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H H Mollenhauer

Publications and source records attributed to H H Mollenhauer.

At least 19 recordsLinked to original sources
PubMed1992

Swelling response of Golgi apparatus cisternae in cells treated with monensin is reduced by cell injury.

The effect of mechanical stress on Golgi apparatus was examined in thin slices of rat liver. The findings should be of relevance both to electron microscopists who routinely mince tissue, and to biochemists who homogenize tissues to isolate membranous components. The swelling response of Golgi apparatus to monensin was used as an assay because the swelling response is distinct and is thought to result from a well-characterized metabolic process, namely the acidification of vesicles. The results showed that the swelling response was compromised by monensin as far away as 6-7 cells from a cut surface even though other aspects of cell ultrastructure were not altered from normal. The monensin-induced swelling response was also evaluated in isolated Golgi apparatus and found to be similar to that with tissue. Thus, mechanical stress such as commonly used to mince tissue or isolate tissue components, appears to markedly alter Golgi apparatus function compared to the situation in vivo. In this example, the altered response of Golgi apparatus to monensin indicated that some aspects associated with the ATP-dependent proton-pumping machinery of the trans-most cisternae and trans Golgi network were compromised.

Animals↗
PubMed1992

Retinol stimulates Golgi apparatus activity in cultured bovine mammary gland epithelial cells.

Biochemical and electron microscopic studies have indicated that the Golgi apparatus responds to retinol. The purpose of this investigation was to visualize and record with living cells the rapidity of the response to retinol. A rapid response of the Golgi apparatus to retinol (1.75-17.5 mumol/L) added to the culture medium was observed using video-enhanced light microscopy with bovine mammary epithelial cells. The response was manifested within 1 min as a marked movement of membranes within the Golgi apparatus zone. In subsequent electron microscope preparations of the cells, only minor changes were observed and were restricted to increased numbers of normal-appearing membranes and vesicles associated with the trans Golgi apparatus face of the retinol-treated cells.

Animals↗
PubMed1991

Perspectives on Golgi apparatus form and function.

In 1898, Camillio Golgi reported a new cellular constituent with the form of an extensive intracellular network (the apparato reticolare interno), which now bears his name. However, the history of Golgi's apparatus is replete with controversy regarding its reality, what components of the cell should be included under its aegis, and what terminology should be used when referring to it. Electron microscopy has resolved many of these controversies and it is appropriate that this volume emphasize that aspect of Golgi apparatus discovery. The principal structural component of the Golgi apparatus is the stack of cisternae, or dictyosome. As determined both biochemically and at the level of electron microscopy, the dictyosome is a highly ordered and polarized structure. The maintenance of order within the stack is thought to result from either intercisternal bonding constituents, or filamentous structures (or both) that bridge the space between adjacent cisternae. Mechanisms proposed for movement of membrane and product into and out of the dictyosome (i.e., the Golgi apparatus stack) include a serial mode which functions exclusively by the formation, displacement, and loss of cisternae from the stack, and a parallel mode which functions exclusively by the movement of membrane, product, or precursor molecules directly into the peripheral edges of the cisternae. In the parallel mode, all cisternae can be accessed either singly or simultaneously, at least in theory, at any position within the stack. It is probable that both the serial and the parallel modes function concomitantly and need not be mutually exclusive. Finally, the peripheral tubules of the cisternae represent a major membranous constituent of the cell with potentially unique functions. These tubules interconnect cisternae of adjacent stacks and may represent the major site of receptors for the shuttle (i.e., parallel) type of transfer among cisternae. Peripheral tubules as extensions of the cisternal lumina into the cytoplasm presumably have other functions, but these, like the tubules themselves, have only rarely been accommodated into functional models of Golgi apparatus dynamics in secretion or membrane flow.

Animals↗
PubMed1990

Alteration of intracellular traffic by monensin; mechanism, specificity and relationship to toxicity.

