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PubMed2005

Uncovering of intracellular water in cultured cells.

The complexity of biologic tissues, with multiple compartments each with its own diffusion and relaxation properties, requires complex formalisms to model water signal in most magnetic resonance imaging or magnetic resonance spectroscopy experiments. In this article, we describe a magnetic susceptibility-induced shift in the resonance frequency of extracellular water by the introduction of a gadolinium contrast agent to medium perfusing a hollow fiber bioreactor. The frequency shift of the extracellular water (+185 Hz at 9.4 T) uncovers the intracellular water and allows direct measurement of motional and relaxation properties of the intracellular space. The proposed method provides a unique tool for understanding the mechanisms underlining diffusion and relaxation in the intracellular space.

Animals↗
PubMed1992

Localization of epidermal growth factor (EGF) binding sites on antiluminal plasma membrane of rat kidney: autoradiographic study using nonfiltering perfused rat kidney.

We previously demonstrated that the specific binding of EGF to the antiluminal plasma membrane was a prerequisite step for the renal uptake of EGF. In the present study, the localization of 125I-EGF binding sites on the antiluminal plasma membrane was investigated by tissue sampling and X-ray autoradiography in the nonfiltering kidney. The binding of 125I-EGF was recognized over the whole kidney and was highest in the inner medulla followed by the cortex and outer medulla. The binding of 125I-EGF in the nonfiltering kidney was completely inhibited in the presence of 20 nM unlabeled EGF, suggesting specific binding of 125I-EGF to its receptor. Further, we used a histologic tissue staining method to confirm the location of the 125I-EGF binding sites. Binding of 125I-EGF was demonstrated on the proximal straight tubules (PST), cortical collecting ducts (CCD), inner medullary collecting ducts (IMCD), and thin limb of Henle in the inner medulla (IMTLH). We found that the binding of 125I-EGF was high in the IMTLH. In addition, we determined the grain density both on the cell surface membrane and in the intracellular space of the proximal straight tubules, where the grain density on the antiluminal plasma membrane was approximately 50% that in the intracellular space at 20 min after the start of 125I-EGF perfusion, suggesting the internalization of 125I-EGF from the antiluminal plasma membrane to the intracellular compartment. In conclusion, the binding sites of 125I-EGF, which were accessible from the antiluminal side, were broadly distributed over the whole kidney and were most dense around the IMTLH.

Animals↗
PubMed1984

[Kinetics of THAM (TRIS) distribution in intra- and extracellular compartments].

The distribution of 14C labelled THAM (tris-hydroxymethylaminomethane) was determined between intra- and extracellular space of nephrectomised Sprague-Dawley rats as a function of time at constant plasma pH of 7.4. The following results were obtained: An equilibrium in the distribution of THAM between ECS and ICS will not occur before 6-12 hours after administration. This indicates that THAM permeates very slowly into the intracellular compartment, which is in contrast to the general assumption that it quickly diffuses into the intracellular space to restore the intracellular acidosis. THAM disappears from the extracellular space in a multiexponential fashion, indicating that it equilibrates with the different body tissues at largely variable rates. The equilibrium which occurs between both body compartments 6-12 hours after THAM application does not agree with the values which are expected for transfer of only the nonionised substance. At plasma pH 7.4 and a "mean whole body pHi" of 6.88, THAM is distributed with a distribution ratio of 4 (ICS/ECS), a value quite different from the value of 11 which would be expected for exclusive nonionic diffusion. Thus THAM is also transferred across the cell membrane in ionised form. These results indicate that the influx of THAM into the intracellular space is too slow (when compared to the renal elimination kinetics) to influence intracellular pH significantly by direct buffer action. Moreover, only a fraction of THAM enters the intracellular space in the nonionised form, thus reducing (to an even greater extent) the direct effect of THAM on the intracellular acid-base equilibrium.

Animals↗
PubMed1983

Increased plasma ammonia may inhibit cellular release of branched-chain amino acids in systemic portal encephalopathy.

