No effects of intermittent 50�Hz EMF on cytoplasmic free calcium and on the mitochondrial membrane potential in human diploid fibroblasts

2004 ◽  
Vol 43 (3) ◽  
pp. 203-207 ◽  
Author(s):  
Alexander Pilger ◽  
Sabine Ivancsits ◽  
Elisabeth Diem ◽  
Melanie Steffens ◽  
Hans-Albert Kolb ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Free Calcium ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts ◽  
Cytoplasmic Free Calcium

scholarly journals Does Cryopreservation of Ovarian Tissue Affect the Distribution and Function of Germinal Vesicle Oocytes Mitochondria?

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Mojdeh Salehnia ◽  
Virpi Töhönen ◽  
Saeed Zavareh ◽  
Jose Inzunza
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Laser Scanning ◽  
Ovarian Tissue ◽  
Germinal Vesicle ◽  
Free Calcium ◽  
Atp Content ◽  
Fertilization Rates

The aim of this study was to evaluate mitochondrial alteration and ATP content of germinal vesicle (GV) oocytes isolated from fresh and vitrified ovaries. After superovulation, the ovaries from adult mice were collected and divided into control and vitrified groups. GV oocytes were isolated mechanically from each group. Half were cultured for 24 hours and their maturation was assessed. Metaphase II oocytes were collected and submitted toin vitrofertilization and their fertilization rates and development to the blastocyst stage were evaluated. In the remaining GV oocytes, ATP levels were quantified, and mitochondrial distribution, mitochondrial membrane potential, and intracellular free calcium were detected with rhodamine 123, JC-1 and Flou-4 AM staining, using laser-scanning confocal microscopy. Maturation and fertilization rates of GV oocytes and the developmental rates of subsequent embryos were significantly lower in vitrified samples (P<0.05). The ATP content and Ca2+levels differed significantly in fresh and vitrified GV oocytes (P<0.05). Most mitochondria were seen as large and homogenous aggregates (66.6%) in fresh GV oocytes compared to vitrified oocytes (50%). No significant differences in mitochondrial membrane potential were found between the groups. The lower maturation and fertilization rates of GV oocytes from vitrified ovaries may be due to changes in their mitochondrial function and distribution.

scholarly journals Myrica rubraExtracts Protect the Liver from CCl4-Induced Damage

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Lizhi Xu ◽  
Jing Gao ◽  
Yucai Wang ◽  
Wen Yu ◽  
Xiaoning Zhao ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Liver Mitochondria ◽  
Mitochondrial Outer Membrane ◽  
Free Calcium ◽  
Dependent Manner ◽  
Protective Effects ◽  
Nuclear Condensation ◽  
Serum Aspartate Aminotransferase

The relationship between the expression of mitochondrial voltage-dependent anion channels (VDACs) and the protective effects ofMyrica rubraSieb. Et Zucc fruit extract (MCE) against carbon tetrachloride (CCl4)-induced liver damage was investigated. Pretreatment with 50 mg kg−1, 150 mg kg−1or 450 mg kg−1MCE significantly blocked the CCl4-induced increase in both serum aspartate aminotransferase (sAST) and serum alanine aminotransferase (sALT) levels in mice (P< .05 or .01 versus CCl4group). Ultrastructural observations of decreased nuclear condensation, ameliorated mitochondrial fragmentation of the cristae and less lipid deposition by an electron microscope confirmed the hepatoprotection. The mitochondrial membrane potential dropped from −191.94 ± 8.84 mV to −132.06 ± 12.26 mV (P< .01) after the mice had been treated with CCl4. MCE attenuated CCl4-induced mitochondrial membrane potential dissipation in a dose-dependent manner. At a dose of 150 or 450 mg kg−1of MCE, the mitochondrial membrane potentials were restored (P< .05). Pretreatment with MCE also prevented the elevation of intra-mitochondrial free calcium as observed in the liver of the CCl4-insulted mice (P< .01 versus CCl4group). In addition, MCE treatment (50–450 mg kg−1) significantly increased both transcription and translation of VDAC inhibited by CCl4. The above data suggest that MCE mitigates the damage to liver mitochondria induced by CCl4, possibly through the regulation of mitochondrial VDAC, one of the most important proteins in the mitochondrial outer membrane.

