HgCl2-induced changes in cytosolic Ca2+ of cultured rabbit renal tubular cells

Smith, Mary W.; Ambudkar, Indu S.; Phelps, Patricia C.; Regec, Annette L.; Trump, Benjamin F.

doi:10.1016/0167-4889(87)90199-6

Cited by 79 publications

(35 citation statements)

References 32 publications

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“…The measurement of [Ca2+]i were done at 30°C. For the calculation of [Ca2+]i, the fluorescence signal obtained from whole cell (F1), after addition of 1 mM EGTA (F2), followed by lysing the cells with 0.04% Triton X-100 in presence of 30 mM Trizma-base (F3) and then 4 mM CaC12 (F4) respectively were used [21]. The formula is:…”

Section: Spectrofluorimetric Methodsmentioning

confidence: 99%

Temperature‐induced rapid increase in cytoplasmic free Ca²⁺ in pathogenic Leishmania donovani promastigotes

Sarkar

Bhaduri

1995

FEBS Letters

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Section: Spectrofluorimetric Methodsmentioning

confidence: 99%

Temperature‐induced rapid increase in cytoplasmic free Ca²⁺ in pathogenic Leishmania donovani promastigotes

Sarkar

Bhaduri

1995

FEBS Letters

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“…Deregulation of calcium is a crucial factor in the progression of reversible to irreversible cell injury (166,190 (184). Lechner et a1 (9 I ) found that low levels (-100 phi) of [Ca2+Ic permitted cell division, whereas high levels (450-1,000 p~) induced squamous differentiation.…”

Section: Significance Of Calciiirn In Cell Ittjtirymentioning

confidence: 99%

Intercellular Communication in Bronchial Epithelial Cells: Review of Evidence for a Possible Role in Lung Carcinogenesis

et al. 1990

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A challenging aspect of lung carcinogenesis is the elucidation of the mechanisms which permit initiated bronchial epithelial cells to attain a growth advantage over normal bronchial epithelial cells, and subsequently evolve into a malignant phenotype. In this review, the effects of interactions between normal and transformed cells, and the potential role of representative extrinsic factors on cell-cell communication are discussed. Evidence is presented to show how cell injury and the effects of serum and calcium may affect morphology and communication, and tumor development. A large number of autocrine-paracnne factors (e.g., TGFp, TGFa) are released by bronchial epithelial cells. These factors may inhibit or promote the proliferation of normal and transformed bronchial epithelial cells, respectively. The ability of certain injurious and tumor promoting agents (e.g., formaldehyde, TPA) to select for the transformed phenotype may involve selective cell injury, the induction of terminal differentiation and an inhibition of gap junction communication among normal BE cells.

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“…An approximate calibration of ratios and the pseudocolor look-up table (LUT) for ratioed images was obtained using the formula nM Ca2+ = &(R -R,J/ (R,,, -R), where & = 224 nM (9). The ratio obtained using the formula nM Ca2+ = &(R -RmJ PM 4-bromo-A23 187 was assumed to be equivalent to Ca2+-saturated fura-2 (R,,,) based on previous studies of cells in suspension (25). The ratio (R) value obtained from untreated cells was assumed to be equivalent to 100 n M based on previous studies in cell suspensions (25).…”

Section: Calibration Of Ratioed Imagesmentioning

confidence: 99%

“…The ratio obtained using the formula nM Ca2+ = &(R -RmJ PM 4-bromo-A23 187 was assumed to be equivalent to Ca2+-saturated fura-2 (R,,,) based on previous studies of cells in suspension (25). The ratio (R) value obtained from untreated cells was assumed to be equivalent to 100 n M based on previous studies in cell suspensions (25). The value for R,,, was calculated by substitution of R,,,, the 0 time values for R, and a 100 nM value for [Ca2+], into the equation.…”

Section: Calibration Of Ratioed Imagesmentioning

confidence: 99%

“…Depending on the type of injury, such increases of [Ca2+Ii were shown to result primarily from influx of extracellular Ca2+, redistribution of intracellular Ca2+ pools, or both (25). Until recently, however, studies of [Ca2+Ii, enabled by the development of fluorescent calcium probes such as fura-2, were confined to cell suspensions in which only an average change in [Ca2+], in a cell population could be measured.…”