Plasma amino acid patterns were determined before and after hemofiltration (HF) and hemodialysis (HD) in 6 patients with portal systemic encephalopathy (PSE) and compared with the plasma AA patterns of 16 patients with chronic renal failure (CRF) treated either by HF or HD. The branched-chain amino acids (BCAA) increased paradoxically in PSE patients during HF but not with HD. There were no differences in BCAA's with HF as compared to HD in the CRF patients. The amount of amino acids lost was the same with both treatment modalities and in both patient groups. Much of the amino acids lost were released from the intracellular space. The BCAA release was significantly higher in PSE patients during HF. No correlation was found between plasma insulin, glucagon, and cortisol levels and BCAA release. An inverse correlation was found between the amount of BCAA's released from the intracellular space and the plasma ammonia levels. It is suggested that a selective cellular transport mechanism for BCAA exists which is inhibited by high plasma ammonia levels in PSE.

Adult↗
PubMed1979

Electrical properties of spherical syncytia.

Syncytial tissues consist of many cells whose intracellular spaces are electrically coupled one to another. Such tissues typically include narrow, tortuous extracellular space and often have specialized membranes at their outer surface. We derive differential equations to describe the potentials induced when a sinusoidal or steady current is applied to the intracellular space with a microelectrode. We derive solutions for spherical preparations with isotropic properties or with a particular anisotropy in effective extracellular and intracellular resistivities. Solutions are presented in an approximate form with a simple physical interpretation. The leading term in the intracellular potential describes an "isopotential" cell in which there is no spatial variation of intracellular potential. The leading term in the extracellular potential, and thus the potential across the inner membranes, varies with radial position, even at zero frequency. The next term of the potentials describes the direct effects of the point source of current and, for the parameters given here, acts as a series resistance producing a large local potential drop essentially independent of frequency. A lumped equivalent circuit describes the "low frequency" behavior of the syncytium, and a distributed circuit gives a reasonably accurate general description. Graphs of the spatial variation and frequency dependence of intracellular, extracellular, and transmembrane potential are given, the response to sinusoidal currents is used to calculate numerically the response to a step function of current.

Cytoplasm↗
PubMed1985

Evidence for plasma membrane impermeability to small ions in acrosome-intact mouse spermatozoa bound to mouse zonae pellucidae, using an aminoacridine fluorescent pH probe: time course of the zona-induced acrosome reaction monitored by both chlortetracycline and pH probe fluorescence.

Previous studies have shown that capacitated mouse spermatozoa bind to zonae pellucidae of mouse eggs with acrosomes apparently intact. The question addressed in this study was the following: are the membrane permeability barriers of the apparently acrosome-intact sperm still retained or is there a preliminary stage of the acrosome reaction in which these barriers are lost and the intracellular space becomes accessible to extracellular substrates? The experimental approach was to use the fluorescent pH probe 9-amino-3-chloro-7-methoxyacridine, which accumulates in intracellular spaces of lower pH than the suspending medium with the result that the cells become fluorescent. Freshly capacitated mouse spermatozoa bound to isolated zonae showed uniform fluorescence over the head and midpiece with this fluorescent probe at early times of binding. The fluorescence was abolished by NH4+ and nigericin, agents that equilibrate H+ across cell membranes. At these early times of binding, the acrosomes were fully intact as judged by chlortetracycline fluorescence pattern, which itself was unaffected by either N4+ or nigericin. The time course of the loss of this chlortetracycline pattern characteristic of acrosome-intactness was closely paralleled by loss of fluorescence of 9-amino-3-chloro-6-methoxyacridine over the first 90 min; thereafter, loss of the chlortetracycline pattern was somewhat more rapid. This result shows that acrosome-intact sperm bound to zonae pellucidae retain the permeability barriers of the plasma membrane to small cations; no evidence was found for an early stage of membrane "leakiness" preceding the acrosome reaction. The ionophore A23187 induced a very rapid acrosome reaction in sperm bound to isolated zonae, as judged with both fluorescence probes. This rapid reaction was partially inhibited by 3-quinuclidinyl benzilate, which, in the absence of ionophore, completely blocks the occurrence of the acrosome reaction in sperm bound to zonae. This suggests involvement of a specific calcium entry mechanism in the acrosome reaction of mouse sperm induced by mouse zonae pellucidae.

