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Diamide acts intracellularly to enhance transmitter release: the differential permeation of diamide, DIP, DIP+1 and DIP+2 across the nerve terminal membrane.

The actions of the new potent thiol oxidizing agents, diazene dicarboxylic acid bis (N'-methyl piperazide) (DIP) and the N'-methyl iodide (DIP + 1) and the bis-N'-methyl iodide (DIP + 2) salts of DIP, were tested at the frog neuromuscular junction. At 20 degrees C, DIP was as fast as the thiol oxidizing agent, diamide, in evoking transmitter release but was appreciably less effective at 6 degrees C. DIP + 1 and DIP + 2 did not increase transmitter release. Since the three agents are potent oxidizers of glutathione and since the effectiveness of the compounds appears to depend on their ability to exist, at least in part, in a neutral form at physiological pH, it is concluded that their action as promoters of transmitter release depends on their ability to permeate nerve terminal membranes. Thus, both diamide and DIP act to increase transmitter release by the intracellular oxidation of glutathione. The two charged agents, DIP + 1 and DIP + 2, are potent muscular depolarizing agents. It is probable that the quaternary nitrogen groups of these compounds render them cholinomimetics.

Acetylcholine

The reduction of diamide by rat liver mitochondria and the role of glutathione.

Diamide is reduced by mitochondria utilizing endogenous substrates with Vmax. 20nmol/min per mg of protein and Km 75micrometer. The reaction is inhibited by: (a) thiol-blocking reagents (N-ethylmaleimide, p-hydroxymercuribenzoate, mersalyl and 2,6-dichlorophenol-indophenol);(b) respiratory inhibitors (arsenicals, malonate and antimycin, but not cyanide or oligomycin; inhibition by antimycin is reversed by ATP); (c) uncouplers (carbonyl cyanide p-trifluoromethoxyphenylhydrazone, 2,4-dinitrophenol and valinomycin with K+; inhibition by the first of these uncouplers is not reversed by cyanide); (d) reagents affecting energy conservation (Ca2+, increasing pH, phosphate; phosphate inhibition is augmented by catalytic ADP or ATP and augmentation is abolished by respiratory inhibitors). Concentrations of mitochondrial glutathione are high when diamide reduction is uninhibited, but low after adding one of the above inhibitors such that the reduction rate is roughly proportional to the glutathione concentration. Endogenous ATP concentrations are lower in the presence of diamide than without, but the difference is abolished by respiratory inhibitors. With oligomycin added, however, ATP concentrations are higher in the presence of diamide and this positive increment is decreased by antimycin, N-ethylmaleimide and malonate. In the presence of diamide and an uncoupler, the mitochondrial glutathione content does not fall if various reducible substrates are present, although the inhibition of diamide reduction is not relieved. Some of these substrates prevent the fall in reduced glutathione concentration found with diamide and phosphate. They also relieve the inhibition of diamide reduction and the relief is sensitive to butylmalonate. The inhibition of diamide reduction by N-ethylmaleimide, mersalyl or p-hydroxymercuribenzoate is not relieved by reducible substrates, but the latter mitigate the fall in the concentration of glutathione. Inhibitors of carriers of tricarboxylic acid-cycle intermediates also inhibit reduction of diamide. The reduced glutathione concentration remains high when they are added singly, but falls when two of them are combined. It is proposed that diamide may enter the matrix as a protonated adduct formed with the thiol groups of mitochondrial carriers and then be reduced in the matrix by glutathione, which is regenerated via NADH, energy-dependent transhydrogenase and NADP+-specific glutathione reductase. Some of the high-energy equivalents required for the transhydrogeneration may be generated by the substrate phosphorylation step of the tricarboxylic acid cycle.

Adenosine Triphosphate

Stimulation of the active transport of serotonin into mouse platelets by the sulfhydryl oxidizing agent diamide.

