid [TCA] cycle). To test this hypothesis, we assessed the ability of oxacillin to induce ROS production and cell death in Staphylococcus epidermidis strain 1457 and an isogenic citric acid cycle mutant. Our results confirm a contributory role for TCA-dependent ROS in enhancing susceptibility of S. epidermidis toward β-lactam antibiotics and also revealed a propensity for clinical isolates to accumulate TCA cycle dysfunctions presumably as a way to tolerate these antibiotics. The increased protection from β-lactam antibiotics could result from pleiotropic effects of a dysfunctional TCA cycle, including increased resistance to oxidative stress, reduced susceptibility to autolysis, and a more positively charged cell surface. IMPORTANCE Staphylococcus epidermidis, a normal inhabitant of the human skin microflora, is the most common cause of indwelling medical device infections. In the present study, we analyzed 126 clinical S. epidermidis isolates and discovered that tricarboxylic acid (TCA) cycle dysfunctions are relatively common in the clinical environment. We determined that a dysfunctional TCA cycle enables S. epidermidis to resist oxidative stress and alter its cell surface properties, making it less susceptible to β-lactam antibiotics.

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