Disease relevance of Taurocyamine

• Guanidinoethanesulfonic acid (GES) is known to induce convulsive seizures when administered intracisternally to rabbits and cats [1].
• Taurocyamine-utilizing mutants from a wild-type strain of Pseudomonas [2].
• Pretreatment with guanidinoethane sulfonate, a competitive antagonist for beta-amino acid transport, as a 1% drinking solution for ten days led to a significant reduction in brain-cell dehydration [3].
• Plasma levels of taurocyamine, guanidinosuccinic acid, alpha-N-acetyl-L-arginine, creatine, guanidinobutyric acid, guanidine, and methylguanidine were significantly increased in patients with chronic renal failure with or without hemodialysis [4].

Psychiatry related information on Taurocyamine

• On the other hand, the antiepileptic potency of phenobarbital and phenytoin against tonic convulsions of maximal electroshock seizures in mice was significantly lessened by chronic administration of guanidinoethane sulfonate [5].

High impact information on Taurocyamine

• Guanidinoacetic acid, guanidinosuccinic acid, guanidinobutyric acid, guanidine, methylguanidine, taurocyamine, and arginine can be detected and quantitated in both plasma and erythrocytes from healthy individuals [6].
• Taurine-deficient cultured cerebellar astrocytes and granule neurons obtained by treatment with guanidinoethane sulfonate [7].
• Taurocyamine in cerebrospinal fluid of neurological and psychiatric patients [8].
• Guanidinoethane sulfonate had no effect on the tissue:serum ratio of radioactivity in brain, thymus, muscle or pancrease 24 hours after an injection of [3H]taurine [9].
• These results indicate that guanidinoethyl sulfonate can modulate extracellular amino acid levels in the nucleus accumbens [10].

Biological context of Taurocyamine

• Both, taurine depletion and impairment of cell migration induced by GES were prevented by adding taurine to the culture medium [11].
• Compared to controls, the duration of ventricular muscle action potentials was significantly increased in GES-treated rats, and this accounted for the prolongation of QT intervals [12].
• Comparative structural studies of the active site of ATP: guanidine phosphotransferases. The essential cysteine tryptic peptide of taurocyamine kinase from Arenicola marina [13].
• These observations suggest that the enzyme of the mutant capable of hydrolyzing taurocyamine has emerged from guanidinobutyrase of the wild-type strain which hydrolyzes taurocyamine at a very low rate, probably as a result of a point mutation in the structural gene [2].

Anatomical context of Taurocyamine

• Taurine and the taurine analogue guanidinoethanesulfonic acid interact with octopamine receptors of cockroach hemocytes to decrease octopamine-stimulated cAMP production [14].

Associations of Taurocyamine with other chemical compounds

• Convulsions and brain levels of amino acids and 5-hydroxytryptamine (5-HT) in E1 mice were examined after oral administration of a 1% guanidinoethane sulfonate (GES) solution [15].

Gene context of Taurocyamine

• Increased seizure susceptibility induced by guanidinoethane sulfonate in E1 mice and its relation to glutamatergic neurons [15].

Analytical, diagnostic and therapeutic context of Taurocyamine

• Intraperitoneal injection of [35S]taurine into lactating rats leads to the appearance of label in the milk, and the dpm/ml milk are significantly decreased by treatment with guanidinoethyl sulfonate (GES), an analog of taurine [16].
• Male C57BL/6 mice were divided into 3 groups: control group (HC), 1% taurine-supplemented group (HCT+), and taurine-deficient group (HCT-) produced by supplying 0.5% guanidinoethyl sulfonate (GES) solution ad libitum instead of water [17].

References