摘要:

AbstractCytochrome P450‐dependent alkoxyphenoxazone dealkylase activity was measured in alveolar type II cells from control and β‐naphthoflavone (ip) treated‐rats. Type II cells were isolated from collagenase/elastase‐digested lung tissue and purified by centrifugal elutriation. The specificity of the cytochrome P450‐dependent activity towards four alkoxyphenoxazones (methoxy‐, ethoxy‐, pentoxy‐, and benzyloxyphenoxazone) was measured under conditions that minimized interference by cytosolic conjugating‐ and NADPH‐dependent quinone reductase activities. Ethoxyphenoxazone dealkylase activity was induced 17‐fold following β‐naphthoflavone treatment and was further characterized by its kinetic parameters and sensitivities towardin vitroinhibitors (Km(app)=0·20 μM,Vmax= 1·74 pmoles resorufin min−1(106cells)−1106cells; I50(α‐naphthoflavone)=0·025 μM, and I50(methyrapone) = 72 μM). β‐Naphthoflavone pretreatment of the rats did not result in statistically significant changes in methoxy‐, pentoxy‐, or benzyloxyphenoxazone dealkylase activity of alveolar type II cells, although, a trend towards decrease activity was observed for benzyloxyphenoxazone. β‐Naphthoflavone pretreatment had no effect on oxygen consumption of trypan blue exclusion in alveolar type II cells and macrophages, or on alveolar macrophage particle‐mediated superoxide release. Furthermore, alveolar macrophage ethoxyphenoxazone dealkylase and benzyloxphenoxazone dealkylase activities were not affected by the β‐naththoflavone pretreatment. The results show that exposure to β‐naphthoflavone resulted in an increase in type II cell cytochrome P450‐dependent ethoxyphenoxazone dealkylase activity but not in other alveolar type II cell or macrophage alkoxyphenoxazone dealkylase activities or in

ISSN:0263-6484    

DOI:10.1002/cbf.290070202

出版商:John Wiley&Sons, Ltd.    

年代:1989

数据来源: WILEY

摘要:

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 IC50value of 11·5 mMand 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

ISSN:0263-6484    

DOI:10.1002/cbf.290070203

出版商:John Wiley&Sons, Ltd.    

年代:1989

数据来源: WILEY

摘要:

AbstractAdministration of clofibrate for 21 days to rats increased the malic enzyme activity in the kidney cortex by about 80 per cent. This effect seems to be specific since the drug did not alter significantly the activity either of lactate dehydrogenase, citrate synthase or total mitochondrial protein content in this organ.The increase in activity of malic enzyme in the 13 000gsupernatant (extramitochondrial) fraction in rats treated with the drug was about 80 per cent, whereas in the pellet (mitochondrial fraction) it was about 40 per cent. The specific activity of malic enzyme in the kidney cortex cytosol from clofibrate‐treated rats was about twice that in controls. In contrast clofibrate treatment did not affect its specific activity in isolated mitochondria.Calculations showed that 0·57 and 0·53 μmoles min−1g−1wet tissue of mitochondrial malic enzyme was obtained in control and clofibrate‐treated rats respectively. Thus, clofibrate feeding increases the amount of cytoplasmic but not mitochondrial malic enzym

ISSN:0263-6484    

DOI:10.1002/cbf.290070204

出版商:John Wiley&Sons, Ltd.    

年代:1989

数据来源: WILEY

摘要:

AbstractNew prostaglandin oligomeric derivatives, termed MR‐256 and MR‐356, were found to inhibit the growth of murine malarial parasites,P. chabaudiandP. vinckei, within red blood cellsin vivo. When mice were infected withP. chabaudi, both MR‐256 and MR‐356 suppressed the growth of parasites, but MR‐356 had a greater inhibitory effect than MR‐256. WithP. 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 dru

ISSN:0263-6484    

DOI:10.1002/cbf.290070205

出版商:John Wiley&Sons, Ltd.    

年代:1989

数据来源: WILEY

摘要:

Abstract3‐Hydroxy‐3‐methylglutaryl‐CoA reductase (EC 1.1.1.34), the major rate‐limiting enzyme of cholesterogenesis, was studied in epithelial cells isolated in a villus to crypt gradient from chick duodenum, jejunum and ileum, in order to resolve the apparent controversy that exists on the anatomical localization of sterol synthesis in the intestine. Consistent separation was demonstrated by using the marker enzymes alkaline phosphatase, specific to the villus cells, and thymidine kinase, specific to the crypt cells. No relative difference in stability was observed, as shown by the equal distribution of acid phosphatase. Cells were 90–95 per cent viable. The highest specific activity of reductase was located in the microsomal fraction (41 per cent of the total). The mitochondria had lower specific activity (8 per cent of the total). The distribution of reductase activity in epithelial cells of the villus–crypt axis was also studied. The specific activity in each cell fraction from chick duodenum was clearly lower than that in jejunum and ileum. The jejunal and ileal crypt regions showed lower specific activity than the villus cells. About 70 per cent of total reductase activity was found in cells from the upper and the mid villus fraction in each intes

ISSN:0263-6484    

DOI:10.1002/cbf.290070206

出版商:John Wiley&Sons, Ltd.    

