AOR^TM certifie qu'aucun ingrédient non mentionné sur l'étiquette n'a été ajouté au produit. Ne contient ni blé, ni gluten, ni maïs, ni noix, ni produits laitiers, ni soja, ni œufs, ni poissons, ni mollusques ou crustacés.

Posologie Adulte: Prendre 1capsule 3 fois par jour ou suivre les recommandations d'un professionnel de la santé qualifié.

Mise en Garde: Consulter un praticien de la santé avant d'utiliser ce produit si vous prenez des médications prescripts ou êtes enceinte ou allaitez.

Applications:
Antioxydant, Amélioration des fonctions immunitaire et cardiaque, Agent détoxifiant

Source:
Produit pharmaceutique de synthèse

La taurine est un acide aminé peu usuel, dû à sa structure chimique unique, qui a une base de soufre par opposition à la base de carbone habituelle. La taurine est décrite comme " conditionnellement essentielle " car bien qu'elle soit essentielle au bon fonctionnement du coeur, des yeux et du cerveau, elle est produite dans le corps à partir de la L-cystéine.

Bon nombre de scientifiques croient que les quantités de taurine que nous produisons ne sont pas suffisantes pour assurer une santé optimale. La taurine agit en tant qu'émulsifiant des lipides et facilite leur absorption. La taurine est également un antioxydant et un stabilisateur de membranes cellulaires.

La taurine est le deuxième acide aminé le plus abondant dans notre corps, et la taurine est l'acide aminé le plus abondant dans le coeur. La taurine a été employée au Japon pour le traitement de divers types de problèmes cardiaques, y compris la congestion cardiaque, les arythmies, la diurèse et l'hypertension. Une étude faite sur 24 sujets souffrant de congestion cardiaque à démontré que l'administration de 2 grammes de taurine, deux fois par jour, a amélioré les symptômes cliniques de 19 d'entre eux. Ces résultats positifs ont été confirmés lors d'une étude clinique dans laquelle la taurine a été combinée à un traitement standard pendant un mois. Comparé au groupe recevant le placebo, la taurine a produit une " amélioration significative " telle qu'évaluée par un certain nombre de tests, y compris des radiographies de la poitrine.

References

Wright, C.E. et al., (1996). Taurine: Biological update. Ann Rev Biochem55: 427-448.

Azuma J, Sawamura A, Awata N, Ohta H, Hamaguchi T, Harada H, Takihara K, Hasegawa H, Yamagami T, Ishiyama T, et al. (1985), Therapeutic effect of taurine in congestive heart failure: a double-blind crossover trial. Clin Cardiol 8(5): 276-82.

Sole MJ, Jeejeebhoy KN. Conditioned nutritional requirements: therapeutic relevance to heart failure. Herz 2002 Mar; 27(2): 174-8.

Saransaari P, Oja SS. Taurine and neural cell damage. Amino Acids. 2000; 19(3-4): 509-26.

Azuma J, Sawamura A, Awata N. Usefulness of taurine in chronic congestive heart failure and its prospective application. Jpn Circ J. 1992 Jan; 56(1): 95-9.

Fujita T, Ando K, Noda H, Ito Y, Sato Y. Effects of increased adrenomedullary activity and taurine in young patients with borderline hypertension. Circulation. 1987 Mar; 75(3): 525-32.

Copyright © 2005, Advanced Orthomolecular Research  

Taurine and neural cell damage.
Amino Acids. 2000; 19(3-4): 509-26.
Saransaari P, Oja SS.

The inhibitory amino acid taurine is an osmoregulator and neuromodulator, also exerting neuroprotective actions in neural tissue. We review now the involvement of taurine in neuron-damaging conditions, including hypoxia, hypoglycemia, ischemia, oxidative stress, and the presence of free radicals, metabolic poisons and an excess of ammonia. The brain concentration of taurine is increased in several models of ischemic injury in vivo. Cell-damaging conditions which perturb the oxidative metabolism needed for active transport across cell membranes generally reduce taurine uptake in vitro, immature brain tissue being more tolerant to the lack of oxygen. In ischemia nonsaturable diffusion increases considerably. Both basal and K+-stimulated release of taurine in the hippocampus in vitro is markedly enhanced under cell-damaging conditions, ischemia, free radicals and metabolic poisons being the most potent. Hypoxia, hypoglycemia, ischemia, free radicals and oxidative stress also increase the initial basal release of taurine in cerebellar granule neurons, while the release is only moderately enhanced in hypoxia and ischemia in cerebral cortical astrocytes. The taurine release induced by ischemia is for the most part Ca2+-independent, a Ca2+-dependent mechanism being discernible only in hippocampal slices from developing mice. Moreover, a considerable portion of hippocampal taurine release in ischemia is mediated by the reversal of Na+-dependent transporters. The enhanced release in adults may comprise a swelling-induced component through Cl- channels, which is not discernible in developing mice. Excitotoxic concentrations of glutamate also potentiate taurine release in mouse hippocampal slices. The ability of ionotropic glutamate receptor agonists to evoke taurine release varies under different cell-damaging conditions, the N-methyl-D-aspartate-evoked release being clearly receptor-mediated in ischemia. Neurotoxic ammonia has been shown to provoke taurine release from different brain preparations, indicating that the ammonia-induced release may modify neuronal excitability in hyperammonic conditions. Taurine released simultane ously with an excess of excitatory amino acids in the hippocampus under ischemic and other neuron-damaging conditions may constitute an important protective mechanism against excitotoxicity, counteracting the harmful effects which lead to neuronal death. The release of taurine may prevent excitation from reaching neurotoxic levels.


Usefulness of taurine in chronic congestive heart failure and its prospective application.
Jpn Circ J. 1992 Jan; 56(1): 95-9.
Azuma J, Sawamura A, Awata N.

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.


Effects of increased adrenomedullary activity and taurine in young patients with borderline hypertension.
Circulation. 1987 Mar; 75(3): 525-32.
Fujita T, Ando K, Noda H, Ito Y, Sato Y.

Recent studies showed that taurine, a sulphonic amino acid, could decrease blood pressure and increase sympathoadrenal tone in DoCA-salt-treated hypertensive rats. To determine whether taurine exerts its antihypertensive action in man in a similar fashion, we studied the effect of oral administration of taurine (6 g for 7 days) on blood pressure and plasma catecholamines in 19 young patients with borderline hypertension in a double-blind, placebo-controlled fashion. Systolic blood pressure in the 10 patients who were treated with taurine decreased by 9.0 +/- 2.9 mm Hg (mean +/- SE; p less than .05 by paired t test), compared with a 2.7 +/- 2.3 mm Hg decrease (NS) in the nine patients treated with placebo and diastolic blood pressure in the taurine-treated patients decreased by 4.1 +/- 1.7 mm Hg (p less than .05) compared with 1.2 +/- 3.0 mm Hg (NS) in the placebo-treated subjects. In the patients receiving taurine plasma epinephrine (E) decreased significantly, with a negligible decrease in plasma norepinephrine (NE). The effect of taurine on plasma catecholamines and the response of plasma E after the stimulation with glucagon was also studied in 12 borderline hypertensive and nine age-matched normotensive subjects. Basal plasma E was significantly higher in borderline hypertensive than in normal subjects, but basal plasma NE did not differ in the two groups.

Copyright © 2005, Advanced Orthomolecular Research