Difference between revisions of "Taurine"

Revision as of 19:00, 16 December 2015

Information on nutritional supplements people with ALS have been taking

Effects on ALS

Taurine inhibits apoptotic caspase-9 [1]. It counteracts increase of Bax and release of cytochrome c from mitochondria [2].

Source collection

Studies on ALS

References

[1] <bibtex> @article{Takatani2004, abstract = {Cardiomyocyte apoptosis contributes to cell death during myocardial infarction. One of the factors that regulate the degree of apoptosis during ischemia is the amino acid taurine. To study the mechanism underlying the beneficial effect of taurine, we examined the interaction between taurine and mitochondria-mediated apoptosis using a simulated ischemia model with cultured rat neonatal cardiomyocytes sealed in closed flasks. Exposure to medium containing 20 mM taurine reduced the degree of apoptosis following periods of ischemia varying from 24 to 72 h. In the untreated group, simulated ischemia for 24 h led to mitochondrial depolarization accompanied by cytochrome c release. The apoptotic cascade was also activated, as evidenced by the activation of caspase-9 and -3. Taurine treatment had no effect on mitochondrial membrane potential and cytochrome c release; however, it inhibited ischemia-induced cleavage of caspase-9 and -3. Taurine loading also suppressed the formation of the Apaf-1/caspase-9 apoptosome and the interaction of caspase-9 with Apaf-1. These findings demonstrate that taurine effectively prevents myocardial ischemia-induced apoptosis by inhibiting the assembly of the Apaf-1/caspase-9 apoptosome.}, author = {Takatani, Tomoka and Takahashi, Kyoko and Uozumi, Yoriko and Shikata, Eriko and Yamamoto, Yasuhiro and Ito, Takashi and Matsuda, Takahisa and Schaffer, Stephen W and Fujio, Yasushi and Azuma, Junichi}, doi = {10.1152/ajpcell.00042.2004}, issn = {0363-6143}, journal = {American journal of physiology. Cell physiology}, keywords = {Animals,Animals, Newborn,Apoptosis,Apoptosis: drug effects,Apoptotic Protease-Activating Factor 1,Blotting, Western,Caspase 9,Caspases,Caspases: drug effects,Cells, Cultured,Disease Models, Animal,Enzyme Activation,Enzyme Activation: drug effects,Enzyme Activation: physiology,In Situ Nick-End Labeling,Ischemia,Ischemia: drug therapy,Ischemia: physiopathology,Membrane Potentials,Membrane Potentials: drug effects,Membrane Potentials: physiology,Mitochondria, Heart,Mitochondria, Heart: drug effects,Mitochondria, Heart: pathology,Myocytes, Cardiac,Myocytes, Cardiac: drug effects,Myocytes, Cardiac: pathology,Precipitin Tests,Proteins,Proteins: drug effects,Rats,Rats, Wistar,Taurine,Taurine: pharmacology}, mendeley-groups = {taurine}, month = oct, number = {4}, pages = {C949--53}, pmid = {15253891}, title = Template:Taurine inhibits apoptosis by preventing formation of the Apaf-1/caspase-9 apoptosome., url = {http://ajpcell.physiology.org/content/287/4/C949}, volume = {287}, year = {2004} } </bibtex>

[2] <bibtex> @article{Sun2011, abstract = {Taurine, an abundant amino acid in the nervous system, is reported to reduce ischemic brain injury in a dose-dependent manner. This study was designed to investigate whether taurine protected brain against experimental stroke through affecting mitochondria-mediated cell death pathway. Rats were subjected to 2-h ischemia by intraluminal filament, and then reperfused for 22 h. It was confirmed again that taurine (50 mg/kg) administered intravenously 1 h after ischemia markedly improved neurological function and decreased infarct volume at 22 h after reperfusion. In vehicle-treated rats, the levels of intracellular ATP and the levels of cytosolic and mitochondrial Bcl-xL in the penumbra and core were markedly reduced, while the levels of cytosolic Bax in the core and mitochondrial Bax in the penumbra and core were enhanced significantly. There was a decrease in cytochrome C in mitochondria and an increase in cytochrome C in the cytosol of the penumbra and core. These changes were reversed by taurine. Furthermore, taurine inhibited the activation of calpain and caspase-3, reduced the degradation of $\alpha$II-spectrin, and attenuated the necrotic and apoptotic cell death in the penumbra and core. These data demonstrated that preserving the mitochondrial function and blocking the mitochondria-mediated cell death pathway may be one mechanism of taurine's action against brain ischemia.}, author = {Sun, Ming and Gu, Yi and Zhao, Yumei and Xu, Chao}, doi = {10.1007/s00726-010-0751-8}, issn = {1438-2199}, journal = {Amino acids}, keywords = {Adenosine Triphosphate,Adenosine Triphosphate: analysis,Adenosine Triphosphate: metabolism,Animals,Brain Ischemia,Brain Ischemia: drug therapy,Brain Ischemia: metabolism,Brain Ischemia: pathology,Calpain,Calpain: metabolism,Caspase 3,Caspase 3: metabolism,Cell Death,Cell Death: drug effects,Cerebral Infarction,Cerebral Infarction: drug therapy,Cerebral Infarction: metabolism,Cerebral Infarction: pathology,Cytochromes c,Cytochromes c: metabolism,Disease Models, Animal,Dose-Response Relationship, Drug,Male,Mitochondria,Mitochondria: drug effects,Mitochondria: metabolism,Nervous System Diseases,Nervous System Diseases: drug therapy,Nervous System Diseases: metabolism,Nervous System Diseases: pathology,Rats,Rats, Sprague-Dawley,Stroke,Stroke: metabolism,Stroke: pathology,Stroke: prevention \& control,Taurine,Taurine: administration \& dosage,Taurine: metabolism,Taurine: pharmacology,bcl-2-Associated X Protein,bcl-2-Associated X Protein: metabolism,bcl-X Protein,bcl-X Protein: metabolism}, mendeley-groups = {taurine}, month = may, number = {5}, pages = {1419--29}, pmid = {20862501}, title = Template:Protective functions of taurine against experimental stroke through depressing mitochondria-mediated cell death in rats., url = {http://www.ncbi.nlm.nih.gov/pubmed/20862501}, volume = {40}, year = {2011} } </bibtex>