Taurine 200 Grams

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SELECTED RESEARCH

 

TAURINE

Taurine deficiency after intensive chemotherapy and/or radiation

Am J Clin Nutr; 55(3):708-11 1992

Taurine, a nonessential amino acid (AA), is the most abundant free AA in the intracellular space. We measured plasma AA concentrations in 36 patients 7-28 d after intensive chemotherapy and/or radiation. Plasma taurine concentrations were uniformly low in all patients (20.0 +/- 6.4 mumol/L, mean +/- SD). Plasma taurine in 11 healthy volunteer control subjects was 45.0 +/- 20.3 mumol/L (P less than 0.001). Other AA concentrations, specifically those of precursor AAs methionine and cystine, were normal. We prospectively measured plasma AA concentrations in 12 patients before starting and 6-10 d after completing intensive cytotoxic treatment. Values before treatment were 37.2 +/- 11.6, 109.6 +/- 30.7, and 18.5 +/- 4.8 for taurine, cystine, and methionine, respectively, and were 24.3 +/- 6.0, 111.2 +/- 23.8, and 24.0 +/- 14.5 after treatment. Pretreatment plasma taurine correlated directly with the magnitude of decrease in plasma taurine during cytotoxic treatment (n = 12, r = 0.85, P less than 0.01). Intensive cytotoxic chemotherapy and/or radiation leads to a reduction in plasma taurine concentrations without any change in its precursor AAs, methionine and cystine. The clinical relevance of plasma taurine depletion will need further study.


Effect of glutaurine and its derivatives and their combinations with radiation protective substances upon irradiated mice

Acta Radiol Oncol Radiat Phys Biol; 20(5):319-324 1981
The radiation protective effects of glutaurine (gamma-L- glutamyl-taurine, Litoralon), and of some of its derivatives, as well as of their combinations with substances of the amino-alkyl-thiol group, have been investigated in mice. The results suggest that glutaurine possesses a radiation protective effect in animals irradiated with LD50/30 of roentgen rays and 60Co gamma rays. The compound has a favorable effect also when administered after irradiation. Among the combinations best results were obtained by its simultaneous administration with subminimal doses of S-beta-aminoethyl-isothiuronium (AET) or cystamine. Some of its derivatives also exhibited considerable protection against irradiation with roentgen rays.


Effect of mixed gamma-neutron irradiation on taurine penetration through cellular membranes of rat peripheral blood leukocytes

Res. Inst. Biology and Biophysics, V. V. Kuibyshev Tomsk State Univ., Tomsk, USSR Capacity of rat peripheral blood WBC for transmembrane transfer of taurine was studied in vitro in normal controls and 24 hr after mixed gamma- neutron (70%) irradiation (GNI: 350 rads). Four hr after GNI, the number of WBC decreased and equaled 31% of the initial level; the amount of taurine increased within the same period, and 24 hr after GNI it was 3x the initial level. At the same time, an increase in the protein content of WBC was seen. Irradiation was found to change the membrane permeability. It was noted that 24 hr after GNI, the system of taurine transport in the irradiated cells became more specific: the affinity to taurine increased, and the d, l-beta-alanine- dependent transfer system began to play a more important role. In another series of experiments, it was found that damage to cell membranes caused by WBC trypsinization decreased the taurine content 5x, showing that the greater part of taurine is localized inside the cells, where it apparently participates in metabolism.


Taurine and sh-group content in the platelets of irradiated rats

Radiobiologiia; 18(2):271-274

The association between the content taurine and SH-groups of platelets during radiation sickness was studied in albino rats. Animals were irradiated with 650 R and sacificed 1, 4, 7, 12 and 21 days later. The levels of taurine and SH-groups in separated platelets was measured per protein unit. The development of radiation sickness resulted in a sevenfold decrease in the content of platelet taurine on days 4-7 of irradiation and twofold decrease in SH-group content on day 12 of irradiation. On day 21,the content of both taurine and SH-groups showed normalization. The decrease in taurine and SH-groups content may have been due to radiation-induced elevation of protein adsorption on platelet membrane.

