The novel ruthenium—γ-linolenic complex [Ru2(aGLA)4Cl] inhibits C6 rat glioma cell proliferation and induces changes in mitochondrial membrane potential, increased reactive oxygen species generation and apoptosisin vitro

2010 ◽  
Vol 28 (1) ◽  
pp. 15-23 ◽  
Author(s):  
Geise Ribeiro ◽  
Marcel Benadiba ◽  
Denise de Oliveira Silva ◽  
Alison Colquhoun
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Proliferation ◽  
Membrane Potential ◽  
Mitochondrial Membrane ◽  
Glioma Cell ◽  
Reactive Oxygen Species Generation ◽  
Oxygen Species ◽  
The Novel ◽  
Rat Glioma ◽  
Glioma Cell Proliferation

Bupivacaine Indirectly Potentiates Glutamate-induced Intracellular Calcium Signaling in Rat Hippocampal Neurons by Impairing Mitochondrial Function in Cocultured Astrocytes

2018 ◽  
Vol 128 (3) ◽  
pp. 539-554 ◽  
Author(s):  
Yuan Xing ◽  
Nan Zhang ◽  
Wei Zhang ◽  
Lei-Ming Ren
Keyword(s):  
Reactive Oxygen Species ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Mitochondrial Membrane ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Laser Scanning Microscopy ◽  
Oxygen Species

Abstract Background Bupivacaine induces central neurotoxicity at lower blood concentrations than cardiovascular toxicity. However, central sensitivity to bupivacaine is poorly understood. The toxicity mechanism might be related to glutamate-induced excitotoxicity in hippocampal cells. Methods The intracellular free Ca2+ concentration ([Ca2+]i), mitochondrial membrane potential, and reactive oxygen species generation were measured by fluorescence and two-photon laser scanning microscopy in fetal rat hippocampal neurons and astrocytes. Results In astrocyte/neuron cocultures, 300 μM bupivacaine inhibited glutamate-induced increases in [Ca2+]i in astrocytes by 40% (P < 0.0001; n = 20) but significantly potentiated glutamate-induced increases in [Ca2+]i in neurons by 102% (P = 0.0007; n = 10). Ropivacaine produced concentration-dependent effects similar to bupivacaine (0.3 to 300 μM). Tetrodotoxin did not mimic bupivacaine’s effects. In pure cell cultures, bupivacaine did not affect glutamate-induced increases in [Ca2+]i in neurons but did inhibit increased [Ca2+]i in astrocytes. Moreover, bupivacaine produced a 61% decrease in the mitochondrial membrane potential (n = 20) and a 130% increase in reactive oxygen species generation (n = 15) in astrocytes. Cyclosporin A treatment suppressed bupivacaine’s effects on [Ca2+]i, mitochondrial membrane potential, and reactive oxygen species generation. When astrocyte/neuron cocultures were incubated with 500 μM dihydrokainic acid (a specific glutamate transporter–1 inhibitor), bupivacaine did not potentiate glutamate-induced increases in [Ca2+]i in neurons but still inhibited glutamate-induced increases in [Ca2+]i in astrocytes. Conclusions In primary rat hippocampal astrocyte and neuron cocultures, clinically relevant concentrations of bupivacaine selectively impair astrocytic mitochondrial function, thereby suppressing glutamate uptake, which indirectly potentiates glutamate-induced increases in [Ca2+]i in neurons.

scholarly journals Paclitaxel resistance development is associated with biphasic changes in reactive oxygen species, mitochondrial membrane potential and autophagy with elevated energy production capacity in lung cancer cells: A chronological study

Tumor Biology ◽  
2017 ◽  
Vol 39 (2) ◽  
pp. 101042831769431 ◽  
Author(s):  
Satabdi Datta ◽  
Diptiman Choudhury ◽  
Amlan Das ◽  
Dipanwita Das Mukherjee ◽  
Nabanita Das ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Resistance Development

Paclitaxel (Tx) is one of the first-line chemotherapeutic drugs used against lung cancer, but acquired resistance to this drug is a major challenge against successful chemotherapy. In this work, we have focused on the chronological changes of various cellular parameters and associated effect on Tx (10 nM) resistance development in A549 cell line. It was observed, at initial stage, the cell death percentage due to drug treatment had increased up to 20 days, and thereafter, it started declining and became completely resistant by 40 days. Expressions of βIII tubulin and drug efflux pumps also increased over the period of resistance development. Changes in cellular autophagy and reactive oxygen species generation showed a biphasic pattern and increased gradually over the course of upto 20 days, thereafter declined gradually; however, their levels remained higher than untreated cells when resistance was acquired. Increase in extracellular acidification rates and oxygen consumption rates was found to be directly correlated with acquisition of resistance. The depolarisation of mitochondrial membrane potential was also biphasic; first, it increased with increase of cell death up to 20 days, thereafter, it gradually decreased to normal level along with resistance development. Increase in activity of catalase, glutathione peroxidase and glutathione content over these periods may attribute in bringing down the reactive oxygen species levels and normalisation of mitochondrial membrane potential in spite of comparatively higher reactive oxygen species production by the Tx-resistant cells.

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