scholarly journals An integrated overview on the regulation of sperm metabolism (glycolysis-Krebs cycle-oxidative phosphorylation)

2021 ◽  
pp. 106805
Author(s):  
Fernando J. Peña ◽  
José M. Ortiz-Rodríguez ◽  
Gemma L. Gaitskell-Phillips ◽  
Maria C. Gil ◽  
Cristina Ortega-Ferrusola ◽  
...  
2005 ◽  
Vol 93 (6) ◽  
pp. 901-909 ◽  
Author(s):  
Selvanathan Saravana Perumal ◽  
Palanivelu Shanthi ◽  
Panchanadham Sachdanandam

Mitochondria are the major intracellular organelles producing ATP molecules via the electron transport chain. Cancer cells have a deviant energy metabolism, and a high rate of glycolysis is related to a high degree of dedifferentiation and proliferation. The overall net ATP production is diminished with cancer, which ultimately leads to cancer cachexia. The present study was designed to investigate the altered energy metabolism in cancer cells and to enhance ATP production in the normal host cell metabolism by enhancing the activities of mitochondrial enzymes, using energy-modulating vitamins, and thus prevent cancer cachexia. Female Sprague–Dawley rats were selected for the experimental study. Mammary carcinoma was induced by the oral administration of 7,12-dimethylbenz[a]anthracene (25 mg/kg body weight), and treatment was started by the oral administration of the energy-modulating vitamins riboflavin (45 mg/kg body weight per d), niacin (100 mg/kg body weight per d) and coenzyme Q10(40 mg/kg body weight per d) for 28 d. Mitochondria were isolated from the mammary gland and liver of all four groups, and the Krebs cycle and oxidative phosphorylation enzymes were assayed. In mammary carcinoma-bearing animals, the activities of the Krebs cycle and oxidative phosphorylation enzymes were significantly decreased. These activities were restored to a greater extent in animals treated with energy-modulating vitamins. From these experimental results, one may hypothesize that the combination therapy of energy-modulating vitamins could be of major therapeutic value in breast cancer.


Protist ◽  
2014 ◽  
Vol 165 (5) ◽  
pp. 701-714 ◽  
Author(s):  
Yonglan Yu ◽  
Haili Zhang ◽  
Fengguang Guo ◽  
Mingfei Sun ◽  
Guan Zhu

Author(s):  
E. Kenneth Parkinson ◽  
Jerzy Adamski ◽  
Grit Zahn ◽  
Andreas Gaumann ◽  
Fabian Flores-Borja ◽  
...  

Abstract It is well established that cancer cells acquire energy via the Warburg effect and oxidative phosphorylation. Citrate is considered to play a crucial role in cancer metabolism by virtue of its production in the reverse Krebs cycle from glutamine. Here, we review the evidence that extracellular citrate is one of the key metabolites of the metabolic pathways present in cancer cells. We review the different mechanisms by which pathways involved in keeping redox balance respond to the need of intracellular citrate synthesis under different extracellular metabolic conditions. In this context, we further discuss the hypothesis that extracellular citrate plays a role in switching between oxidative phosphorylation and the Warburg effect while citrate uptake enhances metastatic activities and therapy resistance. We also present the possibility that organs rich in citrate such as the liver, brain and bones might form a perfect niche for the secondary tumour growth and improve survival of colonising cancer cells. Consistently, metabolic support provided by cancer-associated and senescent cells is also discussed. Finally, we highlight evidence on the role of citrate on immune cells and its potential to modulate the biological functions of pro- and anti-tumour immune cells in the tumour microenvironment. Collectively, we review intriguing evidence supporting the potential role of extracellular citrate in the regulation of the overall cancer metabolism and metastatic activity.


1953 ◽  
Vol 98 (1) ◽  
pp. 81-98 ◽  
Author(s):  
John W. Harman ◽  
Ursula H. Osborne

In pigeon breast muscle the mitochondria are the principal site of oxidative metabolism, whereas the myofibrils are incapable of oxidizing intermediates of the Krebs cycle. The mitochondria contain the oxidative enzymes, and the sarcosomes are associated with a factor which accelerates the mitochondrial oxidative rate. The maintenance of myofibrillar contractility and structure is closely correlated with preservation of mitochondrial oxidative capacity and structure. By use of fluoride and dinitrophenol the connection between mitochondrial metabolism and myofibrillar behavior is shown to occur through the process of oxidative phosphorylation.


2003 ◽  
Vol 285 (4) ◽  
pp. R817-R826 ◽  
Author(s):  
S. C. Leary ◽  
C. N. Lyons ◽  
A. G. Rosenberger ◽  
J. S. Ballantyne ◽  
J. Stillman ◽  
...  

