bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ornithine decarboxylase properties: Is there a role for a microsome‐bound inactivating activity?
Authors: Zuretti M. F. , Brossa O. , Gili P. , Gravela E. 
Published: May 2005

AbstractLiver microsomes have a strong ornithine decarboxylase (ODC) inactivating capacity in vitro. The present results suggest that this may be involved in regulation of ODC activity in vivo: (1) the ODC inactivating capacity of microsomes appears susceptible to in vivo modulation: a single administration of thioacetamide, which induces ODC. also causes a significant increase in the inactivating capacity of the microsomes; (2) under conditions leading to increased microsome‐bound ODC‐inactivating capacity (e.g. liver from thioacetamide‐treated rates versus regenerating liver) ODC displays a greater thermal lability and inactivability in vitro.A possible involvement of this microsomal activity in an autoregulatory pathway of ODC is suggested by the fact that it is induced by the administration of polyamines. However, inhibition of ODC activity by α‐difluoromethylornithine does not prevent the increase of the microsomal activity caused by thioacetamide. Thus, polyamine biosynthesis does not appear to be an absolute requirement for induction of the microsomal ODC‐inactivating capacity.The apparent half‐life of ODC in vivo, as evaluated after cycloheximide administration, does not appear to correlate with the microsomal ODC‐inactivating capacity content and the stability properties of ODC in vitro.
Action of the antileukemic and anti‐HTLV‐III (anti‐HIV) agent avarol on the levels of superoxide dismutases and glutathione peroxidase activities in L5178y mouse lymphoma cells
Authors: Batke Erna , Ogura Ryohei , Vaupel Peter , Hummel Klaus , Kallinowski Friedrich , Gasić Miroslav J. , Schröder Heinz C. , Müllerm Werner E. G. 
Published: May 2005

AbstractThe antileukemic and anti‐HTLV‐III (anti‐HIV) agent avarol, a sesquiterpenoid hydroquinone, was determined to be converted into its corresponding quinone derivative avarone via the semiquinone free radical. Its g‐value was 2·0047; after hyperfine splitting the energy levels revealed 16 isotropic Hfs. The redox reaction products were identified at the pH values 4·0, 7·0 and 12·0 and the overall reaction pathways were formulated. In vivo experiments with L5178y mouse lymphoma cells in the ascites of mice revealed that the cytostatic potencies of avarol and avarone cannot be augmented by lowering the pH value. Incubation studies with L5178y cells in vitro showed that the intracellular levels of superoxide dismutases (SODases) and of glutathione (GSH) peroxidase activities significantly change after avarol administration. While both the Mn‐SODase and the Cu/Zn‐SODase activities dropped significantly, the GSH peroxidase activity increased inversely. From these experiments we assume that the anti‐tumour and the antiviral effects of avarol/avarone may be due to an increase, induced by the drug, of the intracellular concentrations of superoxide radicals.
Effect of phenylhydrazine on red blood cell metabolism
Authors: Magnani M. , Rossi L. , Cucchiarini L. , Stocchi V. , Fornaini G. 
Published: May 2005

AbstractIn addition to the well known effect of phenylhydrazine on red blood cells (methaemoglobin and Heinz body formation, autologous IgG binding, lipid peroxidation, etc.) an increased glucose utilization was observed. Measurement of 14CO2 formation from [1‐14C]‐glucose showed a maximum value at 2 mM phenylhydrazine followed by a progressive inhibition on increasing the drug concentration to 16 mM. Concomitantly we found a reduction in the reduced glutathione concentration but not a corresponding increase in the level of oxidized glutathione. Phenylhydrazine also causes ATP depletion. The ATP is in part dephosphorylated to ADP and AMP and in part converted to inosine monophosphate and hypoxanthine. Measurement of the cell content of reduced and oxidized pyridine nucleotides was also performed and showed a progressive increase in the reduced forms of these coenzymes. Thus phenylhydrazine promotes cellular ATP depletion followed by adenine nucleotide catabolism that is not efficiently counteracted by an increase in glucose utilization. The relevance of these data to the mechanism of phenylhydrazine‐induced anemia is discussed.
Effects of nonionic amphiphiles at sublytic concentrations on the erythrocyte membrane
Authors: Isomaa Boris , Hägerstrand Henry 
Published: May 2005

