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At least 19 recordsLinked to original sources
PubMed1992

Inhibition of actin-activated myosin Mg(2+)-ATPase in smooth muscle by ruthenium red.

Ruthenium red was found to inhibit actin-activated myosin Mg(2+)-ATPase in smooth muscle and to bind to myosin heavy chain, but not to F-actin. The inhibition by Ruthenium red of actin-activated Mg(2+)-ATPase was of the competitive type with respect to actin (Ki 4.4 microM) and of the non-competitive type with respect to ATP (Ki 6.6 microM). However, Ruthenium red scarcely dissociated the acto-heavy meromyosin complex during the ATPase reaction. These results suggest that Ruthenium red interacts directly with the binding site for F-actin on the myosin heavy chain. This site is considered to be necessary not for maintaining the binding affinity of myosin for F-actin, but for activation of the Mg(2+)-ATPase.

Actins↗
PubMed2000

Stimulatory release of hepatic lipase activity from rat hepatocytes by ruthenium red.

Ruthenium Red (RuR; ruthenium oxychloride ammoniated) stimulated the release of hepatic lipase (HTGL) activity from primary cultured rat hepatocytes into medium in a time- and dose-dependent manner. The RuR-stimulated release of HTGL activity was suppressed by tyrosine kinase (TK) inhibitors (ST-638 and biochanin A). The activity of partially purified TK preparation from hepatocytes was found to be increased by incubation with RuR. In addition, treatment of the hepatocytes with H-89, a potent inhibitor of cAMP-dependent protein kinase (PKA), decreased the stimulatory release of HTGL activity by RuR. Moreover, cAMP content in RuR-incubated hepatocytes was rapidly increased, and activation of PKA was observed. The RuR-stimulated release of HTGL activity is also inhibited by uncouplers and glycosylation inhibitors. In addition, incorporation of [3H]leucine into protein was increased in the present of RuR. Under marked inhibition of protein synthesis by cycloheximide, RuR still showed a full effect on the release of HTGL activity. These results suggest that RuR stimulates the release of HTGL activity through mechanisms of action involving TK- and PKA-activating pathways, which require a metabolic energy-sensitive process rather than elevation of enzyme molecule synthesis.

Animals↗
PubMed1986

Dissociation of insulin binding from insulin stimulation of 2-deoxyglucose transport by ruthenium red.

Ruthenium red increased specific insulin binding to isolated adipocytes 5.4 fold and 2.6 fold over binding determined in the absence and presence of Ca2+ and Mg2+. The increase in insulin binding was not accompanied by an increase in insulin sensitivity. The lack of effect of ruthenium red on insulin action argued strongly against an increase in intracellular Ca2+ as a potential messenger/transducer of insulin action and suggested that the enhancing effect of Ca2+ on insulin action was a result of increased receptor affinity.

Adipose Tissue↗
PubMed1986

Hyperthermia inhibition of tumor cells growth in the presence of ruthenium red.

Ruthenium red (RR) is taken up by DS sarcoma cells as a linear function of its concentration. Higher temperatures produce a higher uptake. This increased uptake is coincident with an augmentation of Trypan blue inclusion. A diminution of calcium transport in the presence of RR is observed at hyperthermia, and its uptake is not linear but presents a plateau for all temperatures and concentrations. RR-cell membrane interaction seems to produce two different effects: an early blocking of calcium transport, and a later change of the physicochemical characteristics of the plasma membrane. On the colony forming ability of CA1 cell RR shows clearly an intrinsic toxic effect, and when present during hyperthermia a low but significant enhancement of tumor cells mortality.

Animals↗
PubMed1992

Hepatotoxicity induced by a single ip injection of ruthenium red.

