Stimulation of K+ flux into mitochondria by phenylarsine oxide

Diwan, Joyce Johnson; Srivastava, Jyoti; Moore, Charlest; Haley, Teresa

doi:10.1007/bf00743481

Cited by 19 publications

(2 citation statements)

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“…Sodium or potassium chloride was used as indicated sible for K + movement, may be on the cytoplasmic side of the mitochondria1 inner membrane, and thus may be distinct from the dithiol group on coupling factor B[26]. Evidence has been presented suggesting that another putative dithiol reagent, dibutylchloromethylin chloride, activates K + influx via reaction with some site other than the dithiol site associated with the ATP synthase[14].The rate of H+ efflux shows a linear relationship with the concentration of Cd2 + employed. Concentrations up to 30 pM Cd do not saturate the rate of H f efflux.…”

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confidence: 99%

Activation of potassium ion transport in mitochondria by cadmium ion

1984

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Low levels of CdZ+ (1 -5 pM) produce rapid swelling of mitochondria, which is respiration-dependent and uncoupler-sensitive. No cation requirement is apparent, since the swelling occurs in a medium containing only sucrose and the respiratory substrate. The swelling is inhibited by ruthenium red, suggesting that this effect of Cd2+ requires its entry into mitochondria. In medium containing 9 mM K + , addition of Cd2+ along with ruthenium red increases the rate of K' influx threefold. In the presence of K + , Rb+ or Li', but not of Na', addition of Cd2+ produces first efflux of H + into the medium followed by discharge of the pH gradient or uncoupling. Only the latter effect is inhibited by ruthenium red, showing that the efflux and influx of H f are independent reactions. The H' efflux appears to be an antiport response to the induced K + entry. Its activation by CdZ+ is similar to the known effect ofp-chloromercuriphenyl sulfonate. The H + influx or uncoupling appears to result from binding of Cd2+ to some matrix-facing membrane site, perhaps the dithiol group on coupling factor B, and may relate to apparent permeability changes associated with Cd2 +-induced swelling.Sulfhydryl-group reagents are known to activate mitochondrial monovalent cation transport [l -41. Studies in our laboratory have provided evidence for the presence of at least two types of dithiol groups in rat liver mitochondria that react with cadmium ion (Cd") and phenylarsine oxide. On addition of Cd2+ to respiring rat liver mitochondria, a transient K f -dependent H + efflux occurs, followed by reentry of H + or uncoupling [5]. The initial response is similar to the effect of mercurial reagents on mitochondria [l, 21. Presently available data suggest that mitochondrial accumulation of cation may be due to the interplay between a passive cation uniporter and a cation/proton exchanger [6, 71. Alternatively the possibility of direct involvement of K + transport in the energy transduction process has been considered [4, 8, 91. The existence of a specific K f influx mechanism is indicated by the saturability of K + influx with respect to external K + [lo, 211. An 82-kDa protein, which may function as a K + / H + antiporter, has recently been identified [I21 on the basis of its reactivity with N,N'-dicyclohexyl carbodiimide, a known inhibitor of K + influx and efflux [7, The present communication documents two main events happening in rat liver mitochondria following addition of Cd2+ : (a) activation of cation/proton exchange with considerable specificity towards K + , and (b) subsequent discharge of the proton gradient. 12-141. MATERIALS AND METHODSRat liver mitochondria were prepared by a conventional procedure in 0.25 M sucrose [15] and the protein content was determined by the biuret method [16]. Cation permeability Abbreviation. CIHgPhSO,, p-chloromercuriphenyl sulfonate. was determined by the decrease in absorbance at 546nm, which results from mitochondria1 swelling following uptake of the ions from the medium [l] or by the pH change...

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Activation of potassium ion transport in mitochondria by cadmium ion

1984

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“…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].…”

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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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