AbstractThe interactions of octaethyleneglycol alkylethers (C10–C16), pentaethyleneglycol dodecylether, and dodecyl D‐maltoside with the human erythrocyte membrane were studied. All the amphiphiles protected erythrocytes against hypotonic haemolysis. At concentrations where the amphipiles protected erythrocytes against hypotonic haemolysis they reduced phosphate efflux. The potency of the amphiphiles, at equiprotecting concentrations, was correlated negatively to the length of the alkyl chain. Pottasium fluxes were increased by all the amphiphiles at protective concentrations. The relative potency of the amphiphiles varied but it was not simply related to the length of the alkyl chain. The only amphiphile affecting active potassium influx was octaethyleneglycol decylether which induced a slight decrease. It is concluded that the increase in passive cation fluxes caused by the amphiphiles is due to an increased permeability of the lipid bilayer induced through a nonspecific interaction of the amphiphiles with the bilayer. The effect of the amphiphiles on ion transport mediated by membrane proteins is proposed to be due to an alteration of the state of the transporting protein.
Inhibition of monocyte luminol‐dependent chemiluminescence by tetrahydrobiopterin, and the free radical oxidation of tetrahydrobiopterin, dihydrobiopterin and dihydroneopterin
Authors: Heales Simon J. R. , Blair John A. , Meinschad Christian , Ziegler Irmgard 
Published: May 2005

AbstractLuminol‐dependent chemiluminescence of normal human monocytes activated by zymosan is demonstrated to be inhibited by tetrahydrobiopterin in a concentration‐dependent manner. The reduced pterins tetrahydrobiopterin, dihydrobiopterin, and dihydroneopterin are all shown to be readily oxidized by the hydroxyl radical.The susceptibility of reduced pterins to free radical attack may explain the inhibition of chemiluminescence observed and an additional role of reduced pterins as free radical scavengers in tissues is considered.
Isocitrate dehydrogenase activity and its regulation by estradiol in tissues of rats of various ages
Authors: Yadav R. N. Singh 
Published: May 2005

AbstractThe activity and hormonal regulation of NAD‐ and NADP‐linked isocitrate dehydrogenase (EC.1.1.1.41 and EC.1.1.1.42, respectively) in the brain, liver and kidney cortex of female rats of various ages was investigated. The activity of NAD‐ICDH of brain was greater than extramitochondrial (‐c) or intramitochondrial (‐m) NADP‐ICDH. In contrast, liver c‐NADP‐ICDH was much higher than NAD‐ or m‐NADP‐ICDH, whereas in kidney cortex the activity of m‐NADP‐ICDH is dominant over both NAD‐ and c‐NADP‐ICDH in all the age group of rats studied. The activity of the NAD‐ICDH of brain and all the enzymes of liver and kidney cortex increases until adulthood (33‐weeks) and decreases thereafter in old rats (85‐weeks). In brain c‐NADP‐ICDH was much higher in immature (6‐weeks) rats and decreases with increasing age of the animal, whereas m‐NADP‐ICDH showed no significant change with the age of the rats. Bilateral ovariectomy decreases the level of all the three forms of enzyme in all the tissues of 6‐, 13‐ and 33‐week rats but failed to show any significant effect in 85‐week old rats. Exogenous administration of estradiol induces all the three forms of enzyme in all the tissues of ovariectomized rats. The degree of response is tissue‐ and age‐specific.
Cell density dependent morphological changes in adult rat hepatocytes during primary culture
Authors: Koji T. , Nakane P. K. , Murakoshi M. , Watanabe K. , Terayama H. 
Published: May 2005

AbstractIn order to gain morphological insights about the cell density dependency, hepatocytes cultured at a low cell density (< about 0·1 × 105 nuclei (cm2)−1) and at a high cell density (> about 1 × 105 nuclei (cm2)−1) were examined ultrastructurally 24 h after plating (just prior to the beginning of DNA synthesis). The results were as follows: (i) glycogen rosettes disappeared completely in low density culture as compared with sections from an intact liver. In contrast, glycogen rosettes were still present in high density culture. (ii) Polysomes seemed increased in low density culture in comparison with those seen in sections from an intact liver and from the high density culture. (iii) In low density culture, the shape of mitochondria deviated from that of hepatocytes in an intact liver and the mitochondria often lost a characteristic close contact with rough endoplasmic reticulum (rough ER). (iv) In low density culture, bundles of filamentous structure were detected, which were not found in an intact liver or high density culture. The following features were found only in high density culture; (v) numberous villous cytoplasmic protrusions developed along the area facing adjacent cells, and seemed to intertwine with each other, and (vi) between the hepatocytes, only abortive junctions were found. These results indicate that the hepatocytes cultured at a low density express most of the characteristics of the hepatocytes in a regenerating liver and the features of the cells cultured at a high density are very similar to those of the hepatocytes in sections from an intact liver.
Metabolism of 4‐hydroxynonenal by the rat heptoma cell line MH1C1
Authors: Ferro Margherita , Marinari Umbertom M. , Poli Giuseppe , Dianzani Mario U. , Fauler Günter , Zollner Helmward , Esterbauer Hermann 
Published: May 2005

