scholarly journals Calcium Signals Are Affected by Ciprofloxacin as a Consequence of Reduction of Mitochondrial DNA Content in Jurkat Cells

2006 ◽  
Vol 50 (5) ◽  
pp. 1664-1671 ◽  
Author(s):  
Rafał Kozieł ◽  
Krzysztof Zabłocki ◽  
Jerzy Duszyński
Keyword(s):  
Mitochondrial Dna ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Jurkat Cells ◽  
Atp Formation ◽  
Mitochondrial Dna Content ◽  
Calcium Buffering ◽  
In Cells

ABSTRACT The effects of ciprofloxacin on mitochondrial DNA (mtDNA) content, oxygen consumption, mitochondrial membrane potential, cellular ATP formation, and capacitative Ca2+ entry into Jurkat cells were investigated. In cells incubated for several days with 25 μg/ml ciprofloxacin, a 60% reduction of mtDNA content, inhibition of the respiratory chain, and a significant decrease in mitochondrial membrane potential were observed. These changes led to a decrease in the calcium buffering capacity of mitochondria which, in turn, resulted in a gradual inhibition of the capacitative Ca2+ entry. On days 4, 7, and 11 of incubation with ciprofloxacin, the initial rates of Ca2+ entry were reduced by 33%, 50%, and 50%, respectively. Ciprofloxacin caused a transient decrease in the cellular capability for ATP formation. In cells incubated for 15 min with glucose, pyruvate, and glutamine as exogenous fuel, ciprofloxacin reduced ATP content by 16% and 35% on days 4 and 7, respectively, of incubation with the drug. However, on day 11 of incubation with ciprofloxacin, a recovery of cellular ATP formation was observed. In conclusion, long-term exposure of Jurkat cells to ciprofloxacin at a concentration of 25 μg/ml seriously affects cellular energy metabolism and calcium homeostasis.

scholarly journals Evaluation of Lasting Effects of Heat Stress on Sperm Profile and Oxidative Status of Ram Semen and Epididymal Sperm

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Thais Rose dos Santos Hamilton ◽  
Camilla Mota Mendes ◽  
Letícia Signori de Castro ◽  
Patrícia Monken de Assis ◽  
Adriano Felipe Perez Siqueira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Stress ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Treated Group ◽  
Epididymal Sperm ◽  
Long Term Effects ◽  
Stressed Cells

Higher temperatures lead to an increase of testicular metabolism that results in spermatic damage. Oxidative stress is the main factor responsible for testicular damage caused by heat stress. The aim of this study was to evaluate lasting effects of heat stress on ejaculated sperm and immediate or long-term effects of heat stress on epididymal sperm. We observed decrease in motility and mass motility of ejaculated sperm, as well as an increase in the percentages of sperm showing major and minor defects, damaged plasma and acrosome membranes, and a decrease in the percentage of sperm with high mitochondrial membrane potential in the treated group until one spermatic cycle. An increased enzymatic activity of glutathione peroxidase and an increase of stressed cells were observed in ejaculated sperm of the treated group. A decrease in the percentage of epididymal sperm with high mitochondrial membrane potential was observed in the treated group. However, when comparing immediate and long-term effects, we observed an increase in the percentage of sperm with low mitochondrial membrane potential. In conclusion, testicular heat stress induced oxidative stress that led to rescuable alterations after one spermatic cycle in ejaculated sperm and also after 30 days in epididymal sperm.

BAD Induces Apoptosis in Cells Over-Expressing Bcl-2 or Bcl-xL without Loss of Mitochondrial Membrane Potential

2001 ◽  
Vol 42 (3) ◽  
pp. 429-443 ◽  
Author(s):  
Aaron D. Schimmer ◽  
David W. Hedley ◽  
Nhu-An Pham ◽  
Sue Chow ◽  
Mark D. Minden
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
In Cells

scholarly journals Altered mitochondrial function in fibroblasts containing MELAS or MERRF mitochondrial DNA mutations

1996 ◽  
Vol 318 (2) ◽  
pp. 401-407 ◽  
Author(s):  
Andrew M JAMES ◽  
Yau-Huei WEI ◽  
Cheng-Yoong PANG ◽  
Michael P. MURPHY
Keyword(s):  
Mitochondrial Dna ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Trna Genes ◽  
Primary Fibroblast ◽  
Cultured Fibroblasts ◽  
Mitochondrial Dna Mutations ◽  
Dna Mutations

A number of human diseases are caused by inherited mitochondrial DNA mutations. Two of these diseases, MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) and MERRF (myoclonic epilepsy and ragged-red fibres), are commonly caused by point mutations to tRNA genes encoded by mitochondrial DNA. Here we report on how these mutations affect mitochondrial function in primary fibroblast cultures established from a MELAS patient containing an A to G mutation at nucleotide 3243 in the tRNALeu(UUR) gene and a MERRF patient containing an A to G mutation at nucleotide 8344 in the tRNALys gene. Both mitochondrial membrane potential and respiration rate were significantly decreased in digitonin-permeabilized MELAS and MERRF fibroblasts respiring on glutamate/malate. A similar decrease in mitochondrial membrane potential was found in intact MELAS and MERRF fibroblasts. The mitochondrial content of these cells, estimated by stereological analysis of electron micrographs and from measurement of mitochondrial marker enzymes, was similar in control, MELAS and MERRF cells. Therefore, in cultured fibroblasts, mutation of mitochondrial tRNA genes leads to assembly of bioenergetically incompetent mitochondria, not to an alteration in their amount. However, the cell volume occupied by secondary lysosomes and residual bodies in the MELAS and MERRF cells was greater than in control cells, suggesting increased mitochondrial degradation in these cells. In addition, fibroblasts containing mitochondrial DNA mutations were 3–4-fold larger than control fibroblasts. The implications of these findings for the pathology of mitochondrial diseases are discussed.

