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Biomedical subjects

A Pinson

Publications and source records attributed to A Pinson.

At least 55 records · Page 3Linked to original sources
PubMed1987

Ultrastructural pathology of iron-loaded rat myocardial cells in culture.

The pathological changes induced by in-vitro iron-loading or cultured rat myocardial cells were studied. Cells were exposed to 59Fe-labelled ferric ammonium citrate for up to 24 h followed by 24-72 h chase experiment. After 24 h exposure 29% of the total cellular radioactivity was found in ferritin, 10% in non-ferritin heat supernatant and 61% in an insoluble heat-precipitable form. Mössbauer spectroscopy showed a gradual shift from intracellular iron particles less than 1.8 nm in diameter, through particles of intermediate size, to ferritin-like aggregates over 3.0 nm in diameter, reaching about 20% of total iron by 24 h. Ultrastructural studies showed premature damage such as mitochondrial abnormalities and excessive autophagocytosis. Small, 2.0-5.0 nm electron-dense cytosolic particles were noticed at 3 h of iron loading and reached maximal concentrations at 6 h. This was followed by accumulation of the small particles and of typical iron-rich ferritin cores within siderosomes. Because of the limited duration of iron loading and the high concentrations of non-transferrin inorganic iron employed, the present model is more relevant to acute than chronic iron overload. The efficient incorporation of large amounts of iron within ferritin molecules and its subsequent segregation, together with other smaller particles, within membrane-bound bodies, may represent a defence mechanism limiting iron toxicity in the face of advanced cytosiderosis.

Animals↗
PubMed1985

Studies on oxygen and volume restrictions in cultured cardiac cells. I. A model for ischemia and anoxia with a new approach.

A novel incubation unit is described that is highly suitable for thorough studies of oxygen deprivation states. Its application with cultured heart cells is experimentally demonstrated. The release of enzymes, taken as a marker for cell damage, has clearly shown that restriction of the volume of extracellular medium combined with oxygen plus glucose deprivation caused greatest cellular damage. It may be considered as an experimental ischemia-like state. Furthermore, the onset of cellular damage followed a time table very much like that occurring in vivo under similar conditions, more so than any other previously described studies. A time lag between the release of cytoplasmic enzymes and lysosomal enzymes and other observations made in the present study suggests a sequential order of events in which the release of cytoplasmic enzymes occurs at a stage of reversible damage due to oxygen deprivation, whereas the release of lysosomal enzymes may point at irreparable damage.

Animals↗
PubMed1985

Heart cells in culture: a model of myocardial iron overload and chelation.

The effect of iron loading and chelation was studied in heart cell cultures obtained from newborn rats. Radioactive iron uptake per 2 X 10(6) cells/24 hr was 3.8% for 59Fe-transferrin, 15.8% for 59Fe-ferric ammonium citrate (FeAC) at 20 micrograms Fe/ml in 20% serum, and 37.1% for 59FeAC at 20 micrograms Fe/ml in serum-free medium. About one third of the cellular radioactive iron was in ferritin and the rest in an insoluble lysosomal fraction. Iron uptake was almost completely inhibited by reducing the incubation temperature from 37 degrees C to 10 degrees C. Intracellular concentrations of malonyldialdehyde (MDA) were doubled after 15 minutes of iron loading and reached maximal concentrations at 3 hours. Conversely, iron mobilization by deferoxamine at concentrations ranging from 0.025 mmol/L to 0.3 mmol/L resulted in normalization of cellular MDA concentrations, in direct proportion to the amounts of iron removed. These findings indicate that cultured myocardial cells are able to assimilate large amounts of nontransferrin iron and that iron uptake and mobilization are associated with striking changes in lipid peroxidation as manifested by the respective increase and decrease in cellular MDA concentrations.

Animals↗
PubMed1985

Studies of oxygen and volume restriction in cultured cardiac cells. II. The glucose effect.

An ischaemia-like state in cultured heart cells has been obtained by markedly restricting the volume of extracellular medium combined with total deprivation of oxygen (anoxia) and glucose. Cellular injury, as reflected by the release of both cytoplasmic and lysosomal enzymes was significantly greater than during anoxia alone (oxygen deprivation with a larger extracellular volume). This is most likely due to inadequate washout of metabolites during "ischaemia" rather than reduced energy production since glycolytic flux as reflected by lactate production was similar in both experimental states. Glucose administration during either anoxia or "ischaemia" delayed enzyme release. We believe that cytoplasmic enzymes are released mainly during the reversible period of oxygen deprivation, while lysosomal enzyme release reflects the onset or irreversible injury, occurring at a time when ATP levels and glycogen stores are almost completely exhausted.

Animals↗
PubMed1984

Changes in cytoplasmic and lysosomal enzyme activities in cultured rat heart cells: the relationship to cell differentiation and cell population in culture.

Postnatal rat heart cells in culture enriched with respect to muscle cells were obtained by either high density seeding or by the replating technique. [3H]Thymidine incorporation to DNA and the enzymatic pattern of cytoplasmic and lysosomal enzymes have been studied as a function of the culture's age, of seeding density, and replating. It was shown that replating maintains predominance of myocyte population for at least 2 wk in culture; heavy seeding density allows homogeneous myocyte population for the 1st wk in culture; and the enzyme profile of the culture may serve as an indicator for the type of cell population in culture and its state of differentiation.