AbstractThe metabolism of the toxic lipid peroxidation product 4‐hydroxynonenal was investigated in the well‐differentiated rat heptoma cell line MH1C1.When exposed to 0·1 mM 4‐hydroxynonenal (HNE), MH1C1 cells consumed it in a time‐dependent manner. There was a linear relationship between the amount of aldehyde consumed and cell number in the range 0·5–4 × 106 cells ml−1. This process was unaffected by pyrazole, suggesting that alcohol dehydrogenase is not involved.The whole homogenate of MH1C1 cells consumed added HNE at a rate similar to that in intact cells. Fractionation of the homogenate showed that the highest HNE‐metabolizing activity is in the cytosol. The dialysed cytosol had almost no capacity to metabolize HNE, but this was restored by supplementation with NAD, NADH, NADP and NADPH.The metabolism of HNE in MH1C1 cells is thus different from that in hepatocytes, which were shown to utilize cytosolic alcohol dehydrogenase for this process. Both reductive and oxidative pathways could be implicated in the metabolic activity of MH1C1 cells towards HNE as well as binding by glutathione.
Stimulatory effect of 1,25‐dihydroxyvitamin D3 on the glucose‐6‐phosphate dehydrogenase activity in the MCF‐7 human breast cancer cell line
Authors: Noun Aïcha , Garabedian Michèle , Monet Jean‐Dominique 
Published: May 2005

AbstractHuman breast cancer cell lines have been shown to possess high affinity receptors for 1,25‐dihydroxyvitamin D3 (1,25(OH)2D3) on the activity of glucose‐6‐phosphate dehydrogenase (G6PD) in cells of a human breast cancer cell line MCF‐7. G6PD, an enzyme which controls the hexose monophosphate shunt, is elevated and sensitive to 17β‐estradiol in breast tumors. G6PD activity was stimulated by 1,25(OH)2D3 in a dose‐dependent manner at very low concentrations of steroid (10−10–10−12 M). 1,25(OH)2D3 increased maximum velocity without modifying the affinity constant of the enzyme for glucose‐6‐phosphate.
Some effects of fructose‐1,6‐diphosphate on rat myocardial tissue related to a membrane‐stabilizing action
Authors: Galzigna L. , Rizzoli V. , Bianchi M. , Rigobello M. P. , Scuri R. 
Published: May 2005

AbstractThis study aims at elucidating the mechanism of action of extracellular fructose‐1,6‐diphosphate (FDP). FDP is able to inhibit Ca++ entry into the myocardial tissue with an IC50 value of 11·5 mM and in addition, it is bound by rat heart slices, the binding being activated by Zn and conditions of chemical hypoxia induced by KCN and iodoacetate. The overall effect of extracellular FDP includes an increase of frequency and amplitude of contraction of perfused heart at concentration below 1 mM, and, in general, a stimulation of the oxygen consumption of the tissue. The antihaemolytic effect of FDP suggests its action as a membrane stabilizer. The effects of extracellular FDP on the myocardial cell can be interpreted both on the basis of a limited permeability of the cell membrane to it and as a purely extracellular effect transduced through the cell membrane with a final response consisting of an increase in the intracellular FDP.
Prostaglandin derivatives inhibit the growth of malarial parasites in mice
Authors: Ohnishi S. Tsuyoshi , Ohnishi Noriko , Oda Yoshio , Katsuoka Masayuki 
Published: May 2005

AbstractNew prostaglandin oligomeric derivatives, termed MR‐256 and MR‐356, were found to inhibit the growth of murine malarial parasites, P. chabaudi and P. vinckei, within red blood cells in vivo. When mice were infected with P. chabaudi, both MR‐256 and MR‐356 suppressed the growth of parasites, but MR‐356 had a greater inhibitory effect than MR‐256. With P. vinckei, MR‐356 also inhibited the growth of parasites, and improved the survival rate. The effect of MR‐256 was much less. A possible inhibitory mechanism of action of these drugs is discussed.
Glucose 6‐phosphate plays a central role in the regulation of glycogen synthesis in a glycogen‐storing liver cell line
Authors: Mayer D. , Letsch I. 
Published: May 2005

