Selective electrode for dibenzyl dimethyl amoonium cation as indicator of the membrane potential in biological systems

Muratsugu, Makoto; Kamo, Naoki; Kurihara, Kenzo; Kobatake, Yonosuke

doi:10.1016/0005-2736(77)90035-9

Cited by 84 publications

(27 citation statements)

References 10 publications

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“…DWm (mV) = 59 log(v/V) À 59 log(10 DE=59 À 1) as indicated by Kamo et al [20] and Muratsugu et al [22]. v, V, and DE stand for mitochondrial volume, volume of the incubation medium and deflection of the electrode potential from the baseline, respectively.…”

Section: Membrane Potential (Dw M ) Measurementsmentioning

confidence: 98%

Metformin promotes isolated rat liver mitochondria impairment

et al. 2007

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Metformin, a drug widely used in the treatment of type 2 diabetes, has recently received attention due to the new and contrasting findings regarding its effects on mitochondrial function. In the present study, we evaluated the effect of metformin in isolated rat liver mitochondria status. We observed that metformin concentrations ‡8 mM induce an impairment of the respiratory chain characterized by a decrease in RCR and state 3 respiration. However, only metformin concentrations ‡10 mM affect the oxidative phosphorylation system by decreasing the mitochondrial transmembrane potential and increasing the repolarization lag phase. Moreover, our results show that metformin does not prevent H 2 O 2 production, neither protects against lipid peroxidation induced by the prooxidant pair ADP/Fe 2+ . In addition, we observed that metformin exacerbates Ca 2+ -induced permeability transition pore opening by decreasing the capacity of mitochondria to accumulate Ca 2+ and increasing the oxidation of thiol groups. Taken together, our results show that metformin can promote liver mitochondria injury predisposing to cell death.

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Section: Membrane Potential (Dw M ) Measurementsmentioning

confidence: 98%

Metformin promotes isolated rat liver mitochondria impairment

et al. 2007

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“…This TPP + concentration was chosen to achieve high sensitivity in measurements and to avoid possible toxic effects on mitochondria [18]. The ΔΨ m was estimated by the equation ΔΨ m (mV) = 59 log(v/V) -59 log(10 ΔE/59 -1) as indicated by Kamo et al [17] and Muratsugu et al [19]. v, V, and ΔE stand for mitochondrial volume, volume of the incubation medium, and deflection of the electrode potential from the baseline, respectively.…”

Section: Mitochondrial Membrane Potential Measurementsmentioning

confidence: 99%

Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage

Cardoso

Santos

Carvalho

et al. 2008

Free Radical Biology and Medicine

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This study was aimed at investigating the effects of subchronic administration of doxorubicin (DOX) on brain mitochondrial bioenergetics and oxidative status. Rats were treated with seven weekly injections of vehicle (sc, saline solution) or DOX (sc, 2 mg kg −1 ), and 1 week after the last administration of the drug the animals were sacrificed and brain mitochondrial fractions were obtained. Several parameters were analyzed: respiratory chain, phosphorylation system, induction of the permeability transition pore (PTP), mitochondrial aconitase activity, lipid peroxidation markers, and nonenzymatic antioxidant defenses. DOX treatment induced an increase in thiobarbituric acid-reactive substances and vitamin E levels and a decrease in reduced glutathione content and aconitase activity. Furthermore, DOX potentiated PTP induced by Ca 2+ . No statistical differences were observed in the other parameters analyzed. Altogether our results show that DOX treatment increases the susceptibility of brain mitochondria to Ca 2+ -induced PTP opening and oxidative stress, predisposing brain cells to degeneration and death.© 2008 Elsevier Inc. All rights reserved. IntroductionDoxorubicin (DOX) is a potent broad-spectrum antineoplastic agent effective in the treatment of a wide variety of cancers, including both solid tumors and leukemias [1]. However, the chronic administration of this drug can induce toxicity to nontarget tissues, cardiotoxicity being the best known side effect [2]. DOX-induced cardiotoxicity has been attributed to a number of effects, including the direct inhibition of key transporters involved in ion homeostasis, alterations in cellular iron and calcium metabolism, disruption of sarcoplasmic reticulum function, mitochondrial dysfunction, and apoptotic cell loss [3]. The mechanisms underlying these events seem to be linked to an increased production of reactive oxygen species (ROS) and oxidative damage [3]. Oxidative stress results from an imbalance between the generation of ROS and reactive nitrogen species and their removal by the cellular antioxidant system [4] and has been implicated in many neurodegenerative disorders [5,6].Several studies in breast cancer survivors and other patients undergoing DOX-based chemotherapy have reported persistent changes in cognitive functions, including memory loss and difficulty in the performance of daily life tasks [4]. Despite the well-known side effects of DOX treatment in the heart, little is known about its effects in the brain. Park et al. [7] showed that DOX generates free radicals in cultured astrocytes and decreases cell viability in a concentration-dependent manner. Similarly, in a study made in primary neuronal cultures, Lopes et al. [2] observed that DOX can induce neuronal cell death by necrosis and apoptosis in a concentration-dependent manner.Mitochondria play a central role in both cell life and cell death [8]. These organelles are essential for the production of ATP through oxidative phosphorylation and regulation of intracellular Ca 2+ homeostasis and are t...

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“…as indicated by Kamo et al (1979) and Muratsugu et al (1977). v, V, and ΔE stand for mitochondrial volume, volume of the incubation medium, and deflection of the electrode potential from the baseline, respectively.…”

Section: Mitochondrial Respirationmentioning

confidence: 99%

Estradiol affects liver mitochondrial function in ovariectomized and tamoxifen-treated ovariectomized female rats

Moreira

Custódio

Nunes

et al. 2007

Toxicology and Applied Pharmacology

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Given the tremendous importance of mitochondria to basic cellular functions as well as the critical role of mitochondrial impairment in a vast number of disorders, a compelling question is whether 17β-estradiol (E2) modulates mitochondrial function. To answer this question we exposed isolated liver mitochondria to E2. Three groups of rat females were used: control, ovariectomized and ovariectomized treated with tamoxifen. Tamoxifen has antiestrogenic effects in the breast tissue and is the standard endocrine treatment for women with breast cancer. However, under certain circumstances and in certain tissues, tamoxifen can also exert estrogenic agonist properties. We observed that at basal conditions, ovariectomy and tamoxifen treatment do not induce any statistical alteration in oxidative phosphorylation system and respiratory chain parameters. Furthermore, tamoxifen treatment increases the capacity of mitochondria to accumulate Ca 2+ delaying the opening of the permeability transition pore. The presence of 25 μM E2 impairs respiration and oxidative phosphorylation system these effects being similar in all groups of animals studied. Curiously, E2 protects against lipid peroxidation and increases the production of H 2 O 2 in energized mitochondria of control females. Our results indicate that E2 has in general deleterious effects that lead to mitochondrial impairment. Since mitochondrial dysfunction is a triggering event of cell degeneration and death, the use of exogenous E2 must be carefully considered.

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Selective electrode for dibenzyl dimethyl amoonium cation as indicator of the membrane potential in biological systems

Cited by 84 publications

References 10 publications

Metformin promotes isolated rat liver mitochondria impairment

Metformin promotes isolated rat liver mitochondria impairment

Doxorubicin increases the susceptibility of brain mitochondria to Ca2+-induced permeability transition and oxidative damage

Estradiol affects liver mitochondrial function in ovariectomized and tamoxifen-treated ovariectomized female rats

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