The daily urinary excretion of taurine was studied in six women, 22 to 36 years old. Five subjects collected 24-hour urine specimens for 10 days, and another for 37 days. The subjects were free from any known metabolic disorder. They consumed their normal diet. Urinary taurine was determined by the method of Pentz et al. (1957). Taurine was separated from the other amino acids in urine by treatment with Dowex 50W(H⁺), and reacted with dinitrofluorobenzene to form the dinitrophenol derivative. The derivative was measured photometrically at 360 mμ. In addition to taurine, urinary creatinine was determined by a micro-modification of the method by Folin (Hawk, Oser and Summerson, 1954). The average daily urinary excretion of taurine during the 10 days varied widely among the six subjects, ranging from 60.9 to 196.0 mg per 24 hours. The average excretion of taurine was not related to the subject's age, height, weight or excretion of creatinine. The daily excretion of taurine by each subject varied. Three subjects excreted relatively constant amounts of taurine during the 10-day period; their excretion ranged from 51.0 to 83.3 mg, 66.0 to 105.0 mg and 123.3 to 163.5 mg per 24 hours. The remaining three subjects showed greater variation in taurine execretion; their excretion ranged from 79.5 to 145.5 mg, 84.8 to 187.5 mg and 154.4 to 337.5 mg per 24 hours. This variation in the daily urinary excretion of taurine may have been caused by differences in protein, amino acid and free taurine content of the diet, or stress. A subject who received ACTH to control an allergic reaction to dinitrofluorobenzene excreted increased amounts of taurine on the days the hormone was administered. This subject received seven injections of an ACTH preparation between the 17th and 37th day of urine collection. Taurine excretion was greater on the days ACTH was received than on the day immediately preceding or following each injection. The ingestion of oral contraceptives by two of the subjects did not appear to affect the urinary excretion of taurine. Menstruation appeared to affect the taurine excretion by the two subjects who menstruated during the 10-day period. Results reported by Merrow et al. (1966) indicate that taurine in plasma may be more indicative of vitamin B₆ nutriture than that in urine. In view of this, study on the relationship of taurine in plasma to that excreted in urine by adequately nourished individuals and ones deficient in vitamin B₆ would be of considerable interest. Since the diet consumed by the subjects could affect the urinary excretion of taurine, it is recommended that the subjects be fed a constant diet of known protein, amino acid, taurine and vitamin B₆ content. / Graduation date: 1968

Graduation date: 1969

Thesis (M.A.)--Baylor University, 2007. / Includes bibliographical references (p. 53-74).

Taurine is by far the most abundant of the sulfur amino acids, levels in the heart exceeding the combined quantities of all others. Taurine exhibits extensive cardiovascular pharmacology, including inotropic and antiarrhythmic properties. Many of the actions of taurine appear to involve a modulation of calcium availability. The sarcolemma regulates the entry of calcium into the heart. Binding sites on the cardiac sarcolemma provide calcium for contraction and maintain membrane integrity. The effect of taurine on calcium binding to rat heart sarcolemma varies with the buffer. In Tris and the presence of sodium, taurine increases the affinity of the low affinity binding, but decreases the maximal binding of calcium. In the absence of sodium, taurine decreases affinity of the low affinity binding without altering the maximal binding. These effects on low affinity binding, however, are absent in physiological buffers representative of extracellular conditions. In buffers representative of intracellular ionic conditions, taurine increases the high affinity binding of calcium to sarcolemma in a dose-dependent manner. These results suggest that taurine exerts its cardiotonic actions through a modulation of the high affinity calcium binding on the internal aspect of the sarcolemma. Membrane phospholipids are important calcium-binding molecules in cardiac sarcolemma. Heterogeneous vesicles containing phospholipids in a ratio approximating that of rat heart sarcolemma bind significant quantities of calcium. Taurine increases calcium binding to the artificial liposomes in a manner similar to that observed for sarcolemma. Taurine also increases calcium binding to homogeneous vesicles of phosphatidylserine, but not phosphatidylinositol, phosphatidylcholine or phosphatidylethanolamine. Taurine modulation of calcium may not involve a classical protein-ligand interaction, but, instead, a low affinity attraction to sarcolemmal phospholipids. Taurine binds to sarcolemma with low affinity and positive cooperativity at concentrations normally present in the rat heart. Neither β-alanine nor guanidinoethane sulfonate, inhibitors of taurine transport, affect taurine binding. However, hypotaurine and various cations reduce binding. Heterogeneous phospholipid vesicles also bind taurine with positive cooperativity which was enhanced by the inclusion of cholesterol. Taurine associates with homogeneous vesicles of phosphatidylcholine, phosphatidylserine, or phosphatidylethanolamine. Phosphatidylinositol bind little taurine. These studies support the hypothesis that taurine exerts its modulation of sarcolemmal function through an interaction with membrane phospholipids.