AbstractTwo substrains of the epithelial liver cell line C1 I, one storing large amounts of glycogen, the other one being very poor in glycogen were used as a model for studying glycogen synthesis. The glycogen content of glycogen‐rich cells doubled during the proliferative phase and remained high in plateau phase although glycogen synthase I activity was not significantly altered during growth cycle and was too low to account for the increase in glycogen. However, the activity of the glucose 6‐phosphate (Glc6‐P)‐dependent synthase rose continuously during growth cycle, and intracellular Glc6‐P‐concentration increased about 10‐fold in log phase cells to 0·72 μmol g−1 wet weight. A0·5 of synthase for Glc6‐P was 0·79 mM. It was also found that in contrast to the enzyme from normal liver, glycogen phosphorylase a from C1 I cells was inhibited by Glc6‐P, the apparent Ki being 0·45 mM. It was concluded that glycogen accumulation in C1I cells was due to stimulation of synthase and inhibition of phosphorylase by Glc6‐P. Findings from the glycogen‐poor cell line which revealed similar specific activities of synthase and phosphorylase but only low Glc6‐P (0·056 μmol g−1 wet weight) supported this conclusion. Addition of glucose to starved cells resulted in a transient activation of synthase in both cell lines. Net glycogen synthesis, was, however, only observed in the cells with a high Glc6‐P‐content. Thus, modulation of synthase and phosphorylase by Glc6‐P and not activation/inactivation of the enzymes seems to play a predominant role in glycogen accumulation in this cell line.
Suppressive effect of adrenalectomy on growth of L1210 leukemic cells in ascites
Authors: Kimura Kotohiko , Sakamoto Yukiya 
Published: May 2005

AbstractThis study was designed to evaluate the effect of adrenalectomy on growth of L1210 leukemic cells in ascites of BDF1 mice. Varying doses of 1·5 × 104, 5·0 × 105, and 1·5 × 106 viable tumour cells were inoculated intraperitoneally into groups of either adrenalectomized or sham‐operated mice. At days 4 to 7 after the inoculation, adrenalectomized mice inoculated with 1·5 × 104 or 5·0 × 105 tumour cells had a smaller number of tumour cells in ascites than sham‐operated controls. However, after inoculation of 1·5 × 106 cells, no significant differences were found at days 2 to 4 between adrenalectomized and sham‐operated mice. The growth retardation by adrenalectomy was not observed in adrenalectomized mice supplemented with 4 or 6 μg dexamethasone per day per mouse. It suggested that the ablation of glucocorticoids was at least partially responsible for the growth retardation observed in adrenalectomized mice. Cell kinetic analysis revealed that the difference in a potential doubling time could not explain these results. Tumour retention in the peritoneal cavity was measured using [125I]‐iododeoxyuridine‐labelled tumour cells as a tracer. At days 4 to 6 after inoculation of 5·0 × 105 labelled cells, radioactivity in the peritoneal cavity in adrenalectomized mice was about 70 per cent of that in sham‐operated mice. This ratio was almost equivalent to the ratio of the number of cells in ascites of adrenalectomized mice to that of sham‐operated ones. Consequently, growth retardation observed in adrenalectomized mice resulted from an increase in tumour cell migration and/or in tumour cell death, but not from an increase in doubling time.
Subcellular localization of recently‐absorbed iron in mouse duodenal enterocytes: Identification of a basolateral membrane iron‐binding site
Authors: Snape Sue , Simpson Robert J. , Peters Timothy J. 
Published: May 2005

AbstractThe subcellular distribution of newly absorbed iron in isolated mouse duodenal enterocytes was investigated by analytical subcellular fractionation using sucrose density gradient centifugation. Two major peaks of mucosal 59Fe activity were observed: one soluble and one particulate (density 1·18–1·20 g ml−1). The latter was increased following prior exposure of animals to chronic hypoxia. The particulate 59Fe was localized to the basolateral membranes using the marker enzyme Na+, K+ activated, Mg2+ dependant, ATPase and by washing intact enterocytes with the selective plasma membrane perturbant digitonin.The basolateral membrane can be selectively labelled by in vitro incubation of intact enterocytes at 0°C with 59Fe(III)‐nitrilotriacetate complex, confirming the presence of a 59Fe binding site on this membrane. No significant difference in in vitro iron binding to this site was observed between normal and chronically hypoxic animals. Iron binding to the basolateral membrane was significantly higher in disrupted, compared to intact enterocytes, indicating that this site is present on both sides of the basolateral membrane. It is therfore suggested that the increased labelling of this site in hypoxia, in vivo, is a consequence of an increase in a mucosal Fe pool which is available for binding to a membrane receptor.
Intracellular assembly of newly synthesized canine cardiac myosins
Authors: Seko Yoshinori , Naito Shigeto , Imataka Kouji , Fujii Jun , Nakane Paul K. , Takaku Fumimaro , Yazaki Yoshio 
Published: May 2005