The purpose of this study was to determine the effects of diamide, a reversible sulfhydryl oxidizing agent, on the transport of serotonin (5-HT) by mouse platelets. Diamide produced a concentration-dependent (10-200 microM) stimulation of 5-HT transport that was rapid and sustained over 0-10 minutes of incubation. When platelets were incubated with diamide (10-200 microM) in the presence of glucose, the content of reduced glutathione was significantly decreased only at a final concentration of 200 microM, while washed platelets incubated with diamide (10-200 microM), in the absence of glucose, had a significant concentration-dependent decrease in their content of reduced glutathione. Fluoxetine, an inhibitor of the platelet 5-HT transporter, blocked diamide-induced stimulation of 5-HT transport. The kinetics of 5-HT transport showed that diamide caused a marked increase in the maximal rate of transport (Vmax control = 28.4 +/- 1.4 vs. Vmax diamide = 60.9 +/- 4.1 pM/10(8) platelets/4 min) but did not significantly alter the Km values. Ouabain, an inhibitor of platelet Na(+)-K+ ATPase, blocked the stimulation by diamide in a concentration-dependent manner. Dithiothreitol, a disulfide reducing agent, was able to partially reverse the stimulation of platelet 5-HT transport caused by diamide. This study has shown that diamide can stimulate the active transport of 5-HT by mouse platelets and suggests a possible role for free sulfhydryl groups in the regulation of this process.

Animals

The thiol-oxidizing agent diamide increases transmitter release by decreasing calcium requirements for neuromuscular transmission in the frog.

Diamide, which in concentrations of 10(-5) M and higher oxidizes glutathione intracellularly, produces a dose-related increase in the frequency of miniature end-plate potentials (MEPPs). With high enough doses, quantal release is blocked, apparently through exhaustion. The early phase of MEPP frequency increase is accompanied by an increase in EPP amplitude that may reach more than 10-fold and is therefore not produced by depolarization of axon terminals. Subsequently, EPP amplitude is reduced and falls to zero, associated with failure of invasion of the nerve action into the terminals while the MEPP frequency remains elevated. Both facilitation and PTP follow the time course of change in EPP amplitude. The increase in MEPP frequency with diamide does not require external Ca2+ but raising external Ca2+ increases the MEPP rate in the presence of diamide. External Ca2+ is necessary for EPP appearance and also potentiates the diamide effects. Conversely diamide reduces the requirements for Ca2+ in releasing ACh. Diamide substitutes for external Ca2+ in K+ evoked MEPP release and in the absence of external Ca2+, diamide-evoked MEPP release is increased by raising external Mg2+ levels. The action of diamide may be dependent on the actual release of Ca2+ from intracellular stores or it may work through mimicking some of the actions of Ca2+. The action of diamide bears close resemblance to the effects of prolonged stimulation of the motor axon at 10 Hz.

Acetylcholine

Changes in the distribution and organization of platelet actin induced by diamide and its functional consequences.

Exposure of blood platelets to diamide (azodicarboxylic acid-bis-dimethylamide) results in oxidation of sulphydryl groups present in the cytoskeleton and other proteins. This results in dramatic changes in functional behaviour of the cells. The distribution and level of organization of the major cytoskeletal protein actin has been studied analytically by the DNase-I inhibition assay and morphologically by electron microscopy (EM) of Triton X-100 treated platelets adherent to EM grids. Exposure to diamide results in a redistribution of actin within the cell reflected in an increase in cytoskeletal F-actin and a concomitant decrease in cytosolic actin. The magnitude of these changes depends upon the concentration of diamide and the time of exposure. Diamide also alters platelet aggregatory functions in response to certain stimuli. Treatment of normal human platelets with 0.1 mM diamide proceeds via disaggregation (5 min exposure to diamide), inhibition of aggregation (30 min exposure), to finally a normalization of the aggregation response after 60-120 min incubation with diamide. In parallel with the return to full functional response the distribution of F-actin between the cytoskeleton and cytoplasmic compartments returns to the control pattern. Incubation of the platelets with 0.5 mM diamide for 60 or more minutes leads to total inhibition of the aggregatory ability. In these cells the cytoskeleton associated F-actin remains significantly elevated and the structural organization of the cytoskeleton is markedly altered. In contrast to the network of filaments subadjacent to the surface membrane seen in unstimulated platelets, the cytoskeleton now shows electron dense zones in the more central parts of the cytoplasm. This diamide-induced structural reorganization of platelet cytoskeletal elements, associated with the inhibition of functional responses, emphasizes the dynamic nature of the membrane-cytoskeletal axis and its importance in the expression of shape changes and aggregatory phenomena in response to surface stimuli.

Actins

Modulation of diamide toxicity in thermotolerant cells by inhibition of protein synthesis.

