PubMed Health⌕ Search

Biomedical subjects

E Essner

Publications and source records attributed to E Essner.

At least 55 records · Page 3Linked to original sources
PubMed1978

Localization of lysosomal enzymes in retinal pigment epithelium of rats with inherited retinal dystrophy.

Four acid hydrolase activities are demonstrable by light microscopy in pigment epithelial cell lysosomes of rats (Royal College of Surgeons--RCS) with inherited retinal dystrophy and in control (Fischer) rats. The enzymes include acid phosphatase, aryl sulfatase, N-acetyl-beta-glucosaminidase, and esterase activities. No marked differences are observed in distribution or staining intensity of lysosomes in the two strains of rat. Acid hydrolase activities are not localized in sites other than lysosomes. Acid phosphatase and aryl sulfatase activities are also demonstrable by electron microscopy. In both strains, acid phosphatase reaction product is localized to various forms of lysosomes in pigment epithelial cells. A diffuse precipitate, considered to be nonspecific in origin, is seen in the cytoplasm, apical processes, outer segments (control), and outer segment debris (RCS). The precipitate is probably due to adsorption of lead from the incubation medium or of lead phosphate that diffuses from heavy accumulations in nearby lysosomes. Aryl sulfatase reaction product, in contrast to acid phosphatase, is localized to far fewer lysosomes and there is virtually no nonspecific precipitate. The findings indicate that lysosomes of RCS pigment epithelial cells possess several cytochemically demonstrable acid hydrolase activities. There is no evidence for the localization of acid phosphatase (or aryl sulfatase) activities in sites other than lysosomes.

Acid Phosphatase↗
PubMed1978

Phagocytosis and surface morphology in cultured retinal pigment epithelial cells.

Phagocytosis of latex spheres was studied in explant cultures of retinal pigment epithelium from rabbit, calf, and rat (normal and dystrophic). Calf and rabbit pigment epithelial cells showed a "latent period" of about 12 and 17 hr, respectively, during which latex spheres were not ingested even when the cultures were pre-incubated for up to 24 hr prior to exposure. Scanning electron microscopy demonstrated a profusion of apical processes on the surface of cells from both species that was present throughout the latent period. In contrast, rat pigment epithelial cells showed no latent period and phagocytosed latex spheres after a pulse of 1 hr. It was concluded that the latent period is not common to all species and, when present, is not due to an absence of apical processes. The surfaces of normal and dystrophic pigment epithelial cells showed abundant apical processes that did not differ from each other in morphology, number, or distribution. In cells from pigmented species (calf and rat), frequent fusions were observed between latex phagosomes and melanosomes or melanin granules.

Animals↗
PubMed1977

Ultrastructural study of GERL in beige mouse alveolar macrophages.

Alveolar macrophages of the beige mouse mutant have a system of smooth-surfaced elements with the hallmarks of GERL. GERL also appears to produce residual bodies, and both organelles show cytochemically demonstrable acid phosphatase activity. When cells are exposed to colloidal silver, the tracer is endocytosed via pinocytic vacuoles to GERL.

Acid Phosphatase↗
PubMed1976

Age-related accumulation of ceroid-like pigment in mice with Chediak-Higashi syndrome.

The Chediak-Higashi Syndrome (CHS) is a rare inherited disorder occurring in man and several animal homologs including the beige mouse; it is characterized by pigmentary dilution, susceptibility to pyogenic infections, and the presence of enlarged lysosomes in many cell types. Beige mice 6 months of age and older were found to have darkened livers, kidneys, and spleens, accompanied by splenomegaly. A fluorescence microscopic survey of tissues from beige mice revealed marked accumulations of a microscopic survey of tissues from beige mice revealed marked accumulations of a yellow autofluorescent pigment inhepatocytes, renal proximal tubule cells, and splenic macrophages. Additionally, large amounts of hemosiderin were present in the spleen. In beige mice, the pigment was noted in animals as young as 1 to 2 weeks of age and gradually increased in amount as the animals aged. A histochemical investigation of the pigment showed that it was ceroid-like in nature and contained in lysosomes. Ultrastructurally, the pigment was composed of lipid-like droplets embedded in a dense matrix and surrounded by a limiting membrane. The accumulation of ceroid-like material in beige mice may be a reflection of the metabolic disturbance which underlies CHS.

Aging↗
PubMed1975

Formation of anomalous lysosomes in monocytes, neutrophils, and eosinophils from bone marrow of mice with Chédiak-Higashi syndrome.

