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C K Dorey

Publications and source records attributed to C K Dorey.

28 records · Page 2Linked to original sources
PubMed1989

Superoxide production by porcine retinal pigment epithelium in vitro.

Cultured porcine retinal pigment epithelial cells release superoxide, measured as superoxide dismutase (SOD)-suppressible reduction of cytochrome C, and SOD-suppressible luminol-dependent chemiluminescence. Latex beads stimulated a significant release of superoxide that reached 82 nmol/mg protein in the first 15 min and declined thereafter. Formation of an insoluble blue formazan following reduction of nitroblue tetrazolium histochemically demonstrated that superoxide was released over the region of the cell vicinal to the bead. Dioctanoylglycerol, a synthetic, cell-permeating activator of protein kinase C, also elicited a rapid release of superoxide from RPE cells. This study emphasizes the need to characterize the mechanisms by which superoxide is generated, whether its release is regulated, and how toxicity is prevented in vivo.

Animals↗
PubMed1989

Cell loss in the aging retina. Relationship to lipofuscin accumulation and macular degeneration.

We examined the impact of aging on the numbers of photoreceptors and retinal pigment epithelium (RPE) cells, and the number of photoreceptors per RPE cell profile, in selected regions of 30 human eyes. The mean ratio of photoreceptors to RPE cell was higher in the macula than in the paramacula (P less than 0.01) or the equatorial area (P less than 0.001). We found evidence for an age-related loss of RPE in both whites (P less than 0.02) and blacks (P less than 0.0006), although the rate of loss in whites was significantly slower than in blacks. Photoreceptor loss in blacks was inversely correlated with age (P less than 0.04). In whites, however, photoreceptor loss was very significantly and directly correlated with lipofuscin concentration in the opposing RPE (P less than 0.0001) and unrelated to age. The disparity in the rates of photoreceptor and RPE cell loss produced, in older eyes, a higher ratio of photoreceptors per RPE cell profile. In the macula, the ratio for whites over 50 years of age was significantly higher (P less than 0.05) than that in blacks over 50. Our data suggest that the increased phagocytic and metabolic load on the RPE, which ultimately the macula causes a preferential age-related accumulation of lipofuscin in the RPE, which ultimately leads to photoreceptor death. This may prove a useful model of age-related macular degeneration and Stargardt's disease.

Adolescent↗
PubMed1988

Central sparing in annular macular degeneration.

Using fluorescein angiography and monochromatic photography, we measured the size of the central sparing in 45 patients with annular maculopathy (mean +/- S.D., 0.34 +/- 0.15 disk diameter; range, 0.10 to 0.65 disk diameter) and compared it with the size of macular yellow pigment in 40 subjects (mean +/- S.D., 0.31 +/- 0.12 disk diameter; range, 0.1 to 0.5 disk diameter). The close approximation of these values suggested that macular yellow pigment contributed to the annular pattern through a photoprotective mechanism.

Fluorescein Angiography↗
PubMed1988

Superoxide dismutase activity and growth of retinal pigment epithelial cells are suppressed by 20% oxygen in vitro.

Despite knowledge of the toxicity of oxygen to the retina, its effects on the retinal pigment epithelium have not been considered. We examined the effect of 20%, 10% and 5% oxygen on growth and superoxide dismutase (SOD) activity of porcine retinal pigment epithelial cells (RPE). Growth of RPE cells was very significantly lower in 20% oxygen than in either 10% or 5%; optimal growth occurred at 10% oxygen, the concentration most like their environment in vivo. Inclusion of SOD and catalase in the media very significantly stimulated growth in 20% oxygen. The SOD activity of RPE cells was significantly related to ambient oxygen. In first passage (P1) cells, SOD activity was 44% lower on day 7 than on day 1 of culture in 20% oxygen (p less than or equal to 0.05). Transfer of cells growing in 20% oxygen to 5% oxygen arrested the decrease in SOD and resulted in significantly higher SOD levels. In fourth passage (P4) cells grown in 20% oxygen, SOD was 25% and 44% lower than cells in 10% and 5% oxygen, respectively. After one week, SOD levels in the P4 cells were significantly higher than in P1. A statistical model of SOD activity in RPE cells indicated significant negative correlations with both oxygen concentration and the cell number. Growth of RPE cells was significantly influenced by oxygen level, days of culture and passage number, but not SOD activity. We conclude that traditional culture conditions support generation of free radicals in tissue culture media that suppress both growth and superoxide dismutase activity.

Catalase↗
PubMed1981

Stimulation of aryl sulfatase in rat peritoneal macrophages exposed to bone in vitro.

Rat peritoneal macrophages elicited by injection of thioglycollate were cultured in the absence and presence of non-vital, milled rat bone or latex beads. After 0, 48, 96, and 144 hours exposure to these substances, the levels of aryl sulfatase B were determined. Cells exposed to bone demonstrated a significant (p less than .001) time-dependent increase in the specific activity of aryl sulfatase B. After 144 hours the specific activity of aryl sulfatase in cells exposed to bone was 20 fold higher than that in the 144 hour controls. There were no significant differences in the levels of aryl sulfatase B in controls over time, nor were the levels of enzyme in those exposed to latex beads difference from controls. We conclude that the specific activity of aryl sulfatase B increases when macrophages resorb bone and suggest that this enzyme could be used as a marker or index for bone resportion.

Animals↗
PubMed1977

Ultrastructural analysis of glycosaminoglycan hydrolysis in the rat periodontal ligament. I. Evidence for macrophage involvement in bone remodelling.

We identified the cellular sites of glycosaminoglycan hydrolysis by localizing a key enzyme, N-acetyl-beta-glucosaminidase, in the rat periodonatal ligament. Reaction product was seen in osteoclasts, osteoblasts, fibroblasts, and in macrophages situated perivascularly in areas of bone remodelling. The preferential location of macrophages in areas of both bone formation and bone resorption, and their intense NAGase activity identified the macrophage as a significant participant in the total process of bone remodelling. We considered the presence of reaction product in the Golgi zone and the rough endoplasmic reticulum of osteoblasts and fibroblasts as possible localization of a NAG-transferase.

Acetylglucosaminidase↗
PubMed1977

Ultrahistochemical analysis of glycosaminoglycan hydrolysis in the rat periodontal ligament. II. Aryl sulfatase and bone resorption.

The distribution of aryl sulfatase in the rat periodontal ligament was investigated by ultrastructural histochemistry. In the periodontal ligament aryl sulfatase was localized specifically in osteoclasts and in vicinal perivascular macrophages. Macrophages associated with bone formation did not stain. The authors interpret this specificity as a potential marker for osteoclast differentiation from macrophages--or as a further indication of the capacity of macrophages to modulate their enzymatic complement in response to the environment. To explain the absence of aryl sulfatase in areas of bone formation we suggest that different sulfate esters are mobilized from resorbing and mineralizing matrices, and that only the enzyme associated with bone resorption is histochemically detectable with the artificial substrates currently used.

Animals↗