Although striated muscles differ in mitochondrial content, the extent of fiber-type specific mitochondrial specializations is not well known. To address this issue, we compared mitochondrial structural and functional properties in red muscle (RM), white muscle (WM), and cardiac muscle of rainbow trout. Overall preservation of the basic relationships between oxidative phosphorylation complexes among fiber types was confirmed by kinetic analyses, immunoblotting of native holoproteins, and spectroscopic measurements of cytochrome content. Fiber-type differences in mitochondrial properties were apparent when parameters were expressed per milligram mitochondrial protein. However, the differences diminished when expressed relative to cytochrome oxidase (COX), possibly a more meaningful denominator than mitochondrial protein. Expressed relative to COX, there were no differences in oxidative phosphorylation enzyme activities, pyruvate-based respiratory rates, H2O2 production, or state 4 proton leak respiration. These data suggest most mitochondrial qualitative properties are conserved across fiber types. However, there remained modest differences (∼50%) in stoichiometries of selected enzymes of the Krebs cycle, β-oxidation, and antioxidant enzymes. There were clear differences in membrane fluidity (RM > cardiac, WM) and proton conductance (H+/min/mV/U COX: WM > RM > cardiac). The pronounced differences in mitochondrial content between fiber types could be attributed to a combination of differences in myonuclear domain and modest effects on the expression of nuclear- and mitochondrially encoded respiratory genes. Collectively, these studies suggest constitutive pathways that transcend fiber types are primarily responsible for determining most quantitative and qualitative properties of mitochondria.


2002 ◽  
Vol 14 (6) ◽  
pp. 339 ◽  
Author(s):  
D. Rieger ◽  
L. T. McGowan ◽  
S. F. Cox ◽  
P. A. Pugh ◽  
J. G. Thompson

In cattle embryos, the proportion of ATP produced by glycolysis increases following the major activation of the embryonic genome, and development to the blastocyst stage is improved in the presence of 10 µM 2,4-dinitrophenol (DNP), an uncoupler of oxidative phosphorylation, from Day 5 to Day 7 of culture. In Experiment 1 of the present study, culture of cattle embryos in the presence of 10 µM DNP from Day 5 to Day 7 stimulated development to the blastocyst stage, but had no significant effects on oxygen, pyruvate or glucose uptake, or on lactate production. In Experiment 2, culture of cattle embryos in the presence of 10 µM DNP from Day 5 to Day 7, stimulated the metabolism of [2-14C]pyruvate (a measure of Krebs cycle activity) on all of Days 5, 6 and 7, and stimulated metabolism of [5-3H]glucose (a measure of glycolysis) on Day 7 only. The results show that 10 µM DNP stimulates oxidative and glycolytic metabolism in Day-5 to Day-7 cattle embryos, but this does not fully explain the observed increase in developmental competence. We propose that partial inhibition or uncoupling of oxidative phosphorylation may reduce the level of intracellular reactive oxygen species production, thereby facilitating development.


2019 ◽  
Vol 22 (1) ◽  
pp. 25-34 ◽  
Author(s):  
Sergey A. Afanasiev ◽  
Dina S. Kondratieva ◽  
Margarita V. Egorova ◽  
Shamil D. Akhmedov ◽  
Olesya V. Budnikova ◽  
...  

Background: Metabolic and structural changes in cardiomyocytes in diabetes mellitus lead to aggravation of contractile myocardial dysfunction in coronary heart disease (CHD). The contractility dysfunction of cardiomyocytes is determined by a change in the levels of sarcoplasmic reticulum (SR) Ca2+-ATPase and energetic supply of the cardiomyocytes. Aims: To study the features of functional remodeling of the heart muscle in coronary heart disease with and without type 2 diabetes mellitus (DM2) depend on the level of Ca2+-ATPase and the activity of enzymes involved in energy metabolism. Materials and methods: The work was performed on the heart biopsy of patients with CHD and patients with CHD combined with DM2. The inotropic reaction of myocardial strips on rest periods was assessed. The expression level of Ca2+-ATPase, the activity of enzymes succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH) and the intensity of oxidative phosphorylation processes were determined. Results: The interval-force relationship in patients with CHD with and without DM2 had both negative and positive dynamics. The positive dynamics corresponds to the "high content" of the Ca2+-ATPase and the negative dynamics corresponds to the "low content" were found. At the combined pathology the positive inotropic dynamics is more pronounced and corresponds to a higher protein level. In the patients myocardium with CHD the activity of SDH and LDH was higher, while the oxygen uptake rate by mitochondria was higher in the myocardium with combined pathology. Conclusions: The potentiation of inotropic response of patient myocardium with CHD with and without DM2 corresponds to the "high level" of Ca2+-ATPase. In the combined pathology the inotropic capabilities of the myocardium are more expressed. In CHD the synthesis of ATP in cardiomyocytes is realized mainly due to glycolytic processes and Krebs cycle. In combined pathology the ATP synthesis is realized to a greater extent due to the oxidative phosphorylation.


2011 ◽  
Vol 04 (02) ◽  
pp. 209-214
Author(s):  
PAUL KOSTERIN ◽  
ANA LÍA OBAID ◽  
BRIAN M. SALZBERG

Electrical stimulation of the mammalian neurohypophysial infundibular stalk evokes the entry of Na+ and Ca2+ into the neurosecretory terminals during the action potential. These events, in turn, increase intracellular Ca2+ and activate NaK - and Ca -ATPases, prompting the mitochondria to increase oxidative phosphorylation which can be monitored by recording the changes in FAD and NADH fluorescence. This paper reflects our efforts to determine whether or not modulating the capacity of mitochondria to produce ATP, by changing the concentrations of two important substrates of the Krebs cycle of the nerve terminal mitochondria, pyruvate and glucose, has an effect on the intrinsic fluorescence changes triggered by action potential stimulation.


Sign in / Sign up

Export Citation Format

Share Document