AbstractTo investigate how newly synthesized cardiac myosins are assembled into myofilaments, we analysed the distribution of newly produced α‐myosin heavy chain isozyme in sarcomeres by immunoelectron microscopy using a monoclonal antibody (CMA19), which is specific for α‐myosin heavy chain. Isozymic changes in myosin heavy chains from β to α type were induced in canine ventricular muscles and cultured ventricular myocytes by administration of 1‐thyroxine. We incubated the glycerinated ventricular muscles or cultured ventricular myocytes with the enzyme (horseradish peroxidase) labelled Fab fragment of CMA19. After the reaction with 3, 3′‐diaminobenzidine and osmification, we prepared ultrathin sections of the ventricular muscles or cultured ventricular myocytes and analysed their staining patterns by electron microscopy.There was apparent heterogeneity in the staining intensity of the myofilaments among different cells, among different myofibrils and even intramyofibrillarly. Higher magnification revealed that there were scattered foci of strong reaction which appeared to be foci of assembly of the newly synthesized α‐myosin heavy chain. Immunocytochemical study also showed heterogeneous reactions within myofilaments and that there were scattered foci of myofilament assembly, which were closely associated with polyribosomes producing newly induced α‐myosin heavy chain. These data suggest that newly synthesized cardiac myosins are assembled into myofilaments from the sites of synthesis, that is polyribosomes. This may explain the heterogeneity of the assembly pattern of newly synthesized cardiac myosins at the subcellular level.
Peculiar ultraviolet absorbing moieties of human osteoarthritic cartilage
Authors: Chayen J. , Bitensky Lucille , Nahir A. M. 
Published: May 2005

AbstractThe ultraviolet absorbing components of human cartilage have been measured by microspectrophotometry. The characteristics of the chondrocytes appeared to be identical, irrespective of the pathology. However the matrix of osteoarthritic cartilage contained components that absorbed maximally in the region of 270 to 250 nm; such components were not found in the matrix of cartilage of non‐arthritic joints. Substances that absorb maximally in this region of the ultraviolet could generate free radicals.
Modulation of membrane phenotype, matrix adhesion and microinvasiveness of metastatic tumour cells by HUdR
Authors: Timár J. , Pogány G. , Balázs M. , Szöllösi J. , Ladányi A. , Oláh J. , Timár F. , Lapis K. , Jeney A. 
Published: May 2005

AbstractThe effect of HUdR, proved to be anti‐metastatic in vivo, was studied in vitro on cell proliferation, nucleoside uptake, membrane fluidity, expression of galactosylated glycans and proteoglycans in metastatic HM tumour cells. The observed increase in membrane fluidity and the suppression of nucleoside transport were early events of the HUdR action followed by decrease of galactosylated glycan and HSPG expression. However, these changes did not influence the proliferation capacity of the cells at the concentrations studied. As a consequence of the membrane alterations a reduced adhesiveness and spreading on extracellular matrix components was detected. In addition, the HUdR treated HM cells showed reduced capacity to invade fibroblast monolayers in vitro. Based on these observations, HUdR could be the prototype of new anti‐metastatic agents acting at the level of tumour–host interaction.
Carboxylesterase activities during the establishment of the procambium and procortex in embryos of pisum sativum L.
Authors: Carmignac D. F. , Gahan P. B. , Loukopoulou Z. 
Published: May 2005

AbstractA cytochemical and electrophoretic analysis of alpha‐naphthyl and naphthol AS‐D acetate esterases from the radicles of pea seeds germinated for 24, 36 and 48 h permitted the detection of the loss of activity from the procortex with time after germination, but a stability of this activity in the prostele. Inhibitor studies showed the procambial enzyme as a single band of carboxylesterase activity the remainder being acetylesterase activity. The procambial carboxylesterase which is present in the more mature root apex corresponds to that of the 48‐h embryo (separating at Rf 0·74).