scholarly journals Xiaoyaosan Decoction, a Traditional Chinese Medicine, Inhibits Oxidative-Stress-Induced Hippocampus Neuron Apoptosis In Vitro

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Zhen-zhi Meng ◽  
Jing-hong Hu ◽  
Jia-xu Chen ◽  
Guang-xin Yue
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Low Dose ◽  
Free Calcium ◽  
High Dose ◽  
Hippocampus Neuron ◽  
Neuron Apoptosis

Xiaoyaosan (XYS) decoction is a famous prescription for the treatment of mental disorders in China. In this experiment, we explored the way in which XYS decoction-reverse hippocampus neuron apoptosis in vitro. We used XYS decoction-containing serum to treat oxidative-stress-induced hippocampus neuron apoptosis and used immunofluorescence to determine the concentration of free calcium, mitochondrial membrane potential, and apoptotic rate of neuron. Results showed that 3-hour oxidative stress decrease mitochondrial membrane potential, increase the concentration of free calcium and apoptotic rate of neuron via triggering pathological changes of nucleus such as karyorrhexis, karyopyknosis. Low, medium, high dose of XYS-decoction-containing serum could reverse these phenomenon, and the effect of low-dose XYS-decoction-containing serum was significant in improving mitochondrial membrane potential and apoptotic rate of neuron. These findings suggest that XYS decoction may be helpful in reducing oxidative-stress-induced hippocampus neuron apoptosis.

Intracellular Free Calcium and Mitochondrial Membrane Potential in Ischemia/Reperfusion and Preconditioning

2000 ◽  
Vol 32 (7) ◽  
pp. 1223-1238 ◽  
Author(s):  
Kari V Ylitalo ◽  
Antti Ala-Rämi ◽  
Erkki V Liimatta ◽  
Keijo J Peuhkurinen ◽  
Ilmo E Hassinen
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Ischemia Reperfusion ◽  
Intracellular Free Calcium ◽  
Free Calcium

Exercise delays neutrophil apoptosis by a G-CSF-dependent mechanism

2012 ◽  
Vol 113 (7) ◽  
pp. 1082-1090 ◽  
Author(s):  
Frank C. Mooren ◽  
Klaus Völker ◽  
Rainer Klocke ◽  
Sigrid Nikol ◽  
Johannes Waltenberger ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Annexin V ◽  
Free Calcium ◽  
Neutrophil Apoptosis ◽  
Exercise Tests ◽  
Laboratory Exercise ◽  
Exercise Induced

The aim of the study was to determine whether exercise affects neutrophil apoptosis and to characterize the underlying mechanisms. Using annexin V labeling, neutrophil apoptosis was measured using flow cytometry after various bouts of exercise (marathon run, concentric/eccentric treadmill exercise, moderate/intensive resistance training) and in vitro conditions. Similarly, apoptosis-related markers as death receptors/ligands and mitochondrial membrane potential were detected. Furthermore, concentrations of intracellular free calcium and glutathione were measured using spectrofluorometry. After both marathon run and intensive laboratory exercise tests, neutrophil apoptosis was delayed. Furthermore, neutrophils mitochondrial membrane potential and death receptor/ligand expression were not affected by exercise. Apoptosis delay was accompanied under some exercise conditions by enhanced intracellular calcium transients and decreased glutathione levels. A delay of spontaneous apoptosis in vitro could be induced by incubation of neutrophils in postexercise serum. Heating of postexercise serum abolished the apoptosis delaying effect. In vitro stimulation of resting neutrophils with granulocyte-colony-stimulating factor (G-CSF) and C-reactive protein resulted in apoptosis delay too. Addition of anti-G-CSF antibody to postexercise serum was also effective in reversing its apoptosis-delaying effect. Exercise-induced mobilization of neutrophils is associated with a delay of apoptosis. This fundamental process seems to maintain exercise-induced neutrophilia and to contribute to the alerting and activation of the nonadaptive immune system known from other inflammatory conditions. An important extracellular trigger of apoptosis delay during exercise conditions seems to be G-CSF; intracellular processes may include calcium and redox signaling.

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