Acrosome↗
PubMed1984

Glucocorticoid receptor number and intracellular water space.

In order to elucidate the relationship between cell water content and number of glucocorticoid receptors, eleven normal and malignant lymphoid or myelomonocytic cell types originating from mouse, rat and man were investigated. The cellular water space was measured with 3H2O, and glucocorticoid receptor number was measured in a whole-cell binding assay with [3H]dexamethasone at 30 and 37 degrees C. The intracellular water phase concentration of glucocorticoid receptors (around 40 nmol/l cell water), and the dependence of receptor affinity on temperature were similar in normal and malignant rodent and human cells. It is concluded that comparisons of glucocorticoid receptor levels are best made on the basis of intracellular receptor concentrations.

Animals↗
PubMed1998

An overview of muscle glucose uptake during exercise. Sites of regulation.

The uptake of blood glucose by skeletal muscle is a complex process. In order to be metabolized, glucose must travel the path from blood to interstitium to intracellular space and then be phosphorylated to glucose 6-phosphate (G6P). Movement of glucose from blood to interstitium is determined by skeletal muscle blood flow, capillary recruitment and the endothelial permeability to glucose. The influx of glucose from the interstitium to intracellular space is determined by the number of glucose transporters in the sarcolemma and the glucose gradient across the sarcolemma. The capacity to phosphorylate glucose is determined by the amount of skeletal muscle hexokinase II, hexokinase II compartmentalization within the cell, and the concentration of the hexokinase II inhibitor G6P. Any change in glucose uptake occurs due to an alteration in one or more of these steps. Based on the low calculated intracellular glucose levels and the higher affinity of glucose for phosphorylation relative to transport, glucose transport is generally considered rate-determining for basal muscle glucose uptake. Exercise increases both the movement of glucose from blood to sarcolemma and the permeability of the sarcolemma to glucose. Whether the ability to phosphorylate glucose is increased in the working muscle remains to be clearly shown. It is possible that the accelerated glucose delivery and transport rates during exercise bias regulation so that muscle glucose phosphorylation exerts more control on muscle glucose uptake. Conditions that alter glucose uptake during exercise, such as increased NEFA concentrations, decreased oxygen availability and adrenergic stimulation, must work by altering one or more of the three steps involved in glucose uptake. This review describes the regulation of glucose uptake during exercise at each of these sites under a number of conditions, as well as describing muscle glucose uptake in the post-exercise state.

Animals↗
PubMed1995

Assessment of extracellular glucose distribution and glucose transport activity in conscious rats.

The effects of insulin on extracellular glucose distribution and cellular glucose transport activity were studied by simultaneously analyzing the plasma kinetics of L-[1-14C]glucose and 3-O-[3H]methylglucose after an intravenous injection during saline or insulin infusion (euglycemic glucose clamp) in conscious rats (n = 7 for each). The time profiles of plasma L-glucose were almost superimposable in the two protocols, and compartmental analysis showed that neither distribution volumes nor distribution rate constants were affected with insulin (P > 0.05 for all), suggesting that glucose distribution within the extracellular space was not influenced with insulin. In contrast, the time profile of plasma 3-O-methylglucose (3-MG) was markedly altered with insulin; the initial decrease was much faster during insulin infusion than during saline infusion, indicating stimulation of 3-MG transport into intracellular spaces with insulin. The 3-MG data were analyzed using a comprehensive model separately describing extracellular distribution and cellular transport of 3-MG by incorporating information on extracellular distribution kinetics obtained from L-glucose data. The combined L-glucose and 3-MG kinetic analysis precisely estimated insulin's effect in vivo to stimulate glucose transport into and out of intracellular spaces. We conclude that 1) insulin does not affect extracellular glucose distribution kinetics or volumes in conscious rats and 2) insulin's effects on cellular glucose transport in vivo can be assessed by simultaneous analysis of plasma L-glucose and 3-MG kinetics.

3-O-Methylglucose↗
PubMed2004

Structural changes in glutamate cell swelling followed by multiparametric q-space diffusion MR of excised rat spinal cord.