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The role of taurine in developing rat retina

Ophtalmologie (France),1995, 9/3 (283-286)

Taurine is the most abundant free aminoacid in the retina. A recent study hypothesises the existence of two different functional pools of taurine in the retina: one Ca2-dependent, the other related to high K+ concentration, and to the subsequent cell volume adjustment. Many pathologic conditions, such as hypoxia or ischemia, can induce cell swelling: photoreceptors could prevent volume alteration by a taurine release. The mechanism allowing membrane protection by taurine is still unclear (modification of calcium ion fluxes and inhibition of protein phosphorylation), but many evidence of a key- role played by taurine have been found: we already know that the mother diet-free taurine produce a reduction of neonate optique nerve fibers. We studied the uptake system of taurine with 0.1 mM and 4 mM solution in 7(PN) and 15(PN15) days old rats retina, grown in environmental standard conditions, compared with adult rats. We also studied the effect of neonatal oxygen supplementation (80% O2 in the air followed by 9 days recovery in room air). The data demonstrate that PN 15 rats have a taurine uptake similar to the adult. The PN 7 rats have a hyperactive uptake of this aminoacid. The AA hypothesise that the developing rat retina has a good protection against damages induced by cell swelling during absolute or relative hypoxia. At PN 7 taurine could also play a key role for retinal growth. The oxygen, damaging the taurine uptake system, could stop the normal development of the optic pathway.


Supplemental taurine in diabetic rats: Effects on plasma glucose and triglycerides

BIOCHEM. MED. METAB. BIOL.(USA), 1990, 43/1 (1-9+8)

The present study has indicated that significant shifts in plasma, urinary, and tissue taurine and in non-taurine dialyzable amines occur in the STZ-induced diabetic rat, especially in the kidney. Taurine administration at relatively low dosage ameliorated only kidney taurine concentration.

Anticipated alterations in plasma glucose and creatinine were observed but neiher of these changes was affected by taurine administration. Similarly, urinary output of creatinine, gluycose, and NAG increased significantly among diabetic rats, but none of these were detectably influenced by taurine. Increases in plasma triglycerides observed in STZ-induced diabetes appear to be attenuated by taurine administration, and although cholesterol concentrations were lower in taurine-treated rats, the differences were not statistically significant. These findings should encourage further studies of these effects in rats as a useful model for several complications of human diabetes including atherosclerosis, retinopathy, and nephropathy


Taurine deficiency retinopathy in the cat

J. SMALL ANIM. PRACT. (ENGLAND), 1980, 21/10 (521-534)

The literature on feline central retinal degeneration is reviewed and an experiment reported which investigates whether taurine is essential in cats fed a purified diet. The development of taurine deficiency retinopathy is described and illustrated. The histopathological, ultrastructural and ERG changes are also described. Other retinal degenerations in the cat are discussed.
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Taurine: A therapeutic agent in experimental kidney disease

Amino Acids (Austria), 1996,11/1 (1-13)

Taurine is an abundant free amino acid in the plasma and cytosol. The kidney plays a pivotal role in maintaining taurine balance. Immunohistochemical studies reveal a unique localization pattern of the amino acid along the nephron. Taurine acts as an antioxidant in a variety of in vitro and in vivo systems. It prevents lipid peroxidation of glomerular mesangial cells and renal tubular epithelial cells exposed to high glucose or hypoxic culture conditions. Dietary taurine supplementation ameliorates experimental renal disease including models of refractory nephrotic syndrome and diabetic nephropathy. The beneficial effects of taurine are mediated by its antioxidant action. It does not attenuate ischemic or nephrotoxic acute renal failure or chronic renal failure due to sub-total ablation of kidney mass. Additional work is required to fully explain the scope and mechanism of action of taurine as a renoprotective agent in experimental kidney disease. Clinical trials are warranted to determine the usefulness of this amino acid as an adjunctive treatment of progressive glomerular disease and diabetic nephropathy.


