scholarly journals Computational Model Of Citric Acid Cycle And Oxidative Phosphorylation In Mitochondria

2009 ◽  
Vol 96 (3) ◽  
pp. 242a
Author(s):  
Ardo Illaste ◽  
Marko Vendelin
Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1410 ◽  
Author(s):  
Gerresheim ◽  
Roeb ◽  
Michel ◽  
Niepmann

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.


Biomolecules ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 1068 ◽  
Author(s):  
Joséphine Zangari ◽  
Francesco Petrelli ◽  
Benoît Maillot ◽  
Jean-Claude Martinou

Pyruvate, the end product of glycolysis, plays a major role in cell metabolism. Produced in the cytosol, it is oxidized in the mitochondria where it fuels the citric acid cycle and boosts oxidative phosphorylation. Its sole entry point into mitochondria is through the recently identified mitochondrial pyruvate carrier (MPC). In this review, we report the latest findings on the physiology of the MPC and we discuss how a dysfunctional MPC can lead to diverse pathologies, including neurodegenerative diseases, metabolic disorders, and cancer.


Biomolecules ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 1558
Author(s):  
Chia-Jung Li

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 [...]


2021 ◽  
Vol 64 (1) ◽  
Author(s):  
Eun Ko ◽  
Min Young Um ◽  
Taewon Han ◽  
Sooim Shin ◽  
Moonsung Choi

AbstractCassia tora is an annual herb, which has pharmacological effects such as antioxidant, hypolipidemic, and antidiabetic effects. Accordingly, its effect on diabetes has been well-studied. However, it is unclear whether it has an effect on mitochondrial dysfunction associated with diabetes. In this study, the effects of emodin and rhein in C. tora seed ethanolic extract (ER/CSEE) on retinal mitochondrial function were examined in high-fat diet (HFD)-fed mice. HFD-fed mice exhibited decreased mitochondrial function followed by compensatory increase in the expression levels of mitochondrial enzymes. However, ER/CSEE treatment for 12 weeks ameliorated the activity of retinal mitochondrial complexes and reduced the expression level of enzymes involved in oxidative phosphorylation, except that of complex II and citrate synthase in citric acid cycle. This suggests that repairing capacity of enzymes in electron transport chain and citric acid cycle of mitochondria are different in response to the metabolic state. Therefore, it concluded that emodin and rhein play a pharmacological role in fat metabolism by influencing activities of enzymes in citric acid cycle linked with beta-oxidation in retina.


1963 ◽  
Vol 42 (4) ◽  
pp. 480-484 ◽  
Author(s):  
B. Eckstein ◽  
R. Landsberg

ABSTRACT The succinic, malic and isocitric dehydrogenases in the ovary of immature and mature, normal and serum gonadotrophin injected rats were examined. The Qo2 of these enzymes were markedly enhanced in the gonadotrophin injected rats of both age groups, except in the case of succinic dehydrogenase in the ovary of the immature rats, where a slight non-significant decrease was noted. It is concluded that in the mature rat ovary, gonadotrophin administration stimulates the activity of all the examined dehydrogenases of the citric acid cycle, whereas in the immature rat ovary, at least the isocitric- and malic dehydrogenases are thus stimulated.


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