scholarly journals LIVER PARENCHYMAL CELL INJURY

1963 ◽  
Vol 19 (1) ◽  
pp. 139-157 ◽  
Author(s):  
Edward S. Reynolds
Keyword(s):  
Endoplasmic Reticulum ◽  
Plasma Membrane ◽  
Carbon Tetrachloride ◽  
Cell Injury ◽  
Chemical Interaction ◽  
Parenchymal Cell ◽  
Granular Endoplasmic Reticulum ◽  
Liver Parenchymal Cell ◽  
Cytoplasmic Matrix ◽  
Liver Parenchymal

The structure of the endoplasmic reticulum, plasma membrane, mitochondria, and Golgi apparatus of the liver parenchymal cell is strikingly altered within 1 hour following the administration of a single oral dose of carbon tetrachloride to rats. Progressive loss of glucose-6-phosphatase activity accompanies dispersal of the ergastoplasm. Electron microscopy reveals that these changes are associated with vacuolization of the cisternae of the granular endoplasmic reticulum, degranulation of its membranes, and the appearance of increased number of free ribosomes in the adjacent cytoplasmic matrix. Concomitantly, calcium enters the liver parenchymal cell and is sequestered by mitochondria. First increased at 30 minutes, calcium content is maximal at 1 hour and returns to normal at 2 hours. Although succinic and glutamic dehydrogenase activity patterns within the liver lobule are unaffected, liver cell mitochondria enlarge and some appear to fuse or assume cup-like configurations. Microvilli lining the space of Disse become irregularly indistinct and increasingly pleomorphic by 30 minutes when the plasma membrane becomes increasingly permeable to calcium. Golgi vesicles swell and discharge their granules during the period of poisoning studied. Although all the changes observed may be the result of direct interaction of carbon tetrachloride with the membranes of the cytoplasmic constituents of the liver parenchymal cell, the possibility that the irreversible changes observed in the granular endoplasmic reticulum may be due to the chemical interaction between the poison and this system is discussed.

scholarly journals LIVER PARENCHYMAL CELL INJURY

1965 ◽  
Vol 25 (3) ◽  
pp. 53-75 ◽  
Author(s):  
Edward S. Reynolds
Keyword(s):  
Rat Liver ◽  
Inorganic Phosphate ◽  
Cell Injury ◽  
Parenchymal Cell ◽  
Mitochondrial Atpase ◽  
Liver Parenchymal Cell ◽  
Liver Parenchymal ◽  
Serum Inorganic Phosphate ◽  
Chemical Events ◽  
Parenchymal Cells

Accumulation of calcium in the mitochondria of rat liver parenchymal cells at 16 and 24 hours after poisoning with carbon tetrachloride is associated with an increase in amount of liver inorganic phosphate, the persistence of mitochondrial adenosine triphosphatase activity, and the formation of electron-opaque intramitochondrial masses in cells with increased calcium contents. These masses, which form within the mitochondrial matrix adjacent to internal mitochondrial membranes, resemble those observed in isolated mitochondria which accumulate calcium and inorganic phosphate; are present in a locus similar to that of electron opacities which result from electron-histochemical determination of mitochondrial ATPase activity; and differ in both appearance and position from matrix granules of normal mitochondria. After poisoning, normal matrix granules disappear from mitochondria prior to their accumulation of calcium. As calcium-associated electron-opaque intramitochondrial masses increase in size, mitochondria degenerate in appearance. At the same time, cytoplasmic membrane systems of mid-zonal and centrilobular cells are disrupted by degranulation of the rough endoplasmic reticulum and the formation of labyrinthine tubular aggregates. The increase in amount of inorganic phosphate in rat liver following poisoning is balanced by a decreased amount of phosphoprotein. These chemical events do not appear to be related, however, as the inorganic phosphate accumulated is derived from serum inorganic phosphate.

scholarly journals LIVER PARENCHYMAL CELL INJURY

1969 ◽  
Vol 41 (3) ◽  
pp. 736-752 ◽  
Author(s):  
David A. Sell ◽  
Edward S. Reynolds
Keyword(s):  
Carbon Tetrachloride ◽  
Cell Injury ◽  
Parenchymal Cell ◽  
Liver Protein ◽  
Hepatocellular Injury ◽  
Decomposition Products ◽  
Liver Parenchymal Cell ◽  
Endoplasmic Reticulum Calcium ◽  
Parenchymal Cells ◽  
Histochemical Changes

Iodoform, a relatively water-insoluble yellow solid, chemically reactive in free-radical reactions, produces early hepatocellular injury qualitatively similar to that of carbon tetrachloride. 2 hr after administration of radioactively labeled iodoform, nonvolatile 14C is preferentially recovered in microsomal lipid and protein. By 30 min microsomal properties are profoundly affected: oxidative demethylation decreases abruptly; increased lipoperoxide decomposition products are detected; and amino acid incorporation into liver protein is depressed. By 1 hr glucose-6-phosphatase is suppressed centrolobularly and increased stainable calcium is present in the midzone. Increased cell sap RNA contents are observed by 2 hr. Morphologically, the biochemical and histochemical changes are associated with progressive dispersion, vacuolation, and degranulation of the granular endoplasmic reticulum. Calcium-associated masses accumulate within the mitochondrial matrix, and mitochondria become progressively pleomorphic. Golgi components dilate and disperse. Membranous components of the cytoplasm of parenchymal cells conglomerate into labyrinthine tubular aggregates. Lipid accumulates in cytoplasmic droplets. Ultimately, centrolobular necrosis ensues. The close cytochemical and morphological similarities between the cellular injury produced in the liver by iodoform and that produced by carbon tetrachloride suggest common pathogenetic mechanisms associated with damage to membranes.

