The present investigation is concerned with determining the role of calcium, phospholipids, and phospholipid metabolites on transepithelial sodium and water transport in response to antidiuretic hormone (ADH). These studies utilize the frog skin for determining sodium transport and amphibian urinary bladder for water flow measurements and scanning electron microscopy of cell surface morphology. The results demonstrate that phospholipids and phospholipid metabolites containing arachidonic acid stimulate transepithelial sodium transport through amiloride sensitive channels and the action of these lipids involves the synthesis of prostaglandins. These lipids also inhibited the increase in water flow induced by ADH, and this effect was prevented with prostaglandin synthesis inhibitors. Prostaglandins alter intracellular calcium concentrations and agents effecting calcium metabolism alter cell surface morphology and the changes in surface substructure induced by ADH. These observations support the hypothesis that alterations in membrane permeability to water and ions may involve metabolism of membrane phospholipids and prostaglandin biosynthesis.

Thesis (Ph.D.)--McMaster University, 2004. / Supervisor: Michael J. O'Donnell. Includes bibliographical references (leaves 193-208).

This thesis examines the hypothesis that human erythrocyte net sugar transport is the sum of two serial processes: sugar translocation followed by interaction of newly imported sugar with an intracellular binding complex from which sugar dissociates into the bulk cytosol. This hypothesis suggests that steady-state transport measurements in the human erythrocyte do not accurately reflect the intrinsic catalytic features of the glucose transporter and unless correctly interpreted, may lead to apparent inconsistencies in the operational behavior of the human erythrocyte sugar transport system. Our results support this proposal by demonstrating that although sugar transport measurements in human red blood cells suggest that transport is catalytically asymmetric, ligand binding measurements indicate that transport must be symmetric. In order to examine the serial compartments hypothesis, we set out to determine the following: 1) identify the component(s) of the proposed sugar binding complex, 2) determine whether cytosolic ATP levels and transporter quaternary structure affect sugar binding to the sugar binding complex, and 3) determine whether the sugar binding site(s) are located within or outside the cell. We present findings which support the hypothesis that the sugar binding complex is in fact the sugar transport protein, GLUT1. The number of sugar binding sites and the release of sugar from the GLUT1 complex are regulated by ATP and by GLUT1 quaternary structure. The sugar binding sites are located on a cytoplasmic domain of the GLUT1 complex. We show how these observations can account for the apparent complexity of erythrocyte sugar transport and its regulation by ATP.

Fung, Chun Kit. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 121-135). / Abstracts in English and Chinese. / Declaration --- p.i / Acknowledgement --- p.ii / Abbreviations --- p.iii / Abstract in English --- p.v / Abstract in Chinese --- p.vii / Table of Contents --- p.ix / List of Figures --- p.xii / Chapter Chapter 1 - --- Introduction / Chapter 1.1 --- Genus Cordyceps --- p.1 / Chapter 1.2 --- Cordyceps militaris --- p.4 / Chapter 1.3 --- Biological Functions and Chemical Constituents of Cordyceps militaris --- p.9 / Chapter 1.4 --- "Human Bronchial Epithelial Cell Line, 16HBE14o-" --- p.13 / Chapter 1.5 --- Ion Transport in Human Bronchial Epithelial Cells --- p.16 / Chapter 1.6 --- Objectives of the Experiments --- p.20 / Chapter Chapter 2 - --- Materials and Methods / Chapter 2.1 --- Solutions and Chemicals --- p.21 / Chapter 2.2 --- Preparation of Hot Water Cordyceps militaris Extract --- p.22 / Chapter 2.3 --- Culture of Cells --- p.23 / Chapter 2.4 --- Short-Circuit Current (lsc) Measurement --- p.24 / Chapter 2.5 --- Short-Circuit Current (lsc) Measurement in Nystatin-Permeabilized Monolayer --- p.29 / Chapter 2.6 --- Measurements of [Ca2+]i --- p.31 / Chapter 2.7 --- Measurement of PKA Activity --- p.36 / Chapter 2.8 --- Statistical Analysis --- p.37 / Chapter Chapter 3 - --- Results / Chapter 3.1 --- Regulation of Ion Transport in 16HBE14o- Cells by CM Water Extract --- p.38 / Chapter 3.1.1 --- Dose-Dependent Relationship of CM Water Extract --- p.39 / Chapter 3.1.2 --- "Involvement of CI"" Transport in CM-induced lsc Response" --- p.42 / Chapter 3.1.3 --- Involvement of K+ channels in CM-induced lsc Response --- p.47 / Chapter 3.1.4 --- Involvement of Adenylate Cyclase/cAMP/Protein Kinase A Pathway in CM-induced lsc Response --- p.52 / Chapter 3.1.5 --- Involvement of Ca2+-Dependent Pathway in CM-induced lsc Response --- p.57 / Chapter 3.1.6 --- "Effect of CM Extract on Apical CI"" Current and Basolateral K+ Current in Nystatin-Permeabilized Epithelia" --- p.61 / Chapter 3.1.7 --- Effect of CM Extract on PKA Activity --- p.67 / Chapter 3.2 --- Regulation of Ion Transport in 16HBE14o- Cells by Cordycepin --- p.70 / Chapter 3.2.1 --- Dose-Dependent Relationship of Cordycepin --- p.70 / Chapter 3.2.2 --- "Involvement of CI"" Transport in Cordycepin-induced lsc Response" --- p.73 / Chapter 3.2.3 --- Involvement of K+ channels in Cordycepin-induced lsc Response --- p.79 / Chapter 3.2.4 --- Involvement of Adenylate Cyclase/cAMP/Protein Kinase A Pathway in Cordycepin-induced lsc Response --- p.84 / Chapter 3.2.5 --- Involvement of Ca2+-Dependent Pathway in Cordycepin-induced lsc Response --- p.89 / Chapter 3.2.6 --- Effect of Cordycepin on Intracellular Ca2+ Concentrations --- p.93 / Chapter 3.2.7 --- "Effect of Cordycepin on Apical CI"" Current and Basolateral K+ Current in Nystatin-Permeabilized Epithelia" --- p.98 / Chapter 3.2.8 --- Effect of Cordycepin on PKA Activity --- p.104 / Chapter Chapter 4 - --- Discussion / Chapter 4.1 --- Regulation of Ion Transport in 16HBE14o- Cells by CM Extract --- p.107 / Chapter 4.2 --- Intracellular Signaling Mechanisms behind CM-induced lsc Responses --- p.110 / Chapter 4.3 --- Regulation of Ion Transport in 16HBE14o- Cells by Cordycepin --- p.111 / Chapter 4.4 --- Intracellular Signaling Mechanisms behind Cordycepin-induced lsc Responses --- p.114 / Chapter Chapter 5 - --- Conclusion / Chapter 5.1 --- Summary --- p.117 / Chapter 5.2 --- Future Directions --- p.120 / Chapter Chapter 6 - --- References --- p.121 / Chapter Chapter 7 - --- Publications --- p.136

Thesis (Ph. D.)--University of Virginia, 2008. / Title from title page. Includes bibliographical references. Also available online through Digital Dissertations.