Monensin, a monovalent ion-selective ionophore, facilitates the transmembrane exchange of principally sodium ions for protons. The outer surface of the ionophore-ion complex is composed largely of nonpolar hydrocarbon, which imparts a high solubility to the complexes in nonpolar solvents. In biological systems, these complexes are freely soluble in the lipid components of membranes and, presumably, diffuse or shuttle through the membranes from one aqueous membrane interface to the other. The net effect for monensin is a trans-membrane exchange of sodium ions for protons. However, the interaction of an ionophore with biological membranes, and its ionophoric expression, is highly dependent on the biochemical configuration of the membrane itself. One apparent consequence of this exchange is the neutralization of acidic intracellular compartments such as the trans Golgi apparatus cisternae and associated elements, lysosomes, and certain endosomes. This is accompanied by a disruption of trans Golgi apparatus cisternae and of lysosome and acidic endosome function. At the same time, Golgi apparatus cisternae appear to swell, presumably due to osmotic uptake of water resulting from the inward movement of ions. Monensin effects on Golgi apparatus are observed in cells from a wide range of plant and animal species. The action of monensin is most often exerted on the trans half of the stacked cisternae, often near the point of exit of secretory vesicles at the trans face of the stacked cisternae, or, especially at low monensin concentrations or short exposure times, near the middle of the stacked cisternae. The effects of monensin are quite rapid in both animal and plant cells; i.e., changes in Golgi apparatus may be observed after only 2-5 min of exposure. It is implicit in these observations that the uptake of osmotically active cations is accompanied by a concomitant efflux of H+ and that a net influx of protons would be required to sustain the ionic exchange long enough to account for the swelling of cisternae observed in electron micrographs. In the Golgi apparatus, late processing events such as terminal glycosylation and proteolytic cleavages are most susceptible to inhibition by monensin. Yet, many incompletely processed molecules may still be secreted via yet poorly understood mechanisms that appear to bypass the Golgi apparatus. In endocytosis, monensin does not prevent internalization. However, intracellular degradation of internalized ligands may be prevented.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

An ultrastructural evaluation of toluene toxicity using cultured mammalian cells.

Animal cells were cultured in media containing toluene and then examined by electron microscopy to determine changes in subcellular architecture. Cellular viability and cloning studies indicated toluene toxicity at concentrations of 50-500 ppm. At all dosage levels, toluene accelerated cell death compared to comparable control cells that had not been exposed to toluene. However, media composition and, particularly, the presence or absence of fetal bovine serum (FBS), markedly affected toluene toxicity. In media without FBS reversible changes in filopodia and cell shape were identified after 15 min of exposure to as little as 50 ppm toluene, and cell death occurred within 5 min at concentrations of 500 ppm toluene. In media with FBS, no filopodial changes were observed at 50 ppm toluene, and cell death, although accelerated, was clearly evident only after 24-48 h of exposure to 200-500 ppm toluene. Except for the cell-surface changes, chronic toluene exposures (50-100 ppm without FBS or 200-500 ppm with FBS in the growth medium) produced no unusual intracellular changes until 24-48 h of toluene exposure. With toluene exposures of 24 h or longer, cellular changes included condensation of heterochromatin in nuclei, formation of bulbous protuberances at the cell surface, loss of polyribosomes (but not ribosomes) and, ultimately, degeneration of organelles. These late changes were irreversible and the prelude to cell death.

Animals↗
PubMed1989

Inhibition by mannose of in vitro colonization of chicken small intestine by Salmonella typhimurium.

The in vitro adherence of [3H]thymidine-labeled Salmonella typhimurium isolates to the small intestine of one-day-old chickens was investigated. Bacteria were screened for mannose sensitivity and mannose-resistance binding properties. Type 1 fimbriae positive strains adhered significantly better than Type 2 fimbriae-negative strains. Adherence was significantly (P less than .05) inhibited by D-mannose, methyl-alpha-D-mannoside, arabinose, and galactose. Adherence was both time and temperature dependent. These findings suggest that the small intestine of the chicken has receptors for bacteria with Type 1 fimbriae. The function of the receptors is dependent on a mannose moiety. Bacteria adhered better to fresh intestine cells than to cells held overnight at 4 C. Thus, adherence was dependent upon a metabolically active host cell. The in vitro adherence assay may further be used to study the interaction of bacteria with chicken enterocytes.

Animals↗
PubMed1989

Prevention of Salmonella typhimurium colonization of broilers with D-mannose.

Broiler chickens can be contaminated by Salmonella typhimurium, which is a food safety concern. It has been previously shown that D-mannose blocks S. typhimurium adherence to chicken intestine in vitro. One-day-old broiler chickens were fed normal drinking water or drinking water supplemented with 2.5% mannose for 10 days. On Day 3, both groups were challenged orally with 1 x 10(8) S. typhimurium [ST-10 (Animal Diagnostics Laboratory, Ames, IA)] resistant to Nal and Nov (Sigma, St. Louis, MO). On Day 10 the birds' caecal contents were examined for the antibiotic-marked S. typhimurium. Two additional groups of birds were provided normal drinking water or mannose but were not challenged with the bacteria. Salmonella-challenged control chickens were 78, 82, and 93% colonized whereas Salmonella-challenged mannose-treated chickens were only 28, 21, and 43% colonized. Moreover, the mean log10 counts of control and mannose groups were significantly (P less than .001) reduced by at least 99%. Mannose-supplemented drinking water had no effect on weight gains. Certain carbohydrates may provide a means to reduce S. typhimurium contamination in broilers.