Chinese hamster ovary cells were exposed in vitro to various concentrations of diamide for 1 h at 37 degrees C. This treatment resulted in a dose dependent increase in cytotoxicity. Cells were also heated at 43 degrees C for 15 min, incubated at 37 degrees C for 3 h, and then exposed to various concentrations of diamide. This heat shock has been shown previously to trigger the synthesis of heat shock proteins and the development of thermotolerance. Further, under these experimental conditions both were inhibited if protein synthesis was inhibited by exposure to cycloheximide (M. L. Freeman et al., Radiat. Res., 112: 195-203, 1987). Diamide toxicity was diminished in cells made thermotolerant by the 43 degrees C/15-min heat shock. For example, at the highest dose used, 0.8 mM, survival increased from 0.93% to 6.1%. However, diamide toxicity was unaffected if the cells were exposed to diamide 3 h after a 43 degrees C/60 min heat shock. This latter heat shock produced significant inhibition of protein synthesis whereas the 15-min heat shock did not (M. L. Freeman et al., Cancer Res., 48: 7033-7037, 1988). Further, a 43 degrees C/15-min heat shock did not confer protection against diamide toxicity if the cells were simultaneously exposed to cycloheximide. Exposure to 0.8 mM diamide was shown to oxidize specific cellular proteins as measured by 2-dimensional thiol blotting. However, the degree of protein thiol modification was not affected by a prior heat shock. Nor did the heat shock increase the intracellular concentration of glutathione or the activity of glutathione reductase. The diamide treatment caused specific, as opposed to general, protein thiol oxidation and heat shock did not prevent this. It is hypothesized that it was the oxidation of protein thiols which led to cellular toxicity. Protein synthesis, triggered by heat shock, protected cells from the diamide toxicity without preventing protein thiol modification. These results suggest that the proteins synthesized after heat shock can provide protection against the consequences of aberrant proteins produced by thiol oxidation.

Animals

Incorporation of 3H-N-ethylmaleimide into sheep red cell membrane thiol groups following protection by diamide-induced oxidation.

The thiol oxidant diazene dicarboxylic acid bis [N,N-dimethylamide] (diamide) is known to reversibly activate K-Cl cotransport in sheep red blood cells. Although the detailed mechanism of activation is unknown, functional thiols at the membrane or at the cytoplasmic level are recognized as important. To search for membrane bound thiols involved in the regulation of K-Cl cotransport, sheep red cells were first exposed to diamide at concentrations activating K-Cl cotransport, and then to the alkylating agent N-ethylmaleimide (NEM) in order to block non-oxidized thiols. White ghosts, prepared by osmotic lysis from these cells, were again treated with NEM followed by reduction of the diamide-induced dithiols with dithiothreitol (DTT) concentrations known to reverse the diamide-induced K-Cl flux. Maximum 3H-NEM incorporation into the DTT-reduced thiols occurred at 50 microM DTT. Saturation labelling by 3H-NEM of about 2 x 10(4) diamide-protected thiols/cell occurred at 25 microM NEM. Diamide protected about 0.1% of all membrane thiols chemically determined earlier. Membranes from high K (HK) and low K (LK) sheep red cells did not differ significantly in the number of diamide-protected thiols, and polyacrylamide gels revealed a similar protein distribution of 3H-NEM-labelled thiols. Since diamide is known to stimulate K-Cl flux in LK cells ten times more than in HK cells this finding is consistent with the hypothesis of a cytoplasmic control effecting different K-Cl flux activities in the membranes of the two cation genotypic red blood cells.

Animals

Thiol-dependent K:Cl transport in sheep red cells: VIII. Activation through metabolically and chemically reversible oxidation by diamide.

The sulfhydryl (SH) oxidant diamide activated in a concentration-dependent manner ouabain-resistant (OR), Cl-dependent K flux in both low potassium (LK) and high potassium (HK) sheep red cells as determined from the rate of zero-trans K efflux into media with Cl or Cl replaced by NO3 or methane sulfonate (CH3SO3). Diamide did not alter the OR Na efflux into choline Cl. The diamide effect on K efflux appeared after 80% of cellular glutathione (GSH) was oxidized to GSSG, its disulfide. The stimulation of K efflux was completely reversed during metabolic restitution of GSH, a process that depended on the length of exposure to and the concentration of diamide. The action of diamide on both the K:Cl transporter and GSH was also fully reversed by the reducing agent dithiothreitol (DTT). Diamide apparently oxidized the same SH groups alkylated by N-ethylmaleimide (NEM) (Lauf, P.K. 1983. J. Membrane Biol. 73:237-246). Like NEM, diamide activated K:Cl transport several-fold more in LK cells than in HK cells, and the effect on LK cells was partially inhibited by anti-L1, the allo-antibody known to inhibit OR K fluxes.

