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A Penttila

Publications and source records attributed to A Penttila.

7 recordsLinked to original sources
PubMed1979

Studies on cell surface conformation following injury. II. Scanning and transmission electron microscopy of cell surface changes following anoxic injury in Ehrlich ascites tumor cells.

Exposure of Ehrlich ascites tumor cells to anoxia resulted in rapid and characteristic conformational changes of cell surface topography. Combined scanning and transmission E/M studies revealed rapid alterations including simplification of the cell surface configuration with disappearance of microvilli which were replaced with formation of blebs and recesses at the cell periphery. These surface changes were accompanied by characteristic organelle alterations inside the cells which in this and other cellular systems have been shown to be reversible. Later, the cell surface topography became smoother and monotonic with small blebs and cribriform invaginations in addition to larger eruptions of the cell periphery. Combined transmission E/M studies revealed fragmentation of cellular membrane systems and lysis of organelles indicating the irreversible phase of anoxic injury. The rapid conformational surface changes encountered in Ehrlich ascites tumor cells following anoxia suggest the important role of the plasma membrane and its unfolding as a virtually instantaneous response of the cells to this injury.

Animals↗
PubMed1977

Optical properties of normal and injured cells. Application of cytographic analysis to cell viability and volume studies.

A cell spectrophotometer (Cytograf Model 6300 A, Bio/Physics Systems, Inc.) was tested in a cytotoxic assay using Ehrlich ascites tumor cells as a model system. Several cellular conditions associated with volume expansion, staining of cellular components and fixation of cells were applied and the magnitude of the scattering and extinction signals were tested in these diverse cellular conditions. The magnitude of the scattering pulse of a cell spectrophotometer was found to be greatly dependent on the staining color and intensity of cellular components with vital dyes or following osmium tetroxide fixation. When the absorption wavelength of the vital dye was close to the wavelength used in the cell spectrophotometer (about 630 nm), dead stained and living nonstained cell populations were completely separated from each other. The magnitude of the extinction pulse was greatly dependent on the state (normal, injured cells) and staining intensity (vital dye staining, osmium fixation) of cellular components. The magnitude of the extinction pulse was reduced from that in normal cells when cells were treated with p-chloromercuribenzene sulfonic acid or in a hypotonic solution that caused a marked volume expansion of injured cells. When cells were fixed with a mixture containing glutaraldehyde and osmium tetroxide the cellular components of normal and injured cells turned black and in these conditions the magnitude of the extinction signal was in a linear correlation to the cross-sectional area of cells. In the present study, the cell spectrophotometer proved to be an efficient method for estimation of cellular viability, based on different scattering properties of cells, offering the advantages of high speed and precision. Demonstration of the use of a variety of vital dyes having diverse extinction properties with capabilities to differentiate between living and dead cells has indicated the potential use of the cell spectrophotometer in cytotoxic assay. Modification of the magnitude of the extinction signal in the cell spectrophotometer also shows great promise for accurate automated size determination of both normal and injured cells. Previously, determination of the size of injured cells has been beset with methodologic errors.

4-Chloromercuribenzenesulfonate↗
PubMed1975

Studies on the modification of the cellular response to injury. II. Electron microscopic studies on the protective effect of acidosis on anoxic injury of Ehrlich ascites tumor cells.

Extracellular acidosis (ph 5.9 to 6.5) was found to be significantly retard the subcellular response of Ehrlich ascites tumor cells (EATC) to anoxic injury. The cells initially showed a reversible stage of cell injury with diffuse mitrochondrial condensation and swelling of endoplasmic reticulum (ER) at pH 7.9 by 1 h, while by 3 h at this pH all cells showed high amplitude and intramatrical flocculent densities of mitochondria, and fragmentation of membrane systems. At pH 7.4 cells were normal at 15 min., the mitochondria were condensed as above by 1 h, some cells still showed condensed mitochondria and dilated ER while others showed high amplitude swelling of mitochondria by 3 h and all cells showed irreversible changes by 4 h. At pH 5.9 to pH 6.5 mitochondria remained condensed until 3 h and only by 6 h did some cells show high amplitude swelling, whereas most cells showed persistent mitrochondrial condensation. Not until 8 h did all cells show high amplitude swelling of mitochondria. Furthermore, ultrastructural differences in the pattern of necrosis were seen at the lower pH values consisting of greater density of the cell sap, irregularly dispersed flocculent densities in apposition to fragmented cytoplasmic membranes and in mitochondria, and more prominent persistent clumping of nuclear chromatin.

