Ryan J. Huxtable

Taurine in the central nervous system and the mammalian actions of taurine

Abbreviations

Effect of taurine on a muscle intracellular membrane.

Abstract Sarcoplasmic reticulum from rat skeletal muscle had rates of calcium oxalate uptake dependent upon the speed with which the muscle was removed and homogenized. Rapidly isolated sarcoplasmic reticulum (muscle removed and homogenized within 20 min) showed a 25% increase in rate of calcium oxlate uptake in the presence of 15 mM taurine, and the total sequestering capacity was also increased. The rate of calcium oxalate uptake by more slowly isolated sarcoplasmic reticulum (1 h between sacrifice of first animal and homogenization of the muscle) could be increased by 30% by performing the isolation with 10–15 mM taurine present in all media, compared with a paired isolation in the absence of taurine. Exposure of sarcoplasmic reticulum to taurine throughout isolation led to an increased yield of microsomes and sarcoplasmic reticulum. These effects of taurine on sarcoplasmic reticulum were not duplicated by phosphate, isethionate, KCl, cysteine or histidine, but aminopropane-sulfonic acid showed similar effects. Taurine slowed the rate of loss of calcium transport and ATPase activities of sarcoplasmic reticulum caused by phospholipase C. It is suggested that taurine may function as a membrane stabilizer.

Taurine Concentrations in Congestive Heart Failure

The concentration of taurine in the left ventricular muscle of hearts of patients who died of chronic congestive heart failure was twice that of patients who died of other causes and had no cardiac pathology. There was no corresponding difference in taurine concentrations in aortic tissue between the two groups. Stress-induced hypertension in rats also led to an increase in taurine concentration in the heart, whereas that in skeletal muscle and brain showed no significant alteration when compared to unstressed animals. Spontaneously hypertensive rats, of the Wistar-derived Okamato strain, showed a similar elevation in cardiac taurine compared to age-matched control Wistar rats.

The Harmful Potential of Herbal and Other Plant Products

SummaryHerbs, herbal products, food additives and other dietary supplements derived from plants are widely consumed in many countries. The literature on intoxications from such behaviour is increasing. This article reviews some of the factors predisposing to intoxication from the use of herbs, with examples drawn largely from pyrrolizidine alkaloid-containing plants.Poisonings occur because of the misidentification of a plant, or the unknown or ignored toxicity of a correctly identified plant. Factors contributing to problems include the difficulties of identifying chopped, processed herbs or plant mixtures, persistent use of a toxic plant, variability in the toxic constituents of a plant, problems of nomenclature, adulteration and the difficulty in establishing the chronic toxic potential of a plant.Certain users of herbs are at high risk of intoxication. These include chronic users, those consuming large amounts or a great variety, the very young, fetuses, the elderly, the sick, the malnourished or undernourished and those on long term medication. Members of certain cultural groups in North America are also at higher risk. Certain plant toxins may be gender-selective in their action.To encourage discussion, some approaches to regulation are suggested, and some commonsense guidelines are given.

Activation and pulmonary toxicity of pyrrolizidine alkaloids.

Pyrrolizidine alkaloids unsaturated in the 1,2 position are hepatotoxins. Certain of them, such as monocrotaline, are also pneumotoxins, producing pulmonary arterial hypertension and right ventricular hypertrophy as a delayed response two weeks after administration. Pneumotoxicity is the result of hepatic metabolism, the lung itself being unable to bioactivate pyrrolizidine alkaloids. The changes produced in the lung following exposure to pneumotoxic pyrrolizidine alkaloids are reviewed, together with the factors and interventions which modify or influence these changes. In the main, the earliest changes are seen in vascular smooth muscle and in the interactions between the smooth muscle and the endothelium. The search to identify the pneumotoxic metabolite is reviewed. It is generally accepted that pyrroles, or dehydroalkaloids, are responsible for the toxicity of pyrrolizidines. However, the primary pyrroles are intensely reactive, hydrolyzing and polymerizing within seconds in aqueous solution. Evidence for and against the pneumotoxin being a primary pyrrole or a stabilized secondary conversion product of a primary pyrrole is discussed.

Hepatic metabolism and pulmonary toxicity of monocrotaline using isolated perfused liver and lung

Monocrotaline is a pyrrolizidine alkaloid obtained from the seeds of Crotalaria spectabilis. When perfused through an isolated liver, monocrotaline is metabolized to Ehrlich reactive (E+) metabolites. Metabolism of monocrotaline was faster in livers from male rats than female rats, was inducible with phenobarbital pretreatment, and was inhibited by coperfusion with the P-450 mixed-function oxidase inhibitor SKF-525A, anoxic perfusion conditions, and low temperatures. When metabolites generated by an isolated liver were perfused through isolated lungs in a recirculatory manner, serotonin transport by the pulmonary endothelium was reduced in correlation with the amount of E+ material contained in the perfusion medium. When metabolism of monocrotaline by the liver was inhibited with SKF-525A, low temperature perfusions or anoxic conditions, serotonin transport by the pulmonary endothelium was unchanged from controls. Monocrotaline alone had no effect on the lung. Thus, isolated perfused livers metabolized monocrotaline to chemical species which produced pulmonary damage in vitro. This provides direct evidence that liver metabolites can cause one of the pneumotoxic effects of monocrotaline observed in vivo.