Animals

Investigation of monovalent cation influxes of diamide-treated human erythrocytes in solutions of different ionic strength.

Total and residual i.e. (ouabain + bumetanide + EGTA)-insensitive K+ as well as Na+ influxes were investigated in human erythrocytes before and after treatment with diamide (5 mM). In physiological and in low ionic strength solution these influxes were increased after diamide treatment. Diamide-treated cells do not exhibit significant differences between the total and residual influxes for both Na+ and K+. The diamide-induced cation fluxes in low ionic strength solution are significantly higher compared with the fluxes in physiological ionic strength solution. The diamide-induced K+ influx is not chloride-dependent, and replacement of NaCl by sodium methylsulfate does not significantly reduce this flux. A subsequent incubation of diamide-treated erythrocytes with dithioerythritol which restores the cellular glutathione level to its original value only partly decreases the enhanced K+ influx. From these results it can be concluded that electrodiffusion and K/Cl cotransport are not involved in the diamide-induced stimulation of the residual K+ influx of human erythrocytes.

Biological Transport

Diamide induced shift in protein and glutathione thiol: disulfide status delays DNA rejoining after X-irradiation of human cancer cells.

By treating a human tumor cell line with various concentrations of diamide, we explored the relationship between extent and duration of protein and nonprotein thiol oxidation, initiation of DNA double-strand break rejoining after X-rays, and the degree of radiosensitization. We also examined the relationship between protein thiol status and the non-protein thiol, glutathione (GSH). A549 cells were irradiated and incubated postirradiation with 0, 100, 300 or 500 microM diamide for 1 h. The dose of radiation required to give 10% survival decreased from 4.8 Gy to 3.2 Gy with 300 microM and to 2.7 Gy with 500 microM diamide (enhancement ratios of 1.5 and 1.8, respectively) but was not significantly affected by 100 microM diamide. The time of initiation of double-stranded DNA rejoining after X-irradiation (DNA repair) was delayed by 300 and 500 microM diamide. Furthermore, DNA rejoining began only after total cellular protein thiol content recovered to 55% of pretreatment levels for both concentrations. Intracellular GSH/GSSG ratios decreased immediately after diamide addition to less than 1. Large decreases in GSH/GSSG ratio preceded significant loss of protein thiols, but protein-glutathione mixed disulfides accounted for a minor percentage of the total protein thiol oxidized (up to 20%). We believe that diamide-induced protein thiol loss, and not GSH oxidation, is related to the cessation of DNA strand rejoining after X-irradiation, thereby affecting survival.

Azo Compounds

Reversible elimination of myofibrillar Ca2+ sensitivity by diamide and other sulfhydryl reagents: comparison with reversible contracture produced in intact cells.

Cardiac contractile activity is usually controlled by intracellular Ca2+, but it can also be modified by oxidizing agents. Incubation of guinea pig heart myofibrils with diamide (3 mM, 1 h) increased basal (no Ca2+) ATPase activity by 580% and abolished Ca2+ dependence. The effect was proportional to diamide concentration (0.01-1 mM) and duration of preincubation (up to 2 h). Dithiothreitol (5 mM, 1 h) reversed most of the basal ATPase activation and restored Ca2+ sensitivity. Other sulfhydryl reagents produced a similar effect but also produced inhibition of total ATPase. In intact cell preparations, diamide produced a slow tonic contraction, consistent with myofibril activation. In the perfused rat heart, 1 mM diamide slowly increased diastolic ventricular pressure; this increase was partially reversed by dithioerythritol. In isolated rat heart myocytes, 1 mM diamide produced a slow tonic contraction, increased contractility in response to stimulation. Cardiocytes superfused for 1 h with buffer containing EGTA to deplete Ca2+ did not contract in response to stimulation but showed a slow tonic contraction with diamide. This contraction could be slowly and only partially reversed by dithioerythritol. Response to stimulation was restored by addition of Ca2+. The results show that diamide can produce contraction in viable cells. This contraction does not require extracellular Ca2+ and is unlikely to involve intracellular Ca2+. The direct activation of myofibrillar ATPase may contribute to the increased myocardial stiffness seen in ischemia and to ischemic contracture.

Adenosine Triphosphatases

Anaerobic biosynthesis of the manganese-containing superoxide dismutase in Escherichia coli. Effects of diazenedicarboxylic acid bis(N,N'-dimethylamide) (diamide).