Diffusion in the extracellular and intracellular spaces (ECS and ICS, respectively) was evaluated in excised spinal cords, before and after cell swelling induced by glutamate, by high b-value q-space diffusion MR of specific markers and water. The signal decays of deuterated tetramethylammonium (TMA-d(12)) chloride, an exogenous marker of the ECS, and N-acetyl aspartate (NAA), an endogenous marker of the ICS, were found to be non-mono-exponential at all diffusion times. The signal decays of these markers were found to depend on the diffusion time and the cell swelling induced by the glutamate. It was found, for example, that the mean displacements of the apparent fast and slow diffusion components of TMA-d(12) are 7.21 +/- 0.11 and 1.16 +/- 0.05 microm, respectively at a diffusion time of 496 ms. After exposure of the spinal cords to 10 mM of glutamate, these values decreased to 6.62 +/- 0.13 and 1.01 +/- 0.05 microm, respectively. The mean displacement of NAA, however, showed a less pronounced opposite trend and increased after cell swelling induced by exposure to glutamate. q-Space diffusion MR of water was found to be sensitive to exposure to glutamate, and q-space diffusion MRI showed that a more pronounced decrease in the apparent diffusion coefficient and the mean displacement of water is observed in the gray matter (GM) of the spinal cord. All these changes demonstrate that diffusion MR is indeed sensitive to structural changes caused by cell swelling induced by glutamate. Multiparametric high b-value q-space diffusion MR is useful for obtaining microstructural information in neuronal tissues.

Animals↗
PubMed1979

Cellular site of gastric acid secretion.

Isolated gastric glands of the rabbit were examined both with differential interference-contrast microscopy and with electron microscopy to describe the morphologic correlates of acid secretion. Stimulation of the glands with histamine resulted in the development of intracellular spaces within the parietal cells. A similar transformation was produced by addition of 1 mM aminopyrine, whether the weak base was added in the presence of normal-K+ (5.4 mM) or high-K+ (108 mM) solutions. The intracellular space was compatible with the expanded canaliculus described in stimulated parietal cells. Confirmation that the space produced by histamine is the site of acid secretion was gained by combining fluorescence and interference-contrast methods in the presence of the dye acridine orange, which displays a pH-dependent metachromasia in its emission spectrum. Human gastrin I resulted in an observable discharge of peptic granules.

Acridine Orange↗
PubMed1993

Decreased erythrocyte Na+,K(+)-ATPase activity associated with cellular potassium loss in extremely low birth weight infants with nonoliguric hyperkalemia.

To determine whether a shift of potassium ions from the intracellular space to the extracellular space accounts, in part, for the hyperkalemia seen in extremely low birth weight infants, we examined potassium concentration in serum and erythrocytes from extremely low birth weight infants with hyperkalemia (n = 12) or with normokalemia (n = 27). In addition, to determine whether the shift of potassium was associated with low sodium-potassium-adenosinetriphosphatase (Na+,K(+)-ATPase) activity, we studied the activity of ATPase in the last 16 infants enrolled in the study. Fluid intake and output were measured during the first 3 days of life. Infants were considered to have hyperkalemia if the serum potassium concentration was 6.8 mmol/L or greater. Blood was obtained daily for intracellular sodium and potassium levels by means of lysis of erythrocytes. The remaining erythrocyte membranes were frozen and analyzed for Na+,K(+)-ATPase activity. There were significantly lower intracellular potassium/serum potassium ratios in the infants with hyperkalemia for each day of the 3-day study (p < 0.001). In the hyperkalemic group, there was lower Na+,K(+)-ATPase activity than in the infants with normokalemia (p = 0.006). Low Na+,K(+)-ATPase activity was associated with lower intracellular potassium/serum potassium ratios (p = 0.006), higher serum potassium values (p = 0.02), and lower intracellular potassium concentration (p = 0.009). The urinary data demonstrated that there was no difference in glomerulotubular balance between the two groups. We conclude that nonoliguric hyperkalemia in extremely low birth weight infants may be due, in part, to a shift of potassium from the intracellular space to the extracellular space associated with a decrease in Na+,K(+)-ATPase activity.

Bilirubin↗