Thesis--Copenhagen. / Summary in Danish. Bibliography: p. [88]-107.

Thesis--Copenhagen. / Summary in Danish. Bibliography: p. [88]-107.

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by Lam Ying Wan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1991. / Includes bibliographical references. / Acknowledgement --- p.5 / List of Abbreviations --- p.7 / Abstract --- p.10 / Chapter Chapter 1: --- Introduction --- p.13 / Chapter 1.1 --- Distribution and Biosynthesis of Taurine --- p.14 / Chapter 1.2 --- Physiological Functions of Taurine --- p.17 / Chapter 1.2.1 --- Interaction of Taurine and Calcium --- p.17 / Chapter 1.2.2 --- Neuroinhibitory action of Taurine --- p.18 / Chapter 1.2.3 --- Taurine as an Osmoeffector --- p.20 / Chapter 1.2.4 --- Integrative Model of Taurine Action --- p.22 / Chapter 1.3 --- Taurine and Volume Regulation in Astrocytes --- p.22 / Chapter 1.3.1 --- Response of Cells to Anisosmotic Media --- p.22 / Chapter 1.3.2 --- Mechanism of Regulatory Cell Volume Decrease --- p.23 / Chapter 1.3.3 --- Regulatory Volume Decrease (RVD) in Astrocytes --- p.25 / Chapter 1.3.4 --- Taurine and Volume Regulation in Astrocytes --- p.25 / Chapter 1.4 --- Ion Channels and Transporters in Astrocytes --- p.26 / Chapter 1.4.1 --- Potassium Channels --- p.26 / Chapter 1.4.2 --- Sodium Channels --- p.27 / Chapter 1.4.3 --- Chloride Channels --- p.27 / Chapter 1.4.4 --- Stretch-activated Ion Channels --- p.27 / Chapter 1.4.5 --- (KC1 + NaCl) Carrier --- p.27 / Chapter 1.4.6 --- Na+/H+ exchange --- p.28 / Chapter 1.4.7 --- C1-/HCO3- exchange --- p.28 / Chapter Chapter 2: --- Materials and Methods --- p.30 / Chapter 2.1 --- Cell Culture --- p.30 / Chapter 2.1.1 --- Preparation of Culture Medium --- p.30 / Chapter 2.1.2 --- Preparation of Phosphate Buffered Saline --- p.30 / Chapter 2.1.3 --- Cell Counting Method --- p.31 / Chapter 2.1.4 --- Culture of U373MG Human Astrocytoma Cells --- p.31 / Chapter 2.1.5 --- Culture of Primary Astrocytes --- p.32 / Chapter 2.2 --- Taurine Release Experiment --- p.32 / Chapter 2.2.1 --- Preparation of Physiological Salt Solution (PSS) --- p.32 / Chapter 2.2.2 --- Preparation of Hyposmotic Solution --- p.33 / Chapter 2.2.3 --- Preparation of Chloride Free Solution --- p.33 / Chapter 2.2.4 --- Preparation of Sodium Free Solution --- p.33 / Chapter 2.2.5 --- Preparation of Calcium Free Solution --- p.34 / Chapter 2.2.6 --- Preparation of High Potassium Solution --- p.34 / Chapter 2.2.7 --- Preparation of Urea containing PSS --- p.34 / Chapter 2.2.8 --- Assay of [3H]-Taurine Release --- p.34 / Chapter 2.2.9 --- Drug pretreatment --- p.35 / Chapter 2.2.10 --- Data Calculation --- p.35 / Chapter 2.3 --- Volume Determination --- p.36 / Chapter 2.3.1 --- Experimental procedure --- p.36 / Chapter 2.3.2 --- Drug pretreatment --- p.37 / Chapter 2.3.3 --- Data calculation --- p.40 / Chapter 2.4 --- Taurine Influx Experiment --- p.41 / Chapter 2.4.1 --- Experimental Procedure --- p.41 / Chapter 2.5 --- Drug Preparation --- p.42 / Results / Chapter Chapter 3: --- Hyposmolarity-Induced [3H]-Taurine Release --- p.45 / Chapter 3.1 --- Responses of Astrocytes to Hyposmotic Conditions --- p.45 / Chapter 3.1.1 --- Effect of Hyposmotic Medium on the Release of Preloaded [3H]-taurine in U373MG astrocytoma cell --- p.45 / Chapter 3.1.2 --- Time Course of the Hyposmolarity-induced [3H]-taurine Release --- p.49 / Chapter 3.1.3 --- Response of Primary Astrocytes to Hyposmotic Medium --- p.49 / Chapter 3.2 --- Effect of MK196 on Hyposmolarity-Induce Taurine Release --- p.52 / Chapter 3.3 --- Effects of Inhibitors of (NaCl+KCl) Cotransporter and C1- /HCO3- Anion Exchanger on Hyposmolarity-induced [3H]- taurine Release --- p.56 / Chapter 3.3.1 --- Effect of (NaCl + KC1) Cotransporter Inhibitors on Hyposmolarity-induced [3H]-taurine Release --- p.56 / Chapter 3.3.2 --- "Effects of two stilbene derivatives, SITS and DIDS,on hyposmolarity-induced [3H]-taurine release" --- p.56 / Chapter 3.3.3 --- "Effect of a Chloride Channel Blocker, Antracene-9- Carboxylate on Hyposmolarity-induced [3H]-taurine Release" --- p.57 / Chapter 3.3.4 --- Effect of MK473 on Hyposmolarity-induced [3H]-taurine Release --- p.58 / Chapter 3.4 --- Effect of Chloride Depletion on Hyposmolarity-induced [3H]- taurine Release --- p.58 / Chapter 3.4.1 --- Effect of Replacing Chloride with Nitrate --- p.58 / Chapter 3.4.2 --- Effect of Replacing Sodium Chloride with Sucrose --- p.59 / Chapter 3.4.3 --- Effect of Replacing Chloride with Gluconate --- p.59 / Chapter 3.5 --- Investigation of the Transduction Mechanism of Hyposmolarity- induced [3H]-taurine Release --- p.71 / Chapter 3.5.1 --- Effect of Depleting Extracellular Ca2+ --- p.71 / Chapter 3.5.2 --- Effect of Staurosporine on Hyposmolarity-induced [3H]- taurine Release --- p.71 / Chapter 3.6 --- Effect of SITS on the Swelling Process of U373 MG cells --- p.74 / Chapter 3.6.1 --- Regulatory Volume Decrease (RVD) in U373 MG Cells --- p.74 / Chapter 3.6.2 --- Effect of SITS on RVD in U373 MG Cells --- p.74 / Chapter 3.7 --- Effect of Hyposmotic Medium on Sodium-Independent Taurine Uptake in U373 MG Cells --- p.77 / Chapter Chapter 4 : --- Urea-Induced [3H]-Taurine Release --- p.80 / Chapter 4.1 --- Concentration Dependency of Urea-Induced Efflux of [3H]-taurine from U373 MG Cells --- p.80 / Chapter 4.2 --- Effect of MK 196 on the Urea-Induced [3H]-taurine Release from U373 MG Cells --- p.82 / Chapter 4.3 --- Effect of SITS on the Urea-induced [3H]-taurine Release from U373 MG Cells --- p.82 / Chapter Chapter 5: --- High Potassium-Induced Efflux of [3H]-taurine --- p.86 / Chapter 5.1 --- High Potassium Concentration Induced Release of [3H]-taurine from U373 MG Cells --- p.86 / Chapter 5.1.1 --- High Potassium