Effects of taurine and guanidinoethane sulfonate on toxicity of the pyrrolizidine alkaloid monocrotaline

Biochemical Pharmacology (USA), 1996, 51/3 (321-329)

Monocrotaline (MONO), a pyrrolizidine alkaloid, causes pulmonary ial hypertension and right ventricular hypertrophy due to hepatic metabolism to the alkylating pyrrole dehydromonocrotaline. Taurine, a sulfonic amino acid, is hepato- and cardioprotective in a variety of conditions. We have examined the effects of taurine and its amidino analog, guanidinoethane sulfonate (GES), in rats injected i.p. with MONO (65 mg/kg). Taurine and

GES were given as 1% solutions in drinking water beginning 14 days before administration of MONO and continuing for 14 days thereafter, when the rats were killed. The MONO group had right ventricular hypertrophy and pulmonary hyperplasia. Compared with control, no significant changes in the right ventricle/left ventricle weight ratio, or the right ventricle/body weight ratio occurred in rats also given taurine or GES. Lung weights in these two groups were higher than in the control group, but below that of the MONO-alone group. The lethality of MONO over 14 days was decreased by taurine (LD50 for MONO alone 80 mg/kg; for

MONO + taurine 121 mg/kg). Rats given only MONO had lower hepatic concentrations of GSH and cysteine (Cys), and higher activities of microsomal GSH transferase and gamma-glutamyl transpeptidase. In rats also receiving taurine, hepatic GSH levels and GSH transferase activity were no different from control. gamma-Glutamylcysteine (Glu-Cys) synthetase and gamma-glutamyl transpeptidase activities were elevated. In MONO-injected rats given GES, hepatic GSH levels were higher and Cys levels were lower than in either the MONO alone or MONO + taurine groups. gamma-Glu-Cys synthetase activity was depressed. Microsomal

GSH transferase, GSH peroxidase and gamma-glutamyl transpeptidase activities were elevated. Livers of MONO-injected animals showed higher levels of serine (reversed by both taurine and GES) and glycine (Gly; reversed by GES) and lower levels of glutamine. Compared with control rats, the following changes occurred in serum amino acids: MONO alone: increased aspartate, taurine and lysine; taurine-supplemented: increased taurine, methionine (Met) and lysine, and decreased Gly; GES-supplemented: decreased asparagine, serine, Gly, arginine, taurine, and valine. Compared with the MONO-alone group, the taurine-supplemented group had higher glutamate (Glu), Met and alanine, and the GES-supplemented group higher alanine and lower serine, Gly, arginine and valine. We conclude that taurine protects against MONO-induced lethality and right ventricular hypertrophy. GES also protects against right ventricular hypertrophy. However, these agents act by different mechanisms, taurine preventing many of the biochemical changes induced by MONO, with GES inducing additional changes.


Fish oil and other nutritional adjuvants for treatment of congestive heart failure

Medical Hypotheses (United Kingdom), 1996, 46/4 (400-406)

Published clinical research, as well as various theoretical considerations, suggest that supplemental intakes of the 'metavitamins' taurine, coenzyme Q10, and L-carnitine, as well as of the minerals magnesium, potassium, and chromium, may be of therapeutic benefit in congestive heart failure. High intakes of fish oil may likewise be beneficial in this syndrome. Fish oil may decrease cardiac afterload by an antivasopressor action and by reducing blood viscosity, may reduce arrhythmic risk despite supporting the heart's beta-adrenergic responsiveness, may decrease fibrotic cardiac remodeling by impeding the action of angiotensin II and, in patients with coronary disease, may reduce the risk of atherothrombotic ischemic complications. Since the measures recommended here are nutritional and carry little if any toxic risk, there is no reason why their joint application should not be studied as a comprehensive nutritional therapy for congestive heart failure.


Usefulness of TAURINE in chronic congestive heart failure and its prospective application.

Jpn Circ J (JAPAN) Jan 1992, 56 (1) p95-9

We compared the effect of oral administration of TAURINE (3 g/day) and coenzyme Q10 (CoQ10) (30 mg/day) in 17 patients with congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy, whose ejection fraction assessed by echocardiography was less than 50%. The changes in echocardiographic parameters produced by 6 weeks of treatment were evaluated in a double-blind fashion. In the TAURINE-treated group significant treatment effect was observed on systolic left ventricular function after 6 weeks. Such an effect was not observed in the CoQ10-treated group.


Platelet TAURINE in patients with arterial hypertension, myocardial failure or infarction.