Chédiak-Higashi syndrome, a rare autosomal recessive disorder occurring in man, beige mice, and other homologues, is characterized by abnormally large lysosomes in many cell types. The formation of these anomalous lysosomes in developing monocytes, neutrophils, and eosinophils in beige mouse bone marrow, as well as lysosomal formation in the corresponding normal cells from C57 Black mice, was investigated by electron microscopy, together with a method for the demonstration of peroxidase activity. Localization of peroxidase reaction product was the same in both C57BL and beige mice. In promonocytes and in neutrophilic and eosinophilic proganulocytes, peroxidase reaction product was localized in lysosomes, in the perinuclear cisternae, all cisternae of the endoplasmic reticulum, and the Golgi succules. In the later stages of development, reaction product was localized only in the lysosomes. In promonocytes and progranulocytes from the C57BL mice, lysosomes apparently form from the inner Golgi succule. Fusion of newly formed lysosomes was occasionally seen. Lysosomal fusion was never observed in the more mature monocytes and eosinophils and was only rarely seen in mature neutrophils. In the beige mouse, lysosomes were formed as in the C57BL mice. However, in the beige mouse, fusion of newly formed lysosomes occurred frequently in promonocytes and neutrophilic progranulocytes. Lysosomal fusion was also frequently observed in the more mature cells. As a result of the continued lysosomal fusion, the mature monocytes, neutrophils, and eosinophils from the beige mouse contained fewer but often greatly enlarged lysosomes.

Animals↗
PubMed1974

Fate of exogenous peroxidase in renal lysosomes of mice with Chediak-Higashi syndrome.

The beige mouse is a homolog of Chediak-Higashi syndrome, a disorder which is characterized by the presence of enlarged (anomalous) lysosomes in many cell types. In kidney, anomalous lysosomes are present in cells of the proximal convoluted tubules. In this study, the degradation of injected horseradish peroxidase (HRP) in lysosomes was studied in both the convoluted (S1-S2) and straight (S3) segments of the proximal tubules of beige and control (C57 B1) mice. Tissues were removed at intervals from 18 hours to 7 days after HRP injection. Peroxidase activity was visualized for light and electron microscopy by incubating sections in diaminobenzidine medium. No differences in the rate of degradation of HRP were demonstrable between anomalous lysosomes in S1-S2 cells of beige kidney and those in controls. In both animals, HRP was demonstrable in these lysosomes at 18 and 36 hours but not at 48 hours after injection. By electron microscopy, reaction product appeared as a flocculent precipitate distributed uniformly throughout the lysosome. In contrast to those of S1-S2 cells, lysosomes of beige S3 cells degraded HRP much more slowly than did those of control mice. In controls, HRP was demonstrable in S3 lysosomes at 18 hours but not at 48 hours after injection. In beige mouse kidney HRP was demonstrable in many S3 lysosomes at 48 hours, and it persisted in some lysosomes as long as 5 days after injection. These findings indicate that beige S3 lysosomes are defective in degrading protein. As reported recently, these lysosomes are also markedly enlarged and altered in content. They appear to arise as part of a renal lesion of unknown pathogenesis which is confined to the S3 segments of the proximal tubules. The slower rate of degradation of protein appears to be another manifestation of the alteration in these lysosomes.

Animals↗
PubMed1973

Suppression of pigmentation in mouse melanoma cells by 5-bromodeoxyuridine: effects on tyrosinase activity and melanosome formation.

Low concentrations (1-3 microg/ml) of 5-bromodeoxyuridine (BrdU) reversibly suppress pigmentation in a highly pigmented clone (B(5)59) of cultured B16 mouse melanoma cells. We have found that unpigmented cells (clone C(3)471), derived by long-term culture of B(5)59 cells in 1 microg of BrdU/ml, were completely amelanotic with no biochemically or cytochemically detectable tyrosinase activity or ultrastructural evidence of premelanosomes. The process by which pigmentation is suppressed was studied in B(5)59 cells during a 7-day period of growth with BrdU (3 microg/ml). Assays of tyrosinase activity showed that activity was reduced after 1 day and decreased progressively, approaching zero by 7 days. A quantitatively minor part of this reduction was directly attributable to the appearance of a dialyzable inhibitor of tyrosinase activity. Acrylamide gel electrophoresis revealed two bands of activity corresponding in Rx values to the T(1) and T(2) forms of soluble tyrosinase. Both were progressively reduced during growth with BrdU but one form (T(1)) was consistently affected earlier than the other (T(2)). Ultrastructural-cytochemical studies also showed an early effect on the localization of tyrosinase reaction product. At day 3, reaction product was no longer present in Golgi saccules and Golgi-associated smooth surfaced tubules, but was still seen within premelanosomes, compound melanosomes, and occasional Golgi-associated vesicles. By 7 days tyrosinase reaction product was usually not demonstrable. The number of premelanosomes was progressively decreased during growth with BrdU. Premelanosomes became concentrated in the juxtanuclear region and at day 3 many were contained within abnormally large and numerous compound melanosomes. Premelanosomes and compound melanosomes were rarely seen at 7 days, by which time the cultures were nearly amelanotic. The coordinated suppression of melanogenesis by BrdU may provide a useful model in which to study the normal regulation of this process.