Acidosis↗
PubMed1975

Effects of fixation and postfixation treatments on volume of injured cells;.

The effects of fixation with glutaraldehyde (GA), formaldehyde (FA), glutaraldehyde-formaldehyde (GA-FA), flutaraldehyde-osmium tetroxide (GA-Os04) and osmium tetroxide (OsO4) on cel volume were studied in control, p-chloromercuribenzene sulfonic acid (PCMBS)-treated and hypotonically-treated Ehrlich ascites tumor cells. Among the variables investigated were concentration of the tixative agent, osmolity of the buffer, total osmolaity of the fixation solution, osmolaltity of the postfixation buffer and the time of fixation and postfixation treatment; in addition, the effects of adding calcium and high molecular weight compounds to the fixative solution were studied. When the effects of standard fixatives on control, PCMBS- and hypotonically-treated cells were compared, marked differences were apparent in the behavior of control and injured cells. Control cells retained near prefixation volume in 3% GA and 3% GA-1% OsO4, swelled in 4% FA or 1% OsO4 and phosphate buffer (tkrp), whereas tpcmbs (310 mosM KRP)- and hypotonically-treated cells (103 mos M KRP) shrank in all aldehyde fixatives but swelled in 1% OsO4. Reducing the buffer osmolality had similar effects on control and injured cells although, there were variations in degree...

Animals↗
PubMed1975

Studies on the modification of the cellular response to injury. III. Electron microscopic studies on the protective effect of acidosis on p-chloromercuribenzene sulfonic acid-(PCMBS) induced injury of Ehrlich ascites tumor cells.

Extracellular acidosis (pH 6.5) was found to significantly retard the response of Ehrlich ascites tumor cells (EATC) to direct plasma membrane injury with the non-penetrating organic mercurial compound, p-chloromercuribenzene sulfonic acid (PCMBS). Treatment of cells with 1 mM PCMBS resulted in loss of viability of all cells by 45 minutes at pH 7.4, and by 90 minutes at pH 6.5. Pregression of cellular changes through the various stages of cell injury at the ultrastructural level was correspondingly slower at pH 6.5. The results support the concept that stage 3 of cell injury, associated with condensed mitochondria, dilated ER and swollen cell sap is compatible with cell survival, while stage 5 with high amplitude swelling of mitochondria, fragmentation of membrane systems, and beginning of karyolysis is characteristic of irreversible injury. All cells entered stage 3 at 7.5 minutes at pH 7.4, while essentially all cells entered stage 5 by 45 minutes. At pH 6.5, stage 3 was maintained for 45 minutes and 100% of the cells entered stage 5 by 90 minutes. Although the mechanism of the protection against PCMBS-induced injury is not known, the present electron microscopical results are compatible with the hypothesis that the extracellular acidosis acts to partially stabilize plasma membrane, perhaps by interaction with sulfhydryl (SH) groups.

Acidosis↗
PubMed1975

Studies on modification on the cellular response to injury.

Extracellular acidosis (pH 6.6) has been found to delay the lethal effect of p-chloromercuribenzene sulfonic acid on Ehrlich ascites tumor cells. At pH 6.6, 50 per cent of the cells died within approximately 80 minutes, compared with approximately 10 minutes at pH 7.5 or approximately 5 minutes at pH 8.0. It was also observed that low pH produced a dissociation between potassium loss, ATP levels, cell volume, and cell death. The possible mechanism of this effect is discussed; it is our hypothesis that it involves proton interactions with plasma membrane components which either affect available membrane sulfhydryl groups or otherwise stabilize the cell membrane against loss of semipermeable characteristics and cellular lysis.

4-Chloromercuribenzenesulfonate↗