Ruthenium red (RR) has been used as a marker in morphological observations of the glycocalix because it interacts with polyanionic mucopolysaccharides. This fact may explain its agglutinating effect on rat blood red cells following a single 20 mg/kg intraperitoneal injection, which increases with time post-injection. This study was performed to determine whether such an effect was due to a direct effect of the RR on the blood cells, to interference with coagulation, or to the non-specific general toxicity of this dye. Male rats were injected with 20 mg/kg RR ip and the enzymatic and coagulation parameters, plus the liver morphology were examined. Alanine aminotransferase (ALAT) activity was increased at 30, 60 and 120 min, and aspartic aminotransferase (ASAT) activity was increased 60, 120 and 480 min after RR injection. The prothrombin time (PT) and partially activated thromboplastin time (PTT) were significantly decreased, particularly after 60-120 min. The liver had an external granular appearance with clear signs of congestion and oedema, and showed degenerative changes very soon after RR injection. A single administration of RR induces serious functional and structural changes in the liver. Such a toxicity, and these changes must be taken into consideration, particularly with regard to neurological studies.

Animals↗
PubMed2000

Inhibition of smooth-muscle myosin-light-chain phosphatase by Ruthenium Red.

Ruthenium Red (RuR) is widely used as an inhibitor of ryanodine receptor Ca(2+) release channels, but has additional effects such as the induction of Ca(2+) sensitization of contraction of permeabilized smooth muscles. To address the mechanism underlying this process, we examined the effects of RuR on contractility in permeabilized guinea-pig ileum and on the activity of myosin-light-chain phosphatase (MP). RuR increased the force at submaximal [Ca(2+)] (pCa 6.3) approx. 4-fold. This effect was not observed after thiophosphorylation of MP. RuR also seemed capable of preventing the thiophosphorylation of MP, suggesting a direct interaction of RuR with MP. Consistent with this possibility, smooth-muscle MP was inhibited by RuR in a concentration-dependent manner (IC(50) 23 microM). Exogenous calmodulin significantly increased RuR-induced contraction at pCa 6.3 but had little effect on contraction induced by microcystin at this [Ca(2+)]. Ca(2+)-independent contraction was induced by RuR (EC(50) 843 microM) and by microcystin (EC(50) 59 nM) but the maximal force induced by RuR was smaller than that induced by microcystin. The addition of 300 microM RuR enhanced the contraction induced by 30 nM microcystin but markedly decreased that induced by 1 microM microcystin. Such a dual action of RuR on microcystin-induced effects was not observed in experiments using purified MP. We conclude that the RuR-induced Ca(2+) sensitization of smooth-muscle contraction is due to the direct inhibition of MP by RuR.

Adenosine Triphosphate↗
PubMed1994

Inhibition of the mitochondrial Ca2+ uniporter by pure and impure ruthenium red.

Commercial ruthenium red is often purified by a single recrystallization as described by Luft, J.H. (1971) Anat Rec 171, 347-368, which yields small amounts of material having an apparent molar extinction coefficient of approximately 67,400 at 533 nm. A simple modification to the procedure dramatically improves the yield, allowing crystallization to be repeated. Three times recrystallized ruthenium red has an apparent extinction coefficient of approximately 85,900, the highest value reported to date. Both crude and highly purified ruthenium red can be shown to inhibit reverse activity of the mitochondrial Ca2+ uniporter (uncoupled mitochondria), provided that care is taken to minimize and account for Ca2+ release through the permeability transition pore. Crude ruthenium red is 7-10 fold more potent than the highly purified material in this regard, on an actual ruthenium red concentration basis. The same relative potency is seen against forward uniport (coupled mitochondria), however, the I50 values are 10 fold lower for both the crude and purified preparations. These data demonstrate unambiguously that the energy state of mitochondria affects the sensitivity of the Ca2+ uniporter to ruthenium red preparations, and that both the forward and reverse reactions are subject to complete inhibition. The data suggest, however, that the active inhibitor may not be ruthenium red per se, but one or more of the other ruthenium complexes which are present in ruthenium red preparations.

Animals↗
PubMed1978

Selective inhibition of potassium contracture in guinea pig taenia coli by ruthenium red.