年代:1989

数据来源: WILEY

摘要:

AbstractHepatocytes were isolated from thioacetamide (TAA)‐induced macronodular cirrhotic rat livers by a collagenase perfusion method. In the content of cellular metabolites, fatty acid uptake and lipid secretion there were no substantial differences compared with cells isolated from micronodular cirrhosis described previously. In contrast to isolated hepatocytes from normal livers those from macronodular cirrhosis had a lowered cellular content of triglycerides, phospholipids and cholesterol but not of cholesterol esters and free fatty acids. In macronodular cirrhosis hepatocytes of hypertrophic type, rich in cell organelles, can be distinguished ultrastructurally from those with signs of atrophy and degeneration. Immediately after isolation many hepatocytes isolated from macronodular cirrhosis showed plasma membrane blebbing. Whereas the blebbing was without recognizable effects on the fine structure of the isolated hepatocytes of the hypertrophic type, in the more atrophic ones some mitochondria were swollen. In addition, morphological analysis of the crude and purified suspensions revealed a partial selection of the hypertrophic cells during the isolation procedure, presumably due to a more labile state of those cells which showed signs of atrophy and degeneration. When stabilized in the suspension medium, however, the hepatocytes maintained complex metabolic functions for at least 2 h. Thus, the method described allows the isolation of parenchymal cells from TAA‐induced macronodular cirrhotic livers for studying ultrastructural and biochemical alterations in hyperregenerative experimental liver cirrho

ISSN:0263-6484    

DOI:10.1002/cbf.290070207

出版商:John Wiley&Sons, Ltd.    

年代:1989

数据来源: WILEY

摘要:

AbstractEffects of methotrexate (MTX) on mitochondrial oxidative metabolism and ion transport were studied. MTX decreases the membrane potential (Δψ) upon energization of the mitochondrial membrane by NAD+‐linked substrates and decreases the amplitude and velocity of swelling induced by glutamate and α‐ketoglutarate. MTX also has an inhibitory effect on the activities of the oxidation enzymes of NAD+‐linked substrates without interfering with the oxidation systems of FAD‐linked substrates. The effects of MTX could be interpreted as a consequence of a decrease in the ionic conductivity of the mitochondrial inne

ISSN:0263-6484    

DOI:10.1002/cbf.290070208

出版商:John Wiley&Sons, Ltd.    

年代:1989

数据来源: WILEY

摘要:

AbstractThe effect of methotrexate (MTX) on transplasma‐membrane electron transport and ferricyanide‐induced proton extrusion by HeLa cells was studied. Both systems were inhibited by MTX. It is suggested that inhibition of electron transport and proton extrusion caused by MTX could be associated with other metabolic alterations such as response to the increase in NADH levels and decrease in intracellular

ISSN:0263-6484    

DOI:10.1002/cbf.290070209

出版商:John Wiley&Sons, Ltd.    

年代:1989

数据来源: WILEY

摘要:

AbstractPolyclonal antiserum was generated in guinea pigs immunized with the 116 000 Mrrabbit uterine progesterone receptor (PR). The PR antigen was partially purified by DEAE‐cellulose chromatography and preparative sodium dodecyl sulphate–polyacrylamide gel electrophoresis, transferred to nitrocellulose, and the 116 000 Mrband excised and injected into guinea pigs. The antiserum recognized on protein blots rabbit uterine PR of Mr116 000 and 81 000. The antiserum was judged to be specific for PR from normal and malignant human tissues as determined by sedimentation shift on sucrose gradients, immunoprecipitation studies, protein blotting, and fluorographic analysis using photolabelled samples. Comparison of protein blots probed with this polyclonal antiserum or with a recently obtained monoclonal antibody to human PR indicated that similar PR structures were recognized in rabbit and human samples by both antisera. Characterization of the polyclonal antiserum has demonstrated its suitability for investigating the immunolocalization or PR in normal and malignant human tissues as well as the receptor structure detected on protein bl

ISSN:0263-6484    

DOI:10.1002/cbf.290070210

出版商:John Wiley&Sons, Ltd.    

年代:1989

数据来源: WILEY

摘要:

AbstractA polyclonal antiserum, raised in guinea pigs immunized with the 116 000 Mrrabbit uterine progesterone receptor (PR), was used to demonstrate immunoreactive PR in frozen fixed sections of rabbit and human uterus. In both species, PR localization was exclusively nuclear. For the rabbit uterus, staining intensity was greatest in the myometrium, followed by endometrial stroma, glands, and luminal epithelium. In premenopausal human endometrium and myometrium there was intense staining of nuclei from proliferative phase glands and myometrium. In the secretory phase the glands failed to stain, yet immunostaining persisted in the myometrium.

ISSN:0263-6484    

DOI:10.1002/cbf.290070211

出版商:John Wiley&Sons, Ltd.    

年代:1989

数据来源: WILEY