Anaerobically grown Escherichia coli accumulate active manganese-containing superoxide dismutase (MnSOD) upon exposure to diamide. This induction requires de novo biosynthesis of MnSOD. Catalase, glutathione disulfide reductase, and glucose-6-phosphate dehydrogenase were also induced by diamide in anaerobic E. coli. A GSH-negative strain of E. coli did not produce MnSOD under anaerobic conditions and was as responsive to diamide as was the wild type strain. Diamide which had been prereduced, by incubation with GSH, was ineffective. NO3- plus paraquat, which elicits increased anaerobic biosynthesis of the MnSOD polypeptide, but not of active MnSOD, synergized with diamide in the induction of active MnSOD. A similar increase in the ability of diamide to cause anaerobic biosynthesis of active MnSOD was seen when the production of the MnSOD polypeptide was increased by isopropyl-beta-D-thiogalactopyranoside, in a strain bearing the MnSOD gene under the control of the tac promoter. These results are explained in terms of a dual action of diamide, i.e. at both the transcriptional and the maturational levels of biosynthesis of MnSOD. Oxidative inactivation of an Fe(II)-containing repressor and oxidative facilitation of insertion of manganese, in place of iron, into the nascent MnSOD polypeptide, are the postulated bases of this dual action.

Anaerobiosis

Inhibition of protein phosphorylation and induction of protein cross-linking in erythrocyte membranes by diamide.

This report presents studies on the effect of diamide on protein phosphorylation in erythrocyte membranes. Diamide, a thiol-oxidizing reagent, nonspecifically inhibits cyclic Amp-dependent and -independent autophosphorylation of red cell memvranes, but not the activity of the solubilized membrane cycle AMP-independent protein kinases. Analysis of diamide-treated membranes by gel electrophoresis indicates that diamide is capable of inducing cross-linking of membrane proteins. The action of diamide, both in the inhibition of membrane autophosphorylation and in the cross-linking of membrane proteins, is very similar to that of Cu2+. o-phenanthroline complex. Our data indicate that diamide inhibits erythrocyte membrane autophosphorylation by perturbing the protein substrates.

Adenosine Triphosphate

Effect of diamide on nucleoside and glucose transport in Plasmodium falciparum and Babesia bovis infected erythrocytes.

Normal human erythrocytes, preincubated with the oxidizing agent diamide, did not demonstrate any increased permeability, but showed a significant decrease in their ability to transport the nucleoside adenosine. Diamide appeared to have little effect on glucose permeation in uninfected and Plasmodium falciparum infected cells. The inhibition of adenosine transport in human erythrocytes by diamide pretreatment appeared to be unrelated to the inhibition by the established nucleoside transport inhibitor, nitrobenzylthioinosine (NBMPR). An ID50 for diamide of 0.3 mM was determined for 1 microM adenosine transport in human erythrocytes after preincubation for 45 min at 37 degrees C. However, preincubation of diamide (20 mM, 60 min at 37 degrees C) with Babesia bovis-infected bovine erythrocytes resulted in complete inhibition of the capacity of the parasitised cell to transport adenosine and partial inhibition of glucose permeation. By contrast, diamide was shown to have little or no effect on the new or induced nucleoside permeation site in P. falciparum (trophozoite) infected erythrocytes nor on the glucose transporter in these cells. The results further indicate the differences between the normal human erythrocyte nucleoside and glucose transporters and those new or altered transporters in the membrane of P. falciparum or B. bovis-infected red blood cells.

Animals

The effect of oxidant stress on diamide-treated human granulocytes.

The role of sulfhydryls in the protection of human polymorphonuclear neutrophils against extracellular oxidant attack was investigated by simultaneously exposing polymorphonuclear neutrophils to the thiol-oxidizing agent diamide and the oxidant-generating system xanthine-xanthine oxidase. Neither diamide nor the oxidants generated by the xanthine-xanthine oxidase system alone impaired the burst in chemiluminescence, hexose monophosphate shunt activity or formate oxidation normally seen during polymorphonuclear neutrophil phagocytosis. Incubation of the polymorphonuclear neutrophils simultaneously with diamide and xanthine-xanthine oxidase markedly impaired polymorphonuclear neutrophil phagocytosis, hexose monophosphate shunt activity, chemiluminescence and formate oxidation. Although the polymorphonuclear neutrophils exposed to diamide and xanthine-xanthine oxidase did not respond to a variety of phagocytizable stimuli, trypan blue exclusion was normal and hexose monophosphate shunt activity could be stimulated by diamide. The damaging effect of the diamide xanthine-xamthine oxidase system could be blocked by the addition of superoxide dismutase or catalase, but not by hydroxyl radical or singlet oxygen scavengers. We hypothesize that an unidentified population of thiols may play a role in protecting the polymorphonuclear neutrophil from endogenously derived oxidants.