Administration, Oral↗
PubMed1989

Ultrastructure of hepatic and renal lesions in chickens fed aflatoxin.

Male broiler chicks were given feed and water ad libitum from hatching through 3 weeks of age. The feed contained 0, 1.25, 2.5, and 5.0 micrograms of aflatoxin/g of feed. The chicks were killed by cervical dislocation and specimens of liver and kidney were obtained for electron microscopy on days 3, 6, 9, 17, and 21. In chicks fed 5.0 micrograms of aflatoxin, the primary lesions in liver were hepatocellular lipidosis, enlargement of bile canaliculi, reduction in mitochondrial size, mild lymphocytic infiltration, and hepatocellular degeneration and necrosis. Similar lesions were noticed in some chicks fed 2.5 micrograms of aflatoxin, but none was observed in chicks fed at 1.25 micrograms of aflatoxin. At 5 micrograms of aflatoxin, the most consistent lesion in the kidney was thickening of the glomerular basement membrane. Similar glomerular lesions were observed at 2.5 micrograms of aflatoxin, but not at 1.25 micrograms of aflatoxin. Some foot processes of the glomerular epithelial cells were poorly developed. Fusion of foot processes was not observed and fibrous material was not evident in the basement membrane. The pseudopodia of endothelial cells lining the thickened basement membrane were depleted in number or were absent. Degenerative changes also were observed in the cells of the proximal convoluted tubules, but these were less consistent than those of the glomerulus.

Animals↗
PubMed1989

Ultrastructural lesions induced by T-2 toxin in mice.

Mice were given T-2 toxin daily by stomach tube for a period of 10 days. Three mice were killed on days 1, 2, 7, 9, and 12, and selected tissues were processed for electron microscopy and analyzed for cellular abnormalities. No changes in cellular ultrastructure were observed in either kidney or pancreas. Necrosis of a few cells (estimated as 0.1%) and an occasional slight reduction of brush border microvilli were observed in the intestinal mucosal epithelium at 1 and 2 days post treatment but not at 7, 9, and 12 days post treatment. The most significant changes were observed in the liver and included aberrant forms of endoplasmic reticulum. The liver changes were, however, transitory in that they maximized at 1 and 2 days post treatment and then subsided so that by 7 days post treatment the tissues appeared almost normal. The liver changes induced by T-2 were similar to those induced by aflatoxin as observed in a previous study.

Animals↗
PubMed1987

Some unusual staining properties of tannic acid in plants.

Maize root tips were fixed in glutaraldehyde fixatives containing tannic acid and then processed for electron microscopy. Under these conditions, tannic acid selectively stained the contents of the Golgi apparatus secretory vesicles of some outer root cap cells, the cell walls of all cells, and substances in, and adjacent to, intercellular connections of mature primary walls and of secondary walls. Intercellular connections of the young primary walls were not stained. Plasma membranes, and substances associated with the outer leaflets of the plasma membranes, were also stained. Tannic acid-positive material was associated with the cell plate vesicles of forming walls but very little, or none, was associated with the Golgi apparatus vesicles of dividing cells.

Cell Membrane↗
PubMed1987

Modulation of cell-mediated resistance to listeriosis in mice given T-2 toxin.

The modulating effect of preinoculation and postinoculation treatment with a single oral 4.0 mg/kg dosage of T-2 toxin on cell-mediated resistance was studied in mice inoculated with Listeria monocytogenes. Toxin treatment caused significant decreases in thymus and spleen weights, bone marrow cellularity, and in the total number of circulating leukocytes, lymphocytes, and neutrophils. Enhancement or suppression of resistance to listeriosis was dependent on the time of toxin administration relative to the time of Listeria challenge. Preinoculation treatment on Day 2 or 4 prior to Listeria challenge significantly enhanced resistance and decreased mortality due to listeriosis by as much as 50%. In contrast, resistance was suppressed and mortality was increased by 50% in mice that were treated with toxin after Listeria challenge. Enhanced resistance to listeriosis was accompanied by a significant increase in the influx of macrophages into Listeria-elicited peritoneal exudates. In addition, in vivo phagocytosis of sheep red blood cells by peritoneal macrophages was significantly increased in toxin-treated mice that were sensitized with sheep erythrocytes. The data indicate that T-2 toxin has a modulating effect on cell-mediated resistance and that enhancement of resistance to listeriosis in mice pretreated with T-2 toxin is associated with increased migration/activation of macrophage effector cells.

Animals↗
PubMed1987

Golgi apparatus cisternae of monensin-treated cells accumulate in the cytoplasm of liver slices.

