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Belyaeva, E. S.; Glazunov, V. V.; Никитина, Е. Р.; Коротков, С. М.

doi:10.1023/a:1010607307099

Cited by 51 publications

(26 citation statements)

References 58 publications

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“…Analogously, in the case of Cd 2+ , a swelling was observed on isolated mitochondria [18,[21][22][23][24] and, also in this case the swelling was facilitated by the presence of Ca 2+ . However, there is no agreement between the authors concerning the cyclosporine sensitivity.…”

Section: Discussionmentioning

confidence: 53%

“…However, there is no agreement between the authors concerning the cyclosporine sensitivity. In particular, Pourahmad et al [21] and Dorta et al [23], found cyclosporine sensitivity, while Belyaeva et al [24] and Li et al [18] do not find cyclosporine sensitivity. As a consequence, different mechanisms for Cd 2+ have been proposed; Li et al [18] proposed binding of Co 2+ to the thiol groups in ANT.…”

Section: Discussionmentioning

confidence: 97%

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The interactions of cobalt(II) with mitochondria from rat liver

et al. 2007

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The interactions of Co 2+ with mitochondria have been investigated. The results indicate that Co 2+ inhibits ATP synthesis. Further investigations into ATP synthesis mechanisms indicated that inhibition is due to the opening of a transmembrane pore. The opening of this pore causes the collapse of the high-energy intermediate where, under a pH and a potential gradient, the energy is stored and subsequently utilized to form ATP from ADP.

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 97%

The interactions of cobalt(II) with mitochondria from rat liver

et al. 2007

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“…The onset of increased permeability is favored by massive Ca 2+ accumulation and the influence of an inducing agent [1,2]. With regard to the latter, several dissimilar reagents have been used to open the pore, i.e., inorganic phosphate [3], heavy metals [4][5][6], thiol selective reagents [7][8][9], oxidants, such as reactive oxygen-derived species [10][11][12], and organic hydroperoxides [13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

“…For example, Cd 2+ , a dithiol blocking reagent, triggers mitochondrial K + uptake [17], promotes non-specific permeability [18], and inhibits Ca 2+ influx [6,19,20]. Nonspecific permeability increase to matrix solutes can also be stimulated by the monofunctional thiol reagents, mersalyl [21] and N-ethylmaleimide [22], as well as by the dithiol reagent phenylarsine oxide [23,24].…”

Section: Introductionmentioning

confidence: 99%

On the Opening of an Insensitive Cyclosporin A Non-specific Pore by Phenylarsine Plus Mersalyl

Garcı́a

Martínez-Abundis

Pavón

et al. 2007

Cell Biochem Biophys

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The purpose of this work was addressed to provide new information on the effect of thiol reagents on mitochondrial non-specific pore opening, and its response to cyclosporin A (CSA). To meet this proposal phenylarsine oxide (PHA) and mersalyl were employed as tools to induce permeability transition and CSA to inhibit it. PHA-induced mitochondrial dysfunction, characterized by Ca2+ efflux, swelling, and membrane de-energization, was inhibited by N-ethylmaleimide and CSA. Conversely, mersalyl failed to inhibit the inducing effect of phenylarsine oxide, it rather strengthened it. In addition, the effect of mersalyl was associated with cross-linking of membrane proteins. The content of membrane thiol groups accessible to react with PHA, mersalyl, and PHA plus mersalyl was determined. In all situations, permeability transition was accompanied by a significant decrease in the whole free membrane thiol content. Interestingly, it is also shown that mersalyl hinders the protective effect of cyclosporin A on PHA-induced matrix Ca2+ efflux.

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“…In the case of divalent metals (and of Al 3+ , phenylarsine oxide and oxidising compounds), which are inducers of the cyclosporinesensitive swelling, the proposed molecular mechanism was that the ANT (adenine nucleotide traslocase) (where the metals and the oxidant agents form an intramolecular cross-linking between the Cys 160 and Cys 257 thiol groups) is a target site [17,24,25,[29][30][31][32][33][34][35].…”

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confidence: 99%

Interactions of Cr(VI) and Cr(III) with isolated rat liver mitochondria

Iero

Manente

Pieri

et al. 2010

Inorganic Chemistry Communications

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The mechanism of interaction of Cr(VI) with isolated rat liver mitochondria was investigated in this study. The results suggest that Cr(VI) induces the opening of the membrane permeability transition pore (MPT). The phenomenon is cyclosporine-sensitive and is in agreement with the cyclosporine-sensitive apoptosis observed in the cells incubated with this compound. Moreover the action of Cr(III), that is formed in the cells by a reduction of Cr(VI), has been also analysed. The results obtained demonstrated that the Cr(III) does not induce the opening of the MPT in isolated mitochondria, but it has a protective effect in preventing Cr(VI) MPT opening. Therefore, these results suggest that apoptosis is regulated by a balance between Cr(VI) accumulation in the cytoplasm and Cr(III) formation.Many "in vitro" studies regarding the interactions of Cr(VI) with cellular and sub-cellular structures have been performed directed to discover the biological-molecular mechanism responsible for the high toxicity of this element [1-10].Among the numerous cellular investigations carried out, two significant findings stand out:-Cr(VI) enters into the cell (by means of a carrier-mediated mechanism). Cell apoptosis is subsequently induced and the phenomenon is inhibited by cyclosporine A [1,4,6,9,39,41]; -Once inside the cell, the Cr(VI) is reduced to Cr(III) [2,3,5,8].However, these experiments do not clarify whether the apoptosis is induced by Cr(VI) or by Cr(III) since both compounds are present in the cell. In order to clarify this point, the interactions of both Cr(VI) and Cr(III) with isolated mitochondria were investigated in the present study since mitochondria are involved in all apoptosis mechanisms, and the cyclosporine-sensitive cell apoptosis is correlated with the opening of a mitochondrial pore (a MPT cyclosporinesensitive pore) [11,12].The interactions of chromium as Cr(VI) with isolated plants and animal mitochondria were previously studied [7,10], but the conclusions did not clarify the above cited problem. In particular, the opening of the membrane pore and the cyclosporine-sensitivity of this phenomenon, which is the key experiment for determining the involvement of mitochondria, has never been taken into account [7,10]. This study intends to demonstrate that only Cr(VI) form induces the opening of the mitochondrial cyclosporine-sensitive pore, while Cr(III) has no effect on this process, but, conversely, it seems to have a protective effect against the opening of the pore induced by Cr (VI).In mitochondria, the free energy arising from the oxidation of the substrates by molecular oxygen is utilized to form ATP from ADP. The oxidation of the substrates leads to the production of NADH and FADH 2 which triggers the electron flux along the mitochondrial respiratory chain (RC). The electron flow in the RC gives rise to a proton extrusion, that in turn gives rise to a ΔΨ (electrical gradient) and to a ΔpH (chemical gradient) which constitute the proton-motive force (p.m.f. = ΔΨ + ΔpH), driving the ATP synthesis [15]. T...

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Cited by 51 publications

References 58 publications

The interactions of cobalt(II) with mitochondria from rat liver

The interactions of cobalt(II) with mitochondria from rat liver

On the Opening of an Insensitive Cyclosporin A Non-specific Pore by Phenylarsine Plus Mersalyl

Interactions of Cr(VI) and Cr(III) with isolated rat liver mitochondria

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