Azo Compounds

Endo-exocytotic images and changes in synaptic transmission induced by diamide at a cholinergic junction.

Small tissue fragments excised from the electric organ of Torpedo marmorata were treated with diamide, a penetrating thiol oxidizing agent, until synaptic transmission was blocked. At this stage, we found an unexpected number of exo-endocytotic images in the presynaptic plasmalemma. Omega-shaped profiles, some of them coated, were seen in thin sections of fixed tissue and pits opened in the P-face of the presynaptic membrane in freeze-fracture replicas from rapidly-frozen preparations. Diamide-treated specimens were frozen at 1 ms time intervals before, during and after a single electrical stimulus. This stimulation did not result in a further increase in the density of presynaptic pits, not in any change affecting the density or size distribution of intramembrane particles. This result is in contrast with what is observed in untreated specimens where transmission of a nerve impulse is accompanied by a momentary rise in the number of large particles. The density of synaptic vesicles--especially that of a subpopulation of small size vesicles--transiently increased within the first 2 h of diamide treatment. During the first stages of intoxication, diamide prolonged the time course of postsynaptic potentials--both spontaneous and evoked--probably by altering the gating properties of receptors (acetyl-cholinesterase activity was not impaired). Later on, all evoked responses were blocked. The spontaneous transmitter release greatly increased, first in the form of quantal miniature potentials. These then subsided whereas a class of very small potentials was generated at a high frequency. Also under the action of diamide, calcium progressively accumulated in the tissue but the number of synaptic vesicles containing calcium deposits was reduced. It is concluded that diamide causes a marked increase in the number of exo-endocytotic images in the presynaptic membrane, suppresses quantal but not subquantal release, and interferes with calcium sequestration in and extrusion from terminals.

Animals

Diamide: positive inotropic effect in isolated atria and inhibition of Na+/Ca2+ exchange in cardiomyocytes.

The influence of frequency of stimulation and external calcium on the positive inotropic response of guinea-pig left atria to diamide and the inhibitory action on Na+/Ca2+ exchange activity of rat cardiomyocytes by this oxidant of sulphhydryl groups have been investigated. Diamide (50-500 microM) induces a concentration-dependent positive inotropic effect which is more pronounced when atria are driven at 1.0 Hz rather than at 0.5 and 0.1 Hz, and are bathed in 2.72 mM rather than in 1.36 mM external calcium. A decrease in the positive inotropic effect at 35 degrees C with respect to 29 degrees C is also observed. In addition, diamide in positive inotropic concentrations (100-300 microM) significantly reduces Na+/Ca2+ exchange activity and cytoplasmic glutathione levels in adult rat cardiomyocytes. The thiol reducing agent dithiothreitol either reverses or prevents diamide effects both in isolated atria and cardiomyocytes, suggesting that the actions of diamide are correlated to its property to oxidize sulphhydryl groups to disulphides. In view of the functional importance of Na+/Ca2+ exchange in myocardial contractility, it is proposed that diamide may increase the heart force of contraction by an inhibition of the sarcolemmal Na+/Ca2+ exchange activity.

Animals

Diamide stimulates calcium-sodium exchange in dog red blood cells.

Calcium influx can be stimulated in dog red blood cells by preexposure to diamide under certain conditions. Diamide-activated calcium influx resembles swelling-induced Ca2+-Na+ exchange in several respects. These include saturation of calcium influx at external calcium levels greater than 0.5 mM, suppression of calcium influx by external sodium, and inhibition by quinidine. The ability of diamide to stimulate this transport pathway depends critically on the ionic composition of the medium in which the cells are bathed at the time of diamide exposure. The effect is greatest if the diamide preincubation is conducted in a hypotonic lithium chloride medium containing at least 1 microM calcium. Stimulation of Ca2+-Na+ exchange is seen at diamide concentrations (0.10-0.33 mM) that are lower than those reported to cause major spectrin cross-linking, glutathione depletion, Ca2+-ATPase inhibition, or ion channel formation. The results suggest that dog red cells have a large latent capacity for Ca2+-Na+ exchange.

Adenosine Triphosphate