scholarly journals Geranylgeranyl Acetone Prevents Glutamate-induced Cell Death in HT-22 Cells by Increasing Mitochondrial Membrane Potential

2020 ◽  
Author(s):  
Eriko Sugano ◽  
Yuka Endo ◽  
Akihisa Sugai ◽  
Yuki Kikuchi ◽  
Kitako Tabata ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Oxygen Species ◽  
Mouse Hippocampus ◽  
Calcium Buffering ◽  
Shock Proteins

Geranylgeranyl acetone (GGA) protects against various types of cell damages by upregulating heat shock proteins. We investigated whether GGA protect neuronal cells from cell death induced by oxidative stress. Glutamate exposure was lethal to HT-22 cells which comprise a neuronal line derived from mouse hippocampus. This configuration is often used as a model for hippocampus neurodegeneration in vitro. In the present study, GGA protected HT-22 cells from glutamate-induced oxidative stress. GGA pretreatment did not induce Hsps. Moreover, reactive oxygen species increased to the same extent in both GGA-pretreated and untreated cells exposed to glutamate. In contrast, glutamate exposure and GGA pretreatment increased mitochondrial membrane potential. However, increases in intracellular Ca2+ concentration were inhibited by GGA pretreatment. In addition, the increase of phosphorylated ERKs by the glutamate exposure was inhibited by GGA pretreatment. These findings suggest that GGA protects HT-22 cells from glutamate-provoked cell death without Hsp induction and that the mitochondrial calcium buffering capacity plays an important role in this protective effect.

scholarly journals Mitochondrial Dysfunction in Chronic Respiratory Diseases: Implications for the Pathogenesis and Potential Therapeutics

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Wen-cheng Zhou ◽  
Jiao Qu ◽  
Sheng-yang Xie ◽  
Yang Sun ◽  
Hong-wei Yao
Keyword(s):  
Mitochondrial Dna ◽  
Membrane Potential ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Respiratory Diseases ◽  
Metabolic Reprogramming ◽  
Mitochondrial Calcium ◽  
Chronic Respiratory Diseases ◽  
Cellular Processes

Mitochondria are indispensable for energy metabolism and cell signaling. Mitochondrial homeostasis is sustained with stabilization of mitochondrial membrane potential, balance of mitochondrial calcium, integrity of mitochondrial DNA, and timely clearance of damaged mitochondria via mitophagy. Mitochondrial dysfunction is featured by increased generation of mitochondrial reactive oxygen species, reduced mitochondrial membrane potential, mitochondrial calcium imbalance, mitochondrial DNA damage, and abnormal mitophagy. Accumulating evidence indicates that mitochondrial dysregulation causes oxidative stress, inflammasome activation, apoptosis, senescence, and metabolic reprogramming. All these cellular processes participate in the pathogenesis and progression of chronic respiratory diseases, including chronic obstructive pulmonary disease, pulmonary fibrosis, and asthma. In this review, we provide a comprehensive and updated overview of the impact of mitochondrial dysfunction on cellular processes involved in the development of these respiratory diseases. This not only implicates mechanisms of mitochondrial dysfunction for the pathogenesis of chronic lung diseases but also provides potential therapeutic approaches for these diseases by targeting dysfunctional mitochondria.

Old is new again: a chemical probe for targeting mitochondria and monitoring mitochondrial membrane potential in cells

The Analyst ◽  
2015 ◽  
Vol 140 (17) ◽  
pp. 5849-5854 ◽  
Author(s):  
Lu Zhang ◽  
Wenwen Liu ◽  
Xianhong Huang ◽  
Guanxin Zhang ◽  
Xuefei Wang ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Mitochondrial Activity ◽  
Chemical Probe ◽  
Fluorescence Change ◽  
In Cells

The tetraphenylethene-indolium molecule (TPE-indo) can both image the mitochondria and indicate mitochondrial activity by the fluorescence change of TPE-indo.

scholarly journals Low-Dose Methylmercury-Induced Apoptosis and Mitochondrial DNA Mutation in Human Embryonic Neural Progenitor Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Xinjin Wang ◽  
Mengling Yan ◽  
Lina Zhao ◽  
Qing Wu ◽  
Chunhua Wu ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Membrane Potential ◽  
Progenitor Cells ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Atp Content ◽  
Induced Apoptosis

Methylmercury (MeHg) is a long-lasting organic pollutant primarily found in the aquatic environment. The developing brain is particularly sensitive to MeHg due to reduced proliferation of neural stem cell. Although several mechanisms of MeHg-induced apoptosis have been defined in culture models, it remains unclear whether mitochondrial DNA (mtDNA) mutation is involved in the toxic effect of MeHg, especially in the neural progenitor cells. In the present study, the ReNcell CX cell, a human neural progenitor cells (hNPCs) line, was exposed to nanomolar concentrations of MeHg (≤50 nM). We found that MeHg altered mitochondrial metabolic function and induced apoptosis. In addition, we observed that MeHg induced ROS production in a dose-dependent manner in hNPCs cells, which was associated with significantly increased expressions of ND1, Cytb, and ATP6. To elucidate the mechanism underlying MeHg toxicity on mitochondrial function, we examined the ATP content and mitochondrial membrane potential in MeHg-treated hNPCs. Our study showed that MeHg exposure led to decreased ATP content and reduced mitochondrial membrane potential, which failed to match the expansion in mtDNA copy number, suggesting impaired mtDNA. Collectively, these results demonstrated that MeHg induced toxicity in hNPCs through altering mitochondrial function and inducing oxidative damage to mtDNA.

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