Section: Introductionmentioning

confidence: 99%

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Oxidative Injury Induces Influx-Dependent Changes in Intracellular Calcium Homeostasis

et al. 1991

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Understanding of the mechanisms of cell injury and cell death is fundamental to the understanding of both protection against and initiation ofcell injury and cell death. We subjected primary cultures of proximal tubular epithelium (PTE) from adult rats to an exogenous oxidative stress, generated by xanthine/xanthine oxidase (X/XOD), and studied its effect on the concentration of cytosolic ionized calcium ([Caz+]J by means of digital imaging fluorescence microscopy (DIFM) using a cytosolic calcium probe, fura-2. Exposure to 25 mU/ml X/XOD caused notable increases in [CaZ+], detectable within 15 sec and increasing to micromolar levels with time. Experiments with Ca2+-free medium containing ethylene glycol-bis(/3-aminoethyl ether)N,N,N',N'-tetraacetic acid (EGTA) showed that the increase of [CaZ+], was due to influx from the extracellular space. Smaller and slower increases in [CaZ+li were seen after exposure to lower concentrations of X/XOD (5 and 10 mU/ml). PTE injury and killing were assessed by measuring the release of cytosolic lactate dehydrogenase (LDH), exclusion of trypan blue, and observation of morphologic changes. Exposures to the 25 mU/ml concentration of X/XOD caused significant LDH release after 2 hr and correlated with trypan blue staining of exposed cells. Again, lesser concentrations of X/XOD resulted in a slower release of smaller amounts of LDH, and thus delayed trypan blue staining. Cytoplasmic bleb formation was seen by phase microscopy within minutes of exposure to 25 mU/ml, followed by cell rounding, retraction, and disintegration. Transmission electron microscopy revealed a progression of changes characteristic of lethal cell injury, beginning with dilatation of the endoplasmic reticulum, detachment of ribosomes, condensation of mitochondria, and chromatin clumping and terminating with mitochondria1 swelling and formation of intramitochondrial flocculent densities. These studies clearly show that notable increases of [Ca*+], precede both sub-lethal and lethal changes in rat PTE. These results indicate that interventions designed to minimize or to accelerate calcium entry could be of importance in cell preservation or cell killing, respectively, and therefore to therapeutic strategies for myocardial infarction, stroke, or shock in the former instance and for cancers in the latter.

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HgCl2-induced changes in cytosolic Ca2+ of cultured rabbit renal tubular cells

Cited by 79 publications

References 32 publications

Temperature‐induced rapid increase in cytoplasmic free Ca²⁺ in pathogenic Leishmania donovani promastigotes

Temperature‐induced rapid increase in cytoplasmic free Ca²⁺ in pathogenic Leishmania donovani promastigotes

Intercellular Communication in Bronchial Epithelial Cells: Review of Evidence for a Possible Role in Lung Carcinogenesis

Oxidative Injury Induces Influx-Dependent Changes in Intracellular Calcium Homeostasis

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HgCl2-induced changes in cytosolic Ca2+ of cultured rabbit renal tubular cells

Cited by 79 publications

References 32 publications

Temperature‐induced rapid increase in cytoplasmic free Ca2+ in pathogenic Leishmania donovani promastigotes

Temperature‐induced rapid increase in cytoplasmic free Ca2+ in pathogenic Leishmania donovani promastigotes

Intercellular Communication in Bronchial Epithelial Cells: Review of Evidence for a Possible Role in Lung Carcinogenesis

Oxidative Injury Induces Influx-Dependent Changes in Intracellular Calcium Homeostasis

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Temperature‐induced rapid increase in cytoplasmic free Ca²⁺ in pathogenic Leishmania donovani promastigotes

Temperature‐induced rapid increase in cytoplasmic free Ca²⁺ in pathogenic Leishmania donovani promastigotes