Concentration Induced Release of [3H]- taurine --- p.86 / Chapter 5.1.2 --- Effect of the Concentration of HCO3- on High Potassium Induced Release [3H]-taurine Release --- p.87 / Chapter 5.2 --- Effect of MK 196 on High Potassium Induced [3H]-taurine Release in U373 MG --- p.87 / Chapter 5.3 --- Effect of (NaCl + KC1) Cotransporter Inhibitors on High Potassium Induced Taurine Release from U373 MG Cells --- p.91 / Chapter 5.3.1 --- Effect of Furosemide on High Potassium Induced [3H]- taurine Release --- p.91 / Chapter 5.3.2 --- Effect of Bumetanide on High Potassium Induced [3H]- taurine Release --- p.91 / Chapter 5.4 --- Effect of C1-/HCO3- Anion Exchanger Inhibitors on High Potassium Induced Release of [3H]-taurine from U373 MG Cells --- p.91 / Chapter 5.4.1 --- Effect of SITS on High Potassium Induced [3H]-taurine Release --- p.91 / Chapter 5.4.2 --- Effect of Antracene-9-Carboxylate on High Potassium Induced [3H]-taurine Release --- p.96 / Chapter 5.4.3 --- Effect of MK 473 on High Potassium Induced [3H]- taurine Release --- p.96 / Chapter 5.5 --- Effect of Chloride Depletion on High Potassium-Induced [3H]- taurine Release --- p.96 / Chapter 5.5.1 --- Effect of Replacing C1- by NO3- --- p.96 / Chapter 5.5.2 --- Effect of Replacing C1- by Gluconate --- p.96 / Chapter Chapter 6: --- Discussion --- p.102 / Chapter 6.1 --- Hyposmolarity Induced [3H]-taurine Release --- p.103 / Chapter 6.1.1 --- Hyposmolarity is the Key Stimulation for [3H]-taurine Release --- p.103 / Chapter 6.1.2 --- Hyposmolarity Induced [3H]-taurine Release and the C1- /HCO3- anion exchanger --- p.104 / Chapter 6.1.3 --- Comparision of the Hyposmolarity-induced Release of [3H]-taurine in U373 MG cells and primary astrocytes --- p.106 / Chapter 6.1.4 --- Comparision between the Hyposmolarity-induced Taurine Release and the Na+-independent Uptake for Taurine --- p.106 / Chapter 6.1.5 --- Transduction Mechanisms of Hyposmolarity-induced [3H]-taurine Release --- p.107 / Chapter 6.2 --- Urea-Induced Release of [3H]-taurine --- p.107 / Chapter 6.3 --- High Potassium-Induced [3H]-taurine Release --- p.108 / Chapter 6.3.1 --- Pharmacological Properties of High Potassium-induced [3H]-taurine Release --- p.108 / Chapter 6.3.2 --- Effect of Ionic Environment on High Potassium-Induced [3H]-taurine Release --- p.108 / Chapter 6.4 --- Mechanism of Swelling-Induced Taurine Release --- p.109 / Chapter 6.4.1 --- Involvement Stretched Activated Channel (SACs) in Swelling-Induced Taurine Release --- p.109 / Chapter 6.4.2 --- Involvement of the C1-/HCO3- Anion Exchanger in Swelling-Induced Taurine Release --- p.110 / Chapter 6.4.3 --- Possibility of Taurine as a Substrate of the C1-/HCO3- Anion Exchanger --- p.111 / Chapter 6.4.4 --- Conclusion --- p.114 / Chapter Chapter 7: --- Conclusion --- p.116 / References --- p.119

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