Effects of ruthenium red on isotonic KCl induced contracture (K-contracture), cellular 45Ca uptake and 45 Ca binding to surface membranes were examined in the smooth muscle cells of guinea pig taenia coli. These results were compared with those using lanthanum (La3+). The tonic component of the K-contracture was selectively inhibited by 1 mM ruthenium red. In contrast, 1 mM La3+ inhibited the phasic component of the K-contracture to a large extent. Use of 1 mM ruthenium red selectively inhibited the tonic component of K-contracture and caused a marked decrease in cellular 45Ca uptake in that component of K-contracture. In contrast, 1 mM La3+ largely inhibited the phasic component and caused a significant decrease in cellular 45Ca in that component. According to Scatchard plot analysis, there are two kinds of Ca2+ binding sites of high and low affinity, respectively, on the surface membrane of the taenia coli. One mM ruthenium red suppressed those of low affinity more strongly than those of high affinity. In contrast, 1 mM La3+ suppressed high affinity sites more markedly than low affinity sites. Based on these results, it seems possible to conclude that ruthenium red mainly blocks the initial binding sites linked with Ca2+ influx which is related to the production of the tonic component while La3+ blocks those sites related to the phasic component of the K-contracture of guinea pig taenia coli.

Animals↗
PubMed1979

Potentiation and inhibition of ganglionic transmission by ruthenium red.

The effect of ruthenium red, 2.5 to 5 muM, on ganglionic transmission in rat superior cervical ganglia and frog abdominal ganglia were studied in vitro. In rat ganglia, ruthenium red caused a spontaneous firing of ganglia cells, and an increase in the amplitude and duration of the compound action potential following a single stimulus volley. However, transmission following a conditioning volley or a repetitive stimulus train to the preganglionic nerve was depressed up to 60 sec. The asynchronous firing caused by bethanechol was potentiated by ruthenium red. In the frog, ruthenium red caused repetitive firing of ganglion neurons following either orthodromic or antidromic stimulation. It is suggested that the potentiation of the single potential and the spontaneous firing are due to a ruthenium red-induced increase in intracellular calcium concentration. The depression of transmission may be due to a temporary depletion of readily releasable acetylcholine. It is also suggested that ruthenium red has an effect on the postsynaptic membrane.

Action Potentials↗
PubMed1999

Injection of Xenopus oocytes with mRNA from cultured neurons induces new currents and susceptibility to the damaging action of ruthenium red.

The hexacationic dye ruthenium red produce neuronal death in primary cultures. We injected messenger RNA (mRNA) from cultured neurons into Xenopus laevis oocytes to test whether this treatment can make oocytes sensitive to the damaging action of ruthenium red. Two-microelectrode voltage clamp and resting membrane potential were used to evaluate mRNA expression and to assess the effect of the dye on oocyte survival, when added to the medium or when injected into the cells, at 20, 50, or 100 microM concentrations. Injection of mRNA from cultured cortical or cerebellar granule neurons produced both new outward currents and membrane hyperpolarization. Exposure of mRNA-injected oocytes to extracellular ruthenium red for 24 h induced a remarkable depolarization, but no significant damage was observed. Injection of the dye into buffer-injected oocytes did not cause any change in membrane potential or cell survival, whereas in mRNA-injected oocytes an important depolarization was observed at 24 h after ruthenium red introduction, and 29% of the cells showed serious damage. The results suggest that oocytes become sensitive to intracellular ruthenium red toxicity because they express neuronal-specific proteins involved in cell death.

Animals↗
PubMed1993

The analgesia induced by intrathecal injection of ruthenium red.

Intrathecally (i.t.) administered ruthenium red (40, 80, 160 ng) dose-dependently inhibited formalin-induced nociceptive response. Ruthenium red caused a significant inhibition of pain-related behavioral responses induced by i.t. capsaicin but not by i.t. substance P. These results suggest that ruthenium red produces analgesia by inhibiting the release of neuropeptides in the spinal cord.