Acta Med Scand Suppl (SWEDEN) 1980, 642 p79-84

The content of TAURINE in the hypertrophied left ventricle is increased in congestive heart failure an in spontaneously hypertensive (SH) rats. In SH rats the TAURINE content of and TAURINE uptake by the platelets are also increased. The present results indicate that, as in the heart, the TAURINE content may also increase in the platelets of those patients with congestive heart failure. The TAURINE content and uptake are not increased in the platelets of hypertensive patients as they are in the platelets of SH rats. It is likely that in acute myocardial infarction, a considerable amount of TAURINE is released from the heart into the plasma. However, there is no simultaneous increase in the platelet TAURINE content. From this work on can only conclude that platelets may reflect TAURINE changes in the heart in some pathological states, e.g. congestive heart failure.


Physiological and experimental regulation of TAURINE content in the heart.

Fed Proc (UNITED STATES) Jul 1980, 39 (9) p2685-90

High concentrations of TAURINE are found in the heart and these are increased still further in congestive heart failure. It appears that TAURINE is largely derived by influx from the circulation, and this influx is stimulated by cyclic AMP, whereas influx of alpha-amino acids is unaffected. Influx occurs via a saturable transport system that has strict requirements for ligands. Other substances are transported by this system, including beta-alanine, hypoTAURINE, guanidoethyl sulfonate, and, to a lesser extent, guanidinopropionate; and these are competitive antagonists for TAURINE transport. Guanidinoethyl sulfonate, in vivo, markedly lowers

TAURINE concentrations over the course of a few days in all tissues examined in the rat and mouse (but not in the guinea pig). The concentrations of other amino acids are unaffected. Guanidinoethyl sulfonate may prove to be a useful substance in the study of the biological role of TAURINE, in view of its ability to regulate TAURINE content in a number of species. Despite the numerous pharmacological actions of TAURINE, its physiological function in the heart remains problematic. One function appears to be the modulation of calcium movements. The inotropic actions of TAURINE and beta-adrenergic activation may be linked via the cyclic AMP-dependent regulation of TAURINE influx.


A relation between myocardial TAURINE contest and pulmonary wedge pressure in dogs with heart failure.

Physiol Chem Phys (UNITED STATES) 1977, 9 (3) p259-63

Myocardial TAURINE levels were correlated with pulmonary wedge pressure (PWP) in dogs with congestive heart failure (CHF). Heart failure was induced by creating an infrarenal aortocaval fistula. PWP ranged from 6.6 to 28 mm Hg, suggesting a wide range in severity of heart failure in those dogs. Compared to TAURINE levels of normal dogs, levels of the CHF group were significantly elevated in both left and right ventricles. Linear regression analysis of ventricular TAURINE content yielded a highly significant direct relation to PWP. The results suggest that myocardial TAURINE content increases as heart failure becomes more severe.


Adrenergic stimulation of TAURINE transport by the heart.

Science (UNITED STATES) Oct 28 1977, 198 (4315) p409-11

A high-affinity transport system that is specific for beta- amino acids has been delineated in rat hearts. This system transports the cardiotonic sulfonic amino acid TAURINE. beta-Adrenergic stimulation increases the transport capacity without effect on alpha-amino acid uptake, as does stimulation with adenosine 3',5'-monophosphate or theophylline. The existence of such an uptake system for TAURINE in the heart accounts for the high intra- to extracellular concentration gradient that is maintained, and suggests that cardiac stress is associated with increased TAURINE uptake. This may explain why TAURINE is the only amino acid to be markedly elevated in congestive heart failure. TAURINE is a modifier of calcium fluxes in the heart, as are beta-adrenergic agonists. The presence of this uptake system suggests a link between beta-adrenergic stimulation of calcium and TAURINE fluxes.