Animals↗
PubMed1980

Interactions of cardiac glycosides with cultured cardiac cells. II. Biochemical and electron microscopic studies on the effects of ouabain on muscle and non-muscle cells.

Electron microscopic and biochemical studies revealed a salient difference in the response to toxic doses of ouabain by cultured cardiac muscle and non-muscle cells from neonatal rats. Progressive cellular injury in myocytes incubated with 1 . 10(-4)--1 . 10(-3) M ouabain ultimately leads to swelling and necrosis. The morphological damage in myocytes was accompanied by a drastic decrease in 14CO2 formation from 14C-labeled stearate or acetate but not glucose. Neither morphological nor biochemical impairments were observed in non-muscle cells. The interaction between ouabain and the cultured cells, using therapeutic doses of ouabain (i.e., less than 1 . 10(-7) M), was characterized. Two binding sites were described in both classes of cells, one site is a saturable K+-sensitive site whereas the other is non-saturable and K+-insensitive. The complexes formed between the sarcolemma receptor(s) and ouabain, at low concentrations of the drug (e.g., 7.52 . 10(-9) M), had Kd values of 8.9 . 10(-8) and 2.3 . 10(-8) M for muscle and non-muscle cells, respectively. The formation and dissociation of the complexes were affected by temperature and potassium ions.

Animals↗
PubMed1979

Partial and incomplete oxidation of palmitate by cultured beating cardiac cells from neonatal rats.

The discrepancy in the rate of [14C]O2 formation from either [1-14C]- or [16-14C]palmitate is demonstrated and could be explained by the preferential formation of L-(+)-3-hydroxybutyrate from the four carbon atoms at the omega terminus. The identity of this product as L(+)-3-hydroxybutyrate was established and shown to be the major component of the radioactive products in the extracellular medium from palmitate based on (a) ion-exchange chromatographical properties, (b) gas-liquid chromatography, (c) mass spectrometric analysis, (d) stereoisomeric separation, and (e) its very low rate of utilization by the cells. We therefore propose a shunt to the oxidation of palmitate in these cells occurring at the stage of L(+)-hydroxybutyryl-CoA which undergoes deacylation causing the product to be transported outside the cell.

Animals↗
PubMed1979

Intracellular lipase activities in heart and skeletal muscle homogenates. The absence of trierucin cleavage by the heart: a possible biochemical basis for erucic acid lipidosis.

Rat heart and skeletal muscle homogenates were compared for their intracellular lipolytic activity towards a series of saturated and unsaturated triglycerides from trilaurin (C12:0) to trierucin (C22:1). It is shown that for all triglycerides esterified with fatty acids from C12 to C18, lipolytic activity in heart homogenates was higher than in skeletal muscle homogenates. For these triglycerides there was no relationship between the fatty acid chain length and the lipolytic activity. In both homogenates cleavage of unsaturated triglycerides was higher than cleavage of the homologous saturated triglyceride. Lipolysis of tri-delta-11-eicosenoin (C20:1) was similar in both homogenates but much lower than lypolysis of other triglycerides. Although cleavage of trierucin (C22:1) was very low in skeletal muscle homogenates, it was undetectable in heart homogenates, even when enzyme concentration was increased. A mixture of triglycerides did not show preferential hydrolysis of any simple triglyceride. Trierucin was the only triglyceride that did not complete for lipolytic activity and only with heart homogenates, which shows that that lipase(s) do not cleave trierucin. The absence of lipolytic activity towards trierucin in heart homogenates could explain the selective accumulation of erucic acid-rich triglycerides in hearts of animals fed a diet with a high erucic acid content.

Animals↗
PubMed1979

Glucose and palmitate metabolism by beating rat heart cells in culture.

The metabolism of glucose and palmitate by new born rat heart cell in tissue culture was investigated to ascertain the usefulness of this model system for metabolic studies. Heart cells in culture oxidize palmitate at a rate which is close to the rate reported in vivo. The fate of glucose is shown to differ from in vivo. High rates of lactate release are observed although there are many evidences that cells are not hypoxic. This impaired regulation is likely due to an impaired uptake of glucose.

Amino Acids↗
PubMed1975

Erucic acid metabolism by cultured beating heart cells of the postnatal rat.

Cardiac erucic acid metabolism has been studied with beating heart cells in culture. It has been shown that erucate is taken up by these cultured cardiac myocytes. These cells are unable to oxidize it directly but require delaying intermediary steps to shorten the erucic acid chain before its complete oxidation. This long latency time of erucate oxidation would explain its accumulation within the different cellular lipid classes. It is suggested that the occurrence of large amounts of erucate in the different phospholipids might affect cellular and mitochondrial membrane structures. Evidence is reported that erucate does not affect the oxidative capacity of the myocardial cell but because of its accumulation dilutes other fatty acids which will then be oxidized at a lower rate.

Carbon Dioxide↗