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Biomedical subjects

E Masterson

Publications and source records attributed to E Masterson.

9 recordsLinked to original sources
PubMed1978

The pentose phosphate pathway in developing chick cornea.

Embryonic chick corneas at different stages of development were evaluated for activity of the pentose phosphate pathway. The appearance of activity was concurrent with the onset of corneal transperancy (stage 40). Highest values were found after complete transparency is achieved (stage 45 and after hatching). Phenazine methosulfate, an artificial electron acceptor, increased activity at all stages studied even before endogenous activity was measurable; however, no increase in glucose uptake was observed. Thus, the enzymes for the pathway are present at early stages (i.e., stage 38 and 40) although in latent form. The pathway probably functions in the developing cornea to generate NADPH rather than sugar moieties for macromolecular incorporation.

Age Factors↗
PubMed1978

Glucose oxidation in the chick cornea: effect of diamide on the pentose shunt.

Chick embryo corneas (stages 38 and 45) have been used to study variations in pentose shunt activity following the use of a glutathione-specific oxidizing agent, diamide, and a sulfydryl blocking agent, N-ethylmaleimide (NEM). Shunt activity was measured by the ratio of radiolabeled carbon 1 (14C-1) of glucose to radiolabeled carbon 6 (14C-6) of glucose derived as expired 14CO2. Diamide and NEM were both found to increase pentose shunt activity relative to glycolysis, although by different means. Diamide appeared to exert its effect by oxidizing glutathione and creating a demand for higher shunt activity to facilitate glutathione reduction by NADPH. Both C-1 and C-6 oxidation were increased, but C-1 oxidation was increased to a much greater extent. In contrast, NEM decreased both C-1 and C-6 oxidation, with C-6 preferentially affected. Thus NEM appears to preferentially inhibit the enzymatic machinery of the glycolytic-tricarboxylic acid cycle pathway and acts as an effective metabolic stress on the cornea. Our data suggest that the pentose shunt in the cornea may serve as an important alternative pathway under conditions of metabolic stress for glucose utilization and the production of energy (ATP) in the corneal cells.

Animals↗
PubMed1977

Oxygen consumption in the developing chick cornea.

Embryonic chick corneas at different stages of development were evaluated for O2 consumption. Some embryos were treated with thyroxine or thiouracil. In untreated animals, corneal QO2 (oxygen consumption/hr./mg. dry weight) decreased from 3.60 at stage 38 to 1.58 after hatching. The temperature coefficient Q10 increased from 1.55 at stage 40 to 2.03 after hatching. If O2 consumption is calculated as microliters of O2 consumed per hour per corneal pair, it increases between stage 38 (3.20) and hatched chicks (6.20) with a plateau between stages 40 and 45. Thiouracil treatment reduced O2 consumption by the cornea at stages 42 and 45, and thyroxine treatment elevated it at stage 40.

Age Factors↗
PubMed1977

The role of thyroid hormone in the development of the chick corneal endothelium and epithelium.

Previous studies have established that thyroxine or thiouracil treatments affect the development of corneal transparency in the chick. The effects of these drugs on chick corneal epithelial and endothelial development were investigated because in the adult the integrity of these cell layers is necessary for the maintenance of corneal transparency. Chick embryos were treated with thiouracil or thyroxine at stage 36 or 38; the corneas were excised 2 to 12 days after treatment (between stages 38 and 45), and prepared for electron microscopy. The colloidal tracer ruthenium red was added during fixation to study epithelial and endothelial permeability and to stain the intercellular endothelial spaces. At all stages studied, the epithelium was impermeable to ruthenium red and this property was not affected by drug treatment. The epithelial barrier to this tracer is located in the outermost cell layer. The ease of penetration of ruthenium red through the endothelial intercellular spaces indicated the lack of zonular tight functions and the presence of gap functions in this cell layer. Thiouracil treatment delayed the development of the corneal epithelium so that at stage 45 it resembled epithelium from a normal embryo 3 stages younger. In normal animals, chick corneal endothelial development is characterized by an increasing degree of interdigitation of the lateral plasma membranes of adjacent endothelial cells with advancing embryonic age. Thiouracil treatment delayed this progressive development of adjacent cell membrane interdigitation. In contrast, thyroxine treatment accelerated the development of the lateral borders of the endothelial cells. It also appears that thyroid hormone can affect the development of the cell membranes of apposed cells in epithelium as well as the endothelium of the embryonic chick cornea.

Animals↗