Regulation of pyruvate kinase by 6-phosphogluconate in isolated hepatocytes

1981 ◽  
Vol 240 (3) ◽  
pp. E279-E285
Author(s):  
S. B. Smith ◽  
R. A. Freedland
Keyword(s):  
Pyruvate Kinase ◽  
Parenchymal Cell ◽  
Isolated Hepatocytes ◽  
Hill Coefficient ◽  
Liver Parenchymal Cell ◽  
Liver Parenchymal ◽  
Highly Correlated ◽  
Parenchymal Cells ◽  
The Hill ◽  
Isolated Liver

Isolated liver parenchymal cells from rats fed a 65% sucrose diet for 14 days were incubated in the presence and absence of 10(-6) M glucagon. The pyruvate kinase obtained from homogenates of the glucagon-treated cells displayed and increased Ks 0.5 for phosphoenolpyruvate (P-enolpyruvate), as well as an increased Ka 0.5 for 6-phosphogluconate (6-P-gluconate), compared to pyruvate kinase from untreated cells. Additionally, glucagon treatment decreased the maximal stimulation of pyruvate kinase by 6-P-gluconate by approximately two-thirds and decreased the Hill coefficient value of pyruvate kinase for 6-P-gluconate from 1.76 to 1.56. 6-Aminonicotinamide, an inhibitor of 6-P-gluconate dehydrogenase, increased 6-P-gluconate levels in isolated liver parenchymal cells three- to sevenfold, depending on the substrates present. The flux of P-enolpyruvate through pyruvate kinase was increased from 18 to 40% in these preparations and was highly correlated with the increase in 6-P-gluconate levels. The results suggest that 6-P-gluconate could regulate pyruvate kinase activity in the intact liver parenchymal cell. Furthermore, the activator would be of greatest importance in the lipogenic animal.

l-Thyroxine enters the rat liver cell by simple diffusion

1983 ◽  
Vol 97 (2) ◽  
pp. 277-282 ◽  
Author(s):  
G. S. Rao ◽  
M. L. Rao
Keyword(s):  
Rat Liver ◽  
Arrhenius Plot ◽  
Parenchymal Cell ◽  
Liver Cells ◽  
Liver Parenchymal Cell ◽  
Simple Diffusion ◽  
Liver Parenchymal ◽  
Isolated Rat Liver ◽  
Centrifugation Technique ◽  
Parenchymal Cells

The mode of uptake of l-[125I]thyroxine by freshly isolated rat liver parenchymal cells was studied by a rapid centrifugation technique. Using conditions for measuring initial rates of uptake, uptake by liver cells was not saturable when exposed to hormone concentrations in the incubation medium ranging from 2 pmol/l to 10 μmol/l. The Arrhenius plot was linear from 2 to 37°C; the temperature coefficient was 1·4. The uptake of l-[125I]thyroxine by liver cells was 35% when compared with that of l-[125I]tri-iodothyronine. In the presence of 2·8% bovine serum albumin the rate of uptake of l-[125I]thyroxine by liver cells was reduced by 90%. These results suggest that l-[125I]thyroxine enters the rat liver parenchymal cell by simple diffusion and only the free hormone crosses the plasma membrane.

scholarly journals Active Synthesis of Collagen by Albumin-Producing Liver Parenchymal Cell Clones in Culture

1978 ◽  
Vol 54 (7) ◽  
pp. 391-396 ◽  
Author(s):  
Ryu-ichiro HATA ◽  
Yoshifumi NINOMIYA ◽  
Yutaka NAGAI ◽  
Kooko SAKAKIBARA ◽  
Yutaka TSUKADA
Keyword(s):  
Parenchymal Cell ◽  
Active Synthesis ◽  
Liver Parenchymal Cell ◽  
Liver Parenchymal ◽  
Cell Clones

scholarly journals SUBSURFACE CISTERNS AND THEIR RELATIONSHIP TO THE NEURONAL PLASMA MEMBRANE

1962 ◽  
Vol 13 (3) ◽  
pp. 405-421 ◽  
Author(s):  
Jack Rosenbluth
Keyword(s):  
Endoplasmic Reticulum ◽  
Plasma Membrane ◽  
Nerve Cell ◽  
Plasma Membranes ◽  
Granular Endoplasmic Reticulum ◽  
Supporting Cells ◽  
Golgi Membranes ◽  
Subsurface Cisterns ◽  
Central Nervous Systems ◽  
Neuronal Plasma Membrane

Subsurface cisterns (SSC's) are large, flattened, membrane-limited vesicles which are very closely apposed to the inner aspect of the plasma membranes of nerve cell bodies and the proximal parts of their processes. They occur in a variety of vertebrate and invertebrate neurons of both the peripheral and central nervous systems, but not in the surrounding supporting cells. SSC's are sheet-like in configuration, having a luminal depth which may be less than 100 A and a breadth which may be as much as several microns. They are separated from the plasmalemma by a light zone of ∼50 to 80 A which sometimes contains a faint intermediate line. Flattened, agranular cisterns resembling SSC's, but structurally distinct from both typical granular endoplasmic reticulum (ER) and from Golgi membranes, also occur deep in the cytoplasm of neurons. It is suggested that membranes which are closely apposed may interact, resulting in alterations in their respective properties. The patches of neuronal plasmalemma associated with subsurface cisterns may, therefore, have special properties because of this association, resulting in a non-uniform neuronal surface. The possible significance of SSC's in relation to neuronal electrophysiology and metabolism is discussed.

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