Analgesics↗
PubMed1999

Ruthenium red and the bacterial glycocalyx.

Ruthenium red, a promising cationic reagent for electron microscopy (EM), has long been an important tool in histology. The reagent was initially used by botanists as a semispecific stain for pectic substances, but it has gradually been embraced by investigators in microbiology and the animal sciences as a stain for anionic glycosylated polymeric substances. Luft developed a reliable method and demonstrated that ruthenium red was a useful reagent for visualizing ultrastructural detail. Many investigators, using modifications of Luft's approach, have identified numerous applications for this important reagent. Ruthenium red has been used to show the ultrastructural detail of bacterial glycocalyces. Strong, sharp and consistent observations of this ultrastructural component of the bacterial cell have given a better understanding its fibrous anionic matrix. Any variations in staining owing to artifactual alteration of the fine delicate ultrastructural features have been overcome by incorporation of diamine lysine into ruthenium red methods, thus providing flexible processing times under less than ideal laboratory sampling conditions. Ruthenium red has broad utility in the biological sciences, and in combination with lysine, it is an excellent EM stain for enhanced visualization of bacterial glycocalyx from culture or from clinical specimens.

Animals↗
PubMedDate not supplied

Influence of ruthenium red on rat heart subcellular calcium transport.

Ruthenium red inhibited Ca2+-ATPase and ATP-independent Ca2+ binding with rat heart sarcolemma in a concentration dependent manner; significant effects were evident at 0.25 microM and higher concentrations. The apparent Ka for Ca2+-ATPase was 1.02 +/- 0.02 mM Ca2+ and 1.47 +/- 0.12 mM Ca2+ in the absence and presence of 2.5 microM ruthenium red, respectively; however, no change in the Vmax (41.2 +/- 1.6 mumol Pi/mg/h) was observed. Likewise, the affinity of Ca2+ for both low and high affinity Ca2+ binding sites in sarcolemma was decreased by ruthenium red. Sarcolemmal Na+-dependent Ca2+ uptake, ATP-dependent Ca2+ accumulation, Mg2+-ATPase and Na+,K+-ATPase activities were not affected by ruthenium red. In sarcoplasmic reticulum preparations, ruthenium red (0.25 to 25 microM) enhanced Ca2+ uptake without altering the Ca2+-stimulated ATPase activity. The observed increase in Ca2+ uptake appears to be due to the depressant effect of the dye on Ca2+ release from the sarcoplasmic reticulum. In mitochondrial preparations, ruthenium red (0.025 to 25 microM) showed a marked inhibitory effect on Ca2+ uptake activity whereas the Mg2+-ATPase activity was unaltered. In isolated rat hearts, 0.025 microM ruthenium red produced a slight negative inotropic effect, whereas 0.25 to 2.5 microM ruthenium red elicited a biphasic response both in terms of developed tension and resting tension. High concentrations of ruthenium red (12.5 to 25 microM) resulted in the development of contracture. Electron microscopic studies revealed the presence of ruthenium red in the myoplasm of hearts perfused for 15 to 30 mins with 2.5 to 5 microM dye.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Muscle satellite cells in urodele amphibians: faciliatated identification of satellite cells using ruthenium red staining.

The ruthenium red (RR) stained forelimb musculature of three species of urodeles Triturus (Notophthalmus) viridescens, Amblystoma maculatum, Amblystoma opacum in various stages of growth were examined with the electron microscope for the presence of satellite cells. It was found that RR staining facilitated greatly the identification of satellite cells. In young larvae of all three species satellite cells were detected with a frequency of 29% to 48% per total number of nuclei. In adult Triturus and Amblystoma maculatum satellite cells were no longer detected; instead "pericytes" as described by Hay ('74) were seen with a frequency of 12% and 3% respectively. During metamorphosis of Triturus satellite cells, with part of their myofiber-satellite cell intercellular space filled with basement membrane material, occurred at a peak frequency. The cells presumably are intermediate in the formation of "pericytes." At ten days after metamorphosis satellite cells and intermediate cells were no longer detected and the limb musculature contained only "pericytes" similar to the ones observed in adult newts. The significance of the presence of satellite cells in relation to limb regeneration and muscle regeneration is discussed.