Taurine and serine supplementation modulates the metabolic response to tumor necrosis factor alpha in rats fed a low protein diet

J. NUTR. (USA), 1992, 122/7 (1369-1375)

Plasma taurine and serine decrease following trauma and in severe inflammatory disease. These changes may signify an increase in requirements for sulfur amino acids. We previously demonstrated that cysteine supplementation can restore the impaired ability of rats fed an 8% casein diet to increase hepatic zinc, glutathione (GSH) and protein concentrations in response to tumor necrosis factor alpha (TNFalpha). Here we examined whether serine or taurine produces a similar effect, because serine provides the carbon skeleton of cysteine and taurine is its major metabolite. After 7 d of receiving either a 20% casein diet supplemented with cysteine or an 8% casein diet supplemented with alanine, serine or taurine, rats received an intraperitoneal injection of human TNFalpha. Tumor necrosis factor caused no change in hepatic GSH but resulted in a lower GSH concentration in lung in rats fed the alanine-supplemented diet. Neither taurine nor serine increased liver GSH relative to that in rats fed alanine, but the depression in lung due to TNF injection was lessened. The absolute increase in ceruloplasmin in response to TNF was enhanced in rats fed the alanine-supplemented diet relative to those fed the 20% casein diet. Serine normalized this response. This observation-the effects of taurine and serine on lung GSH and a significant negative correlation between ceruloplasmin and liver and lung GSH concentration in rats fed TNF-suggests that supplemental serine and taurine may improve antioxidant defenses when dietary supplies of cysteine are low but do not influence cysteine availability for a normal response to TNF.


Taurine deficiency after intensive chemotherapy and/or radiation

Am J Clin Nutr; 55(3):708-11 1992

Taurine, a nonessential amino acid (AA), is the most abundant free AA in the intracellular space. We measured plasma AA concentrations in 36 patients 7-28 d after intensive chemotherapy and/or radiation. Plasma taurine concentrations were uniformly low in all patients (20.0 +/- 6.4 mumol/L, mean +/- SD). Plasma taurine in 11 healthy volunteer control subjects was 45.0 +/- 20.3 mumol/L (P less than 0.001). Other AA concentrations, specifically those of precursor AAs methionine and cystine, were normal. We prospectively measured plasma AA concentrations in 12 patients before starting and 6-10 d after completing intensive cytotoxic treatment. Values before treatment were 37.2 +/- 11.6, 109.6 +/- 30.7, and 18.5 +/- 4.8 for taurine, cystine, and methionine, respectively, and were 24.3 +/- 6.0, 111.2 +/- 23.8, and 24.0 +/- 14.5 after treatment. Pretreatment plasma taurine correlated directly with the magnitude of decrease in plasma taurine during cytotoxic treatment (n = 12, r = 0.85, P less than 0.01). Intensive cytotoxic chemotherapy and/or radiation leads to a reduction in plasma taurine concentrations without any change in its precursor AAs, methionine and cystine. The clinical relevance of plasma taurine depletion will need further study.


Effect of glutaurine and its derivatives and their combinations with radiation protective substances upon irradiated mice

Acta Radiol Oncol Radiat Phys Biol; 20(5): 319-324 1981

The radiation protective effects of glutaurine (gamma-L-glutamyl-taurine, Litoralon), and of some of its derivatives, as well as of their combinations with substances of the amino-alkyl-thiol group, have been investigated in mice. The results suggest that glutaurine possesses a radiation protective effect in animals irradiated with LD50/30 of roentgen rays and 60Co gamma rays. The compound has a favorable effect also when administered after irradiation. Among the combinations best results were obtained by its simultaneous administration with subminimal doses of S-beta-aminoethyl-isothiuronium (AET) or cystamine. Some of its derivatives also exhibited considerable protection against irradiation with roentgen rays. (Author abstract) (19 Refs)


[Effect of mixed gamma-neutron irradiation on taurine penetration through cellular membranes of rat peripheral blood leukocytes]

Res. Inst. Biology and Biophysics, V. V. Kuibyshev Tomsk State Univ., Tomsk,USSR

Capacity of rat peripheral blood WBC for transmembrane transfer of taurine was studied in vitro in normal controls and 24 hr after mixed gamma-neutron (70%) irradiation (GNI: 350 rads). Four hr after GNI, the number of WBC decreased and equaled 31% of the initial level; the amount of taurine increased within the same period, and 24 hr after GNI it was 3x the initial level. At the same time, an increase in the protein content of WBC was seen. Irradiation was found to change the membrane permeability. It was noted that 24 hr after GNI, the system of taurine transport in the irradiated cells became more specific: the affinity to taurine increased, and the d, l-beta-alanine- dependent transfer system began to play a more important role. In another series of experiments, it was found that damage to cell membranes caused by WBC trypsinization decreased the taurine content 5x, showing that the greater part of taurine is localized inside the cells, where it apparently participates in metabolism. (16 Refs)