Protein transport via the endoplasmic reticulum Golgi apparatus-cell surface export route was blocked when slices (6-15 cells thick) of livers of 10-day-old rats were incubated with 1 microM monensin. Production of secretory vesicles by Golgi apparatus was reduced or eliminated and, in their place, swollen cisternae accumulated in the cytoplasm at the trans Golgi apparatus face. The swelling response was restricted to the six external cell layers of the liver slices, and the number of cells showing the response was little increased by either a greater concentration of monensin or by longer times of incubation. When monensin was added post-chase to the slices, flux of radioactive proteins to the cell surface was inhibited by about 80% as determined from standard pulse-chase analyses with isolated cell fractions. Radioactive proteins accumulated in both endoplasmic reticulum and Golgi apparatus and in a fraction that may contain monensin-blocked Golgi apparatus cisternae released from the stack. The latter fraction was characterized by galactosyltransferase/thiamine pyrophosphatase ratios similar to those of Golgi apparatus from control slices. The use of monensin with the tissue slice system may provide an opportunity for the cells to accumulate monensin-blocked Golgi apparatus cisternae in sufficient quantities to permit their isolation and purification by conventional cell fractionation methods.

Animals↗
PubMed1987

Regulation of murine macrophage phagocytosis of sheep erythrocytes by T-2 toxin.

The effect of a single oral dose of 4 mg of T-2 toxin/kg of body weight on in vivo phagocytosis of sheep RBC by peritoneal macrophages was evaluated in nonsensitized mice and in mice sensitized with sheep RBC. T-2 toxin treatment had no effect on the viability or phagocytic activity of resident peritoneal macrophages in nonsensitized mice. However, a significant (P less than 0.005) increase in phagocytic activity occurred in cells from mice treated with toxin and subsequently sensitized with sheep RBC. In contrast, phagocytosis of sheep RBC was significantly (P less than 0.05) suppressed in cells from mice treated with toxin after sensitization. Toxin treatment induced necrosis of lymphocytes and significant decreases in thymus and spleen weights. Seemingly, T-2 toxin, administered at a dose that caused marked lymphoid depletion, suppressed or enhanced in vivo macrophage phagocytic activity in antigenically sensitized mice, and enhancement or suppression of phagocytosis was a function of the time of toxin treatment in relation to antigenic stimulation.

Administration, Oral↗
PubMed1985

Effects of dietary cobalt on testicular structure.

Adult male rats were maintained on a diet containing 265 ppm cobalt for up to 98 days. Three rats were sacrificed weekly and assayed for testicular damage by light and electron microscopy. Testicular damage was first apparent after 70 days of treatment, followed by a progressive deterioration of cell architecture and decrease in testicular volume. The degenerative changes were of a very general nature; e.g., thickening of basal lamina and basement membranes, increased packing of red blood cells in veins and arteries, formation of "giant" cells, loss of sperm tail filaments, and degeneration of sperm mitochondria. No cobalt residues could be detected by energy dispersive x-ray microanalysis. These data indicate that testicular degeneration was not a primary response to cobalt and suggest that the testes become hypoxic due both to blockage of veins and arteries by red blood cells and to changes in permeability caused by thickening of basal lamina and basement membranes.

Animals↗
PubMed1979

Combinative effects of hexachlorobenzene and crowding on rat adrenal cell mitochondria.

The effects of social stress (crowding) on hexachlorobenzene (HCB) toxicity in male rats was evaluated by a morphometrical analysis of adrenal cortex mitochondria. The social stress was produced by transferring singly-housed rats from cages of ample size (1000 cm2 floor space) into small cages (100 cm2 floor space) each containing four rats. Differences in cage design as well as size may have contributed to the overall stress experienced by the rats. The food of the treated rats was supplemented with 250 ppm HCB. Structural changes in mitochondrial volume, surface area, or cristae area were not significant in HCB-treated or in crowded animals when compared with those of the controls. However, increases in mitochondrial volume and diameter were significant in those animals simultaneously challenged by HCB and crowding. The results strongly suggest that even a relatively mild social stress may adversely affect the ability of an animal to resist the effects of some exogenous chemicals.

Adrenal Cortex↗
PubMed1978

Polyribosomes associated with forming acrosome membranes in guinea pig spermatids.

Ribosomes, some of which are arranged in polyribosomal configurations, are attached to specialized regions of the acrosomal membrane in guinea pig spermatids. This finding indicates a new functional dimension for the acrosomal membrane, that of protein synthesis, and suggests that during acrosome formation, proteins of the acrosomal membrane or acrosomal contents need not be synthesized before or during passage through the Golgi apparatus.

Acrosome↗