scholarly journals Functional Changes Induced by Short Term Caloric Restriction in Cardiac and Skeletal Muscle Mitochondria

2020 ◽  
Author(s):  
Julian David C. Serna ◽  
Camille C. Caldeira da Silva ◽  
Alicia J. Kowaltowski
Keyword(s):  
Skeletal Muscle ◽  
Hydrogen Peroxide ◽  
Caloric Restriction ◽  
Calcium Uptake ◽  
Atp Synthesis ◽  
Calcium Handling ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Uptake Rates ◽  
Hydrogen Peroxide Release

AbstractCaloric restriction (CR) is widely known to increase life span and resistance against different types of injuries in several organisms. We have previously shown that mitochondria from livers or brains of CR animals exhibit higher calcium uptake rates and lower sensitivity to calcium-induced mitochondrial permeability transition (mPT), an event related to the resilient phenotype exhibited by these organs. Given the importance of calcium in metabolic control and cell homeostasis, we aimed here to uncover possible changes in mitochondrial calcium handling, redox balance and bioenergetics in cardiac and skeletal muscle mitochondria. Unexpectedly, we found that CR does not alter the susceptibility to mPT in muscle (cardiac or skeletal), nor calcium uptake rates. Despite the lack in changes in calcium transport properties, CR consistently decreased respiration in the presence of ATP synthesis in heart and soleus muscle. In heart, such changes were accompanied by a decrease in respiration in the absence of ATP synthesis, lower maximal respiratory rates and a reduced rate of hydrogen peroxide release. Hydrogen peroxide release was unaltered by CR in skeletal muscle. No changes were observed in inner membrane potentials and respiratory control ratios. Together, these results highlight the tissue-specific bioenergetic and ion transport effects induced by CR, demonstrating that resilience against calcium-induced mPT is not present in all tissues.

Caloric Restriction Followed by High Fat Feeding Predisposes to Oxidative Stress in Skeletal Muscle Mitochondria

2013 ◽  
Vol 45 (12) ◽  
pp. 874-879 ◽  
Author(s):  
R. Crescenzo ◽  
F. Bianco ◽  
P. Coppola ◽  
A. Mazzoli ◽  
G. Liverini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Caloric Restriction ◽  
High Fat ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Fat Feeding

The Effect of Sodium and Potassium on Calcium Uptake by Frog Skeletal Muscle Mitochondria and Vesicles

1972 ◽  
Vol 50 (12) ◽  
pp. 1157-1161 ◽  
Author(s):  
Satish Batra
Keyword(s):  
Skeletal Muscle ◽  
Calcium Uptake ◽  
Frog Skeletal Muscle ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Sucrose Medium ◽  
Ca Uptake ◽  
Sodium And Potassium

Calcium uptake by mitochondria of frog skeletal muscle increased when K replaced Na or sucrose in the medium. There was no difference in passive binding of Ca and the amount of ATP split when K replaced Na. Ca uptake was increased by substituting K for Na in the medium and was maximal in a medium containing 100 mM K and no Na. Azide and dinitrophenol (DNP) inhibited K-stimulated Ca uptake completely. Inhibition by these agents in Na medium was relatively small. Ca uptake by vesicles was little affected by changing from Na to K medium, by azide, or by DNP. Ageing reduced Ca uptake in both fractions and stimulation by K of mitochondrial Ca uptake nearly disappeared after 4 h of storage (at 4 °C). Since Ca was taken up to the same extent in Na or sucrose medium, it is concluded that Ca uptake by mitochondria is stimulated by K rather than inhibited by Na.

scholarly journals Effects of magnesium and nucleotides on the proton conductance of rat skeletal-muscle mitochondria

2000 ◽  
Vol 348 (1) ◽  
pp. 209-213 ◽  
Author(s):  
Susana CADENAS ◽  
Martin D. BRAND
Keyword(s):  
Skeletal Muscle ◽  
Atp Synthase ◽  
Atp Synthesis ◽  
Proton Conductance ◽  
Rat Skeletal Muscle ◽  
Maximal Inhibition ◽  
Muscle Mitochondria ◽  
Mitochondrial Inner Membrane ◽  
Skeletal Muscle Mitochondria ◽  
The Matrix

During oxidative phosphorylation most of the protons pumped out to the cytosol across the mitochondrial inner membrane return to the matrix through the ATP synthase, driving ATP synthesis. However, some of them leak back to the matrix through a proton-conductance pathway in the membrane. When the ATP synthase is inhibited with oligomycin and ATP is not being synthesized, all of the respiration is used to drive the proton leak. We report here that Mg2+ inhibits the proton conductance in rat skeletal-muscle mitochondria. Addition of Mg2+ inhibited both oligomycin-inhibited respiration and the proton conductance, while removal of Mg2+ using EDTA activated these processes. The proton conductance was inhibited by more than 80% as free Mg2+ was raised from 25 nM to 220 μM. Half-maximal inhibition occurred at about 1 μM free Mg2+, which is close to the contaminating free Mg2+ concentration in our incubations in the absence of added magnesium chelators. ATP, GTP, CTP, TTP or UTP at a concentration of 1 mM increased the oligomycin-inhibited respiration rate by about 50%. However, these NTP effects were abolished by addition of 2 mM Mg2+ and any NTP-stimulated proton conductance was explained completely by chelation of endogenous free Mg2+. The corresponding nucleoside diphosphates (ADP, GDP, CDP, TDP or UDP) at 1 mM had no effect on oligomycin-inhibited respiration. We conclude that proton conductance in rat skeletal-muscle mitochondria is very sensitive to free Mg2+ concentration but is insensitive to NTPs or NDPs at 1 mM.

scholarly journals Caloric restriction prevents age-associated accrual of oxidative damage to mouse skeletal muscle mitochondria

1998 ◽  
Vol 25 (9) ◽  
pp. 1089-1097 ◽  
Author(s):  
Achim Lass ◽  
Barbara H. Sohal ◽  
Richard Weindruch ◽  
Michael J. Forster ◽  
Rajindar S. Sohal
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Damage ◽  
Caloric Restriction ◽  
Muscle Mitochondria ◽  
Mouse Skeletal Muscle ◽  
Skeletal Muscle Mitochondria
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