[Sources of taurine hyperexcretion in irradiated rats]

Radiobiologiia; 20(3):455-459 1980

The correlation between postradiation excretions of taurine and its final metabolite, an inorganic sulfate, in the urine of white male rats (irradiated totally with a single dose of 700 rads) is discussed. The levels of taurine in the thymus, spleen, and mesenteric lymph nodes are also considered. Taurine concentrations in the thymus, spleen, and lymph nodes were found to be approx the same (10.2 +-0.6, 12.7 +-0.5 and 11.8 +-1.4 umole/g of tissue, respectively). The obtained data show that radiation-induced destructive changes in cells of lymphoid organs cause the loss of taurine from these tissues and the increase in taurine excretion in the urine. The study of intracellular taurine distribution in the thymocytes of intact rats showed that it was localized primarily in the cytosolic fraction of cells. Disorders in taurine transformation into inorganic sulfate during radiation sickness accounted for additional taurine removal from the body. It was suggested that postradiation taurine excretion from the organism is a significant symptom of radiation injury.


[Taurine and sh-group content in the platelets of irradiated rats]

Radiobiologiia; 18(2):271-274

The association between the content taurine and SH-groups of platelets during radiation sickness was studied in albino rats. Animals were irradiated with 650 R and sacificed 1, 4, 7, 12 and 21 days later. The levels of taurine and SH-groups in separated platelets was measured per protein unit. The development of radiation sickness resulted in a sevenfold decrease in the content of platelet taurine on days 4-7 of irradiation and twofold decrease in SH-group content on day 12 of irradiation. On day 21,the content of both taurine and SH-groups showed normalization. The decrease in taurine and SH-groups content may have been due to radiation-induced elevation of protein adsorption on platelet membrane.


Prophylactic effects of taurine and diltiazem, alone or combined, on reperfusion arrhythmias in rats

Acta Pharmacologica Sinica(China), 1996, 17/2 (122-124)

Aim: To study the effects of taurine (Tau) and diltiazem (Dil), alone or in combination, on reperfusion arrhythmias in anesthetized rats.

Methods: The arrhythmias were produced by coronary artery ligation for 15 min followed by reperfusion. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were measured by thiobarbituric acid fluorescence assay and colorimetric determination.


Results:

Taurine 70 mg . kg-1 in combination with Dil 1 mg . kg-1 were more effective on prevention of the reperfusion arrhythmias than each drug alone. The combination of both drugs not only decreased the content of MDA, but also increased the activity of SOD in reperfusion myocardium.


Conclusion:

The inhibition of lipoperoxides formation as well as the inhibition of the calcium influx was involved in the anti- arrhythmic effect of both taurine and diltiazem.


The antiarrhythmic effects of taurine alone and in combination with magnesium sulfate on ischemia/reperfusion arrhythmia

Chinese Pharmacological Bulletin (China), 1994, 10/5 (358- 362)

The effect of tauring (Taur) alone and in combination with magnesium sulfate (MgSO4) on ischemia/reperfusion arrhythmia was investigated. The arrhythmia as produced by coronary artery occlusion for 10 min followed by reperfusion. In addition, the present study also observed the effect of MgSO4 alone and in combination with Taur on hemodynamics. The results showed that Taur (50 mg . kg-1) and MgSO4 (25 mg . kg-1) had partly antiarrhythmic effect. Taur (100, 150mg. kg-1) MgSO4 (50, 100mg. kg-1) had significantly antiarrhythmic effect. Taur (50 mg. kg-1) combined with MgSO4 (25 mg. kg-1) shortened the duration of ventricular tachycardia (VT) more than that either drug did alone. The hypotensive effect of MgSO4 (25 mg. kg-1) was not increased by coadministration of Taur, but the myocardial oxygen consumption was reduced. These findings indicate that Taur in combination with MgSO4 is more effect on reperfusion arrhythmia, and that the mechanism of antiarrhythmic effect of Taur and MgSO4 may be involved in the effect of defence on myocardium.