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A Reith

Publications and source records attributed to A Reith.

34 records · Page 2Linked to original sources

Two hypolipidemic peroxisome proliferators increase the number of lamellar bodies in alveolar cells type II of the rat lung.

Male rats treated with either clofibrate or nafenopin, two peroxisome proliferating compounds with potent hypolipidemic properties, show identical structural changes in their lungs. In both cases, two types of lung cells were affected by these agents: (i) the alveolar epithelial cells type II and (ii) the intraalveolar macrophages. These lung cells are known to be involved in the metabolism of the pulmonary surfactant which serves to reduce the surface tension within alveoli. The size of the alveolar cells type II was conspicuously increased in the treated lungs. Compared to controls, intraalveolar macrophages apparently were slightly more numerous. Their enlarged cytoplasm was strongly vacuolated. The osmiophilic lamellar bodies within alveolar cells type II represent the intracellular presecretory pulmonary surfactant. Their number per individual alveolar cell type II was estimated by means of light microscopic morphometry on Epon-embedded semithin sections. Compared to control lungs, the number was increased by about 30% in rats treated with clofibrate (11.4 +/- 0.5 lamellar inclusions in the control cells; P less than 0.001). The increase in the number of lamellar bodies per type II cell was close to 60% in animals fed the nafenopin diet. In contrast the frequency of alveolar cells type II, estimated per area of lung tissue, remained unchanged. These results demonstrate that clofibrate and nafenopin, two drugs with hypolipidemic properties, cause identical structural changes in the rodent lung. It is concluded from these data that (i) the morphological changes observed in the surfactant metabolizing cells represent a specific action of hypolipidemic agents at the lungs and (ii) hypolipidemic peroxisome proliferators influence the metabolism of the pulmonary surfactant.

Animals

Clofibrate increases the number of peroxisomes and of lamellar bodies in alveolar cells type II of the rat lung.

The hypolipidemic drug clofibrate, which causes a striking proliferation of hepatic peroxisomes, and the induction of peroxisomal lipid metabolizing enzymes, was tested for its influence on rat lung. Alveolar cells type II of the lung are the major source of the surface-active phospholipid-apoprotein complex. Their surfactant-containing lamellar bodies are part of the pulmonary surfactant system. To test the possible relationship between lung peroxisomes and the phospholipid-rich lamellar bodies in alveolar cells type II, clofibrate was administered to male rats. Drug treatment for 7 days resulted in a 30% (p less than 0.001) increase in the number of lamellar bodies within the type II cells, as estimated by morphometry on semithin sections of the lung. In contrast, the average number of type II cells per area of lung remained unchanged which indicates that type II cell proliferation did not occur. Intraalveolar macrophages were consistently vacuolated and markedly increased in size in the lungs of the treated rats. Peroxisomes (microperoxisomes) were identified cytochemically using the alkaline diaminobenzidine (DAB) method for catalase, a marker enzyme of these organelles. Ultrastructural-morphometric analysis of the lungs showed that clofibrate treatment resulted in a 60% increase in the profile number of DAB-positive peroxisomes (p less than 0.005) in alveolar cells type II which are known to be actively involved in the synthesis of the pulmonary surfactant. The number of mitochondria remained unchanged. A great variation in shape and size of the proliferated peroxisomes was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Keratin and involucrin in preneoplastic and neoplastic lesions. Distribution in the nasal mucosa of nickel workers.

Nasal mucosal biopsy specimens encompassing normal and pathological epithelia were obtained from nickel workers, a population with an increased incidence of carcinomas of the respiratory tract. The immunohistochemical detection of keratins was carried out using monoclonal antibodies AE1 and AE3. The antibody AE1 stained only the basal cells of normal mucociliary epithelium. Regular metaplasias showed an increased stain with AE3; all layers of the surface epithelium were stained. The dysplastic and neoplastic lesions exhibited an extraordinary increase in the staining patterns with AE3 and to a lesser extent with AE1. Involucrin, which was absent from the normal pseudostratified epithelium, appeared in all metaplastic-dysplastic lesions and in keratinized areas of carcinomas. The combined detection of keratins and involucrin proved useful in detecting the degree of maturity and differentiation of preneoplastic and neoplastic lesions of the nasal mucosa.

Antibodies, Monoclonal

Spatial visualization of junctional complexes by backscattered electron imaging and silver staining.

A method for the observation of junctional complexes by backscattered electron imaging in scanning electron microscopy, in tissue blocks, is presented. The junctional complexes are revealed by a modified silver staining method (originally devised for nucleolar organizer regions), used "en bloc" after formalin or glutaraldehyde fixation. Backscattered electron imaging allows, after this staining, the observation of junctional complexes through the surface of intact superficial cells, in the three tissues studied (liver, jejunum and urinary bladder). The interest of this approach is to offer the possibility of observing junctional complexes "by transparence," in nondissociated and nonsectioned tissues.

Animals

Ultrastructural and cytochemical study of the early stages of liver colonization by transplanted neoplastic hepatocytes.

Neoplastic liver cell colonies were induced in the livers of isogeneic F344 rats by intraportal injection of a hepatic cell suspension from diethylnitrosamine-treated donor rats. Examination of the livers 12 days after cell implantation revealed well-demarcated groups of liver cells. The colonies showed alterations of the normal hepatocyte phenotype, which were clearly demonstrated by histologic, cytochemical, and electron microscope techniques. The hepatocytes were markedly deficient in glucose-6-phosphatase and bile canalicular ATPase activities, and they contained numerous mitotic figures. Scanning and transmission electron microscopy allowed characterization of hepatocyte interfaces and the shape of sinusoids and the biliary network. The nodular colonies displayed disorganized, thickened trabeculae separated by dilated sinusoids. In these colonies the hepatocytes proliferated intensely and formed, inside the host parenchyma, revascularized, integrated nodular structures. However, these hepatocytes showed ultrastructural anomalies: large nuclei with prominent nucleoli, many free polysomes, and areas of proliferated smooth endoplasmic reticulum in connection with unfolded cisternae of the rough endoplasmic reticulum. All of these features agreed with the hypothesis previously proposed that the colonies may be precursors of the hepatocarcinomas that ultimately develop in animals given injections of treated liver cells. Direct confirmation, however, still is needed.

Adenosine Triphosphatases

Ammonia inhibits protein secretion in isolated rat hepatocytes.

The general secretion of proteins by isolated rat hepatocytes in suspension is inhibited by colchicine, anoxia, or ammonia (NH4Cl). The inhibition by ammonia is accompanied by the cytoplasmic retention and swelling of protein secretory vesicles, suggesting that ammonia accumulates in the vesicles and thereby prevents their translocation to the cell periphery. General protein synthesis appears to be relatively unaffected by ammonia.

Ammonia

Morphometry and ultrastructure of prismatic cristae in mitochondria of a crayfish muscle. A hypothesis of the structural principle.

Approximately 40% of the mitochondria in the sphincter muscle of the crayfish vas deferens have prismatic-type cristae. In cross section, the angular cristae have either triangular or rhomboid profiles which are surrounded by a hexagonal array of electron-dense dots. In longitudinal section, these mitochondria exhibit both thick and thin parallel lines, which represent cristae and filaments, respectively. It is postulated that the matrix of the prismatic-type mitochondria is packed with rodlets composed of an electron-dense core and a less dense shell. Close packing of these rodlets results in the regular hexagonal dot array. Deletion of fascicles of 3 or 4 rodlets results in spaces with triangular or rectangular cross sections. Lining of these spaces with membranes results in cristae with triangular or rhomboid cross sections.

Animals

[Morphology].

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Anatomy