Animals↗
PubMed1973

A hereditary alteration in kidneys of mice with Chediak-Higashi syndrome.

The beige mouse is considered to be a homologue of Chediak-Higashi syndrome (CHS). Cytochemical and electron microscopic studies have revealed an inherited lesion in the kidneys of these mice. The alteration was confined to the distal segments (S3) of the proximal tubules and was characterized by the accumulation of numerous massive polysaccharide-rich granules. These granules were reactive for acid phosphatase and beta-glucuronidase activities and were therefore considered to be lysosomes. Small numbers of lymphocytes were also observed in the perivascular spaces and within the tubules of the S3 segment. The fine structure of S3 cells was also markedly altered. In addition to the massive lysosomes, dense material was found associated with the brush border and was present in pinocytotic vesicles at the base of the brush border and between basal invaginations of the plasma membranes. Despite these changes, reabsorption of exogeneous peroxidase by S3 cells appeared to be normal. The presence of a congenital defect in the kidney of the beige mouse appears to provide a useful model for studying the morphology and function of the S3 region of the nephron.

Acid Phosphatase↗
PubMed1972

Protein transport in mouse kidney utilizing tyrosinase as an ultrastructural tracer.

The morphological basis of glomerular filtration and protein reabsorption in mouse kidney was examined by using mushroom tyrosinase subunits (mol wt 34,500), as an ultrastructural tracer. Almost immediately after injection tyrosinase reaction product was visualized in the glomerulus, and within the capillary lumen extending into the endothelial fenestrae. The entire basement membrane showed accumulations of tyrosinase in the subendothelial and subepithelial layers. The urinary space contained considerable amounts of reaction product, some of which was adsorbed to the cell coat of the podocytes. Reaction product could also be seen in the brush border region of the proximal tubule cells. By 30 min after injection, no tyrosinase reaction product was demonstrable in the glomerulus except for dense vesicles in mesangial cells. Most of the reaction product was localized in absorption droplets in the apical cytoplasm of proximal tubule cells. Occasionally, some tyrosinase reaction product was present within the basal infoldings of these cells. The behavior of tyrosinase in the mouse kidney is in accordance with that of other low molecular weight tracers. The pattern of localization within the basement membrane provides additional support for the presence of two filtration barriers in the glomerulus. The adherence of tyrosinase to the cell coat of the glomerular epithelial cells suggests that this may be an additional mechanism whereby protein is removed from the glomerular filtrate. Tyrosinase subunits may prove to be a useful new tracer for the study of protein transport.

Animals↗
PubMed1972

Myeloperoxidase and crystalline bodies in the granules of DMBA-induced rat chloroma cells.

Chloroma (chloroleukemia) was induced in a splenectomized rat by repeatedly administering dimethylbenz(a)anthracene (DMBA) and was serially transplanted thereafter. Composed of immature myeloid cells, the tumor imparted a green discoloration to the tissues that it infiltrated extensively. Chloroma cells fluoresced red in ultraviolet light, produced a characteristic curve in spectrophotometry, and contained large amounts of myeloperoxidase. They included numerous intracytoplasmic granules of both types A and B, which contained occasional crystalline bars. Permanent lines of chloroma cells were established in tissue culture. These cells, while maintaining their initial morphology, ceased producing myeloperoxidase and subsequently induced white tumors when they were isotransplanted.

Animals↗
PubMed1971

Hypolipidemia in a mutant strain of "acatalasemic" mice.

Mutant "acatalasemicm" mice have an unstable catalase in hepatic and renal peroxisomnes that is readily degraded, apparently into peroxidase subunits. The hypothesis that an in situ cataloperoxidase would affect serum lipids was tested in these mutants and serum triglycerides and cholesterol were found to be significantly lower than in the wild strain. This finding is in accordance with reports that a hypolipidemic response to the injection of peroxidase subunits of hepatic catalase occurs in humans and rabbits.

Age Factors↗