Ambystoma↗
PubMed1999

Cooperative block of the plant endomembrane ion channel by ruthenium red.

Effects of ruthenium red (RR) on the slow Ca(2+)-activated Ca(2+)-permeable vacuolar channel have been studied by patch-clamp technique. Applied to the cytosolic side of isolated membrane patches, RR at concentrations of 0.1-5 microM produced two distinct effects on single channel kinetics, long lasting closures and a flickering block of the open state. The first effect was largely irreversible, whereas the second one could be washed out. The extent of flickering block steeply increased (zdelta = approximately 1.35) with the increase of cytosol-positive voltage, dragging RR into the channel pore. At least two RR ions are involved in the block according to Hill coefficient n = approximately 1.30 for the dose response curves. The on-rate rate of the drug binding linearly depended on the RR concentration, implying that one RR ion already plugged the pore. The blocked state was further stabilized by binding of the second RR. This stabilization was in excess of that predicted by independent binding as the dependence of unblocking rate on RR concentration revealed. A cooperative model was therefore employed to describe the kinetic behavior of RR binding. At zero voltage the half-blocking RR concentration of 36 microM and the bimolecular on-rate constant of 1.8 x 10(8) M(-1) s(-1) were estimated.

Binding Sites↗
PubMed1976

Convulsions or flaccid paralysis induced by ruthenium red depending on route of administration.

Ruthenium red was administered to mice and cats intracranially or intraperitoneally. In mice, intracisternal administration produced status epilepticus and tonic convulsions. In contrast, intraperitoneal administration induced total flaccid paralysis lasting several hours. These effects of Ruthenium red were partially blocked by the simultaneous administration of CaCl2. EDTA, at doses much greater than those of Ruthenium red, produced effects similar to those of the dye, which were also blocked by CaCl2 administration. In cats, intraventricular or intrahippocampal administration of Ruthenium red through a permanently implanted cannula produced after a few minutes subclinical paroxysmal activity in all brain regions recorded. After several hours the animals developed typical grand mal seizures. Intraperitoneal injection of Ruthenium red to cats did not affect the EEG but markedly depressed muscular activity. Administration of carbachol to the latter animals produced myoclonic responses. These results are discussed in relation to the inhibitory effect of Ruthenium red on Ca2+ transport and binding to membranes, and to the role of this cation on neurotransmitter release.

Animals↗
PubMed1974

The inhibition of mitochondrial calcium transport by lanthanides and ruthenium red.

An EGTA (ethanedioxybis(ethylamine)tetra-acetic acid)-quench technique was developed for measuring initial rates of (45)Ca(2+) transport by rat liver mitochondria. This method was used in conjunction with studies of Ca(2+)-stimulated respiration to examine the mechanisms of inhibition of Ca(2+) transport by the lanthanides and Ruthenium Red. Ruthenium Red inhibits Ca(2+) transport non-competitively with K(i) 3x10(-8)m; there are 0.08nmol of carrier-specific binding sites/mg of protein. The inhibition by La(3+) is competitive (K(i)=2x10(-8)m); the concentration of lanthanide-sensitive sites is less than 0.001nmol/mg of protein. A further difference between their modes of action is that lanthanide inhibition diminishes with time whereas that by Ruthenium Red does not. Binding studies showed that both classes of inhibitor bind to a relatively large number of external sites (probably identical with the ;low-affinity' Ca(2+)-binding sites). La(3+) competes with Ruthenium Red for most of these sites, but a small fraction of the bound Ruthenium Red (less than 2nmol/mg of protein) is not displaced by La(3+). The results are discussed briefly in relation to possible models for a Ca(2+) carrier.

Animals↗