Taurine in nutrition and neurology

I Physicochemical Properties of Taurine: Introduction.- Coordination and Binding of Taurine as Determined by Nuclear Magnetic Resonance Measurements on 13C-Labeled Taurine.- II Taurine in Nutrition and Development: Introduction.- Sources and Turnover Rates of Taurine in Newborn, Weanling, and Mature Rats.- Studies on the Renal Handling of Taurine: Changes During Maturation and After Altered Dietary Intake.- Taurine and Tapetum Structure.- Taurine Deficiency: A Rationale for Taurine Depletion.- Taurine Nutrition in Man.- III Transport and Metabolism of Taurine: Introduction.- Hypotaurine Aminotransferase.- Hypotaurine Uptake in Mouse Brain Slices.- The Sulfur-Containing Amino Acid Pathway in Normal and Malignant Cell Growth.- Taurine Transport by Reconstituted Membrane Vesicles.- IV Taurine and the Heart: Introduction.- Electrophysiological Effects of Taurine in Cardiac Purkinje Fibers and Myocardial Taurine Loss during Ischemia. Is There a Relationship?.- Observations on the Action of Taurine at Arterial and Cardiac Levels.- Elevated Blood Taurine Levels After Myocardial Infarction or Cardiovascular Surgery: Is There any Significance?.- V The Neurochemistry of Taurine: Introduction.- Interaction of Taurine with Its Precursor, Cysteine Sulfinic Acid, in the Central , Nervous System.- Differential Effects of Light and Dark Adaptations on Function and Metabolism of Retinal Taurine and ?-Aminobutyric Acid (GABA).- Changed Taurine-Glutamic Acid Content and Altered Nervous Tissue Cytoarchitecture.- Taurine, Cysteinesulfinic Acid Decarboxylase and Glutamic Acid in Brain.- VI The Neuropharmacology of Taurine: Introduction.- The Role of Taurine in Nervous Tissue, Its Effects on Ionic Fluxes.- Taurine Receptors in CNS Membranes: Binding Studies.- Specific Binding of Taurine in Central Nervous System.- Central Neuropharmacology of D-Ala2-Met-Enkephalinamide and its Interactions with Taurine in Rats.- Central Effects of Taurine: Antagonistic Effects on Central Actions of Angiotensin.- Taurine and Thermoregulation: Behavioral and Cellular Studies.- Influence of Centrally Administered Taurine on Thermoregulation and Fever.- Taurine and Friedreichs Ataxia: An Update.- Discussions on Taurine: Introduction.- Session I: How are Tissue Taurine Concentrations Regulated?.- Session II: Are the Pharmacological Actions of Taurine Related to its Physiological Functions?.- Session III: What Does Taurine Do?.- Session IV: Do Taurine and Its Analogs or Cogeners Have Actions in Common?.- Session V: Is Taurine Essential in Development?.- Session VI: Does Taurine Have Clinical Significance?.- List of Participants.

Fluorimetric determination of monobromobimane and o-phthalaldehyde adducts of γ-glutamylcysteine and glutathione : application to assay of γ-glutamylcysteinyl synthetase activity and glutathione concentration in liver

The reversed-phase HPLC separation of fluorescent o-phthalaldehyde (OPA) derivatives has been applied to the assay of hepatic gamma-glutamylcysteine and glutathione (GSH) levels and the enzymes producing these peptides. The method has been compared to the assay using monobromobimane (MB) as the derivatizing agent. The OPA method has the advantage of faster derivatization, the lack of need to adjust the pH, isocratic separation and selectivity for GSH and gamma-glutamylcysteine. The MB method requires pH adjustment following derivatization and gradient elution chromatography. MB is also non-selective, yielding fluorescent derivatives of all biological thiols and more interfering peaks on the chromatogram. MB-based analyses are also approximately sixty times more expensive per sample. MB yields fluorescent degradation products on exposure to light. OPA adducts are stable for up to ten days when stored at -20 degrees C. OPA detection is sensitive to 12.5 pmol in the sample, at a signal-to-noise ratio of 2.5. The two methods correlate well. Hepatic gamma-glutamylcysteine synthetase in the same liver preparation was found to be 4.85 +/- 0.47 nmol min-1 mg-1 protein by the OPA method and 4.42 +/- 0.52 nmol min-1 mg-1 protein by the MB method. GSH concentrations were found to be 90.4 +/- 6.5 nmol/mg protein for the OPA method and 92.5 +/- 3.4 for the MB method.

Increase in type I adenosine 3',5'-monophosphate-dependent protein kinase during isoproterenol-induced cardiac hypertrophy.

Abstract The amount of type I and type II cyclic AMP-dependent protein kinase present in the rat heart was determined at various times during isoproterenol-induced cardiac hypertrophy. Wistar rats were injected twice daily with isoproterenol (5 mg/kg, s.c.) for 2, 5 or 10 days. Cardiac weight increased gradually over the 10-day period of drug administration, and by day 10, heart weight was 156% of control. Following the cessation of isoproterenol administration, the cardiac weight regressed toward the control value by day 15. An increase in the specific activity of type I protein kinase to 197% of control occurred by day 10. The specific activity of type II protein kinase did not change significantly during either the hypertrophy or regression stage. The increase in the specific activity of type I protein kinase during a chemically-induced trophic response of the heart may indicate that type I cyclic AMP-dependent protein kinase plays a regulatory function in this process.

Elevation of taurine in human congestive heart failure.

Abstract The concentration of taurine in the left ventricle of the heart was doubled in patients who had died of chronic congestive heart failure compared to patients who had died of other causes and had no cardiac pathology. In the absence of congestive heart failure, a similar elevation in taurine level was seen in patients with high blood pressure compared to patients with lower blood pressures. The levels of taurine in heart failure were not affected by digitalis treatment. The concentration of taurine in the aorta was almost the same in patients who had died of congestive heart failure and patients who had died of other causes, suggesting that the increase in concentration of taurine might be specific to the heart.