Three distinct mechanisms generate oxygen free radicals in neurons and contribute to cell death during anoxia and reoxygenation. Mechanisms underlying the loss of mitochondrial membrane potential in glutamate excitotoxicity. MELAS: mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes ND6: NADH-ubiquinone oxidoreductase chain 6 mt IS: motochodrial intermembrane space mtIM: mitochondrial inner membrane LS: light strand HS: heavy strand.Ībramov AY, Duchen MR. On the other hand, taurine deficiency has normal aminoacylation of tRNA Leu(UUR) by leucine, but exhibits reduced formation of the taurine conjugate of τm 5UAA-tRNA Leu(UUR), which also prevents decoding of mitochondrial ND6 mRNA, resulting in increased superoxide generation and reduced ATP generation. Both reduced aminoacylation of tRNA Leu(UUR) by leucine and formation of the taurine conjugate of τm 5UAA-tRNA Leu(UUR) prevent decoding of mitochondrial UUG-dependent proteins, including ND6, which is one of 44 protein subunits of complex I of the electron transport chain located in the mitochondria inner membrane. MELAS patients also show reduced aminoacylation of taurine deficient tRNA Leu(UUR) by leucine catalyzed by aminoacyl-tRNA synthetase (AS). The mutation in MELAS alters the structure of the tRNA Leu(UUR) preventing the conjugation of taurine with the uridine base of the UAA anti-codon from forming 5-taurinomethyluridine (τm 5U). The gene of tRNA Leu(UUR) responsible for MELAS is located adjacent to ND1. In mtDNA, ND genes are shown in red color and tRNA genes are depicted as blue circles. Most of the point mutations of MELAS with 80% frequency occur at A3243G while mutations at T3271C exist with 10% frequency. The mitochondrial disease, MELAS, is caused by specific point mutations in mitochondrial DNA (mtDNA) that codes for tRNA Leu(UUR). CNS: central nervous system FXS: fragile X syndrome SSDD: succinic semialdehyde dehydrogenase deficiency MELAS: mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes.Ĭomparison of MELAS and taurine deficiency in mitochondria. Taurine prevents sarcopenia in aged person by minimizing gradual muscle loss. Taurine depletion or taurine transporter KO leads to cardiac and skeletal muscle dysfunction. The anti-inflammatory activity of taurine involves either the formation of taurochloramine in neutrophils or the attenuation of nitric oxide and prostaglandin E2 in inflammatory diseases, such as rheumatoid arthritis and osteoarthritis. Supplementation of taurine ameliorates symptoms of MELAS and diabetes mellitus. Protection of the cardiovascular system by taurine occurs through regulation of cell signaling, such as Ca 2+ transport, ROS generation and protein phosphorylation. Taurine protects CNS by decreasing ER stress and antagonizing neurotransmitter receptors of GABA A, glycine and NMDA. High concentrations of taurine in most cells regulate physiological function of excitable tissues and mitochondria. Taurine-mediated protection against pathology and disease. The review also addresses the functions of taurine (regulation of antioxidation, energy metabolism, gene expression, ER stress, neuromodulation, quality control and calcium homeostasis) underlying these therapeutic actions.Īntioxidation Cytoprotection ER stress MELAS Neurodegenerative diseases Taurine. In addition, taurine is extremely effective in the treatment of the mitochondrial disease, mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and offers a new approach for the treatment of metabolic diseases, such as diabetes, and inflammatory diseases, such as arthritis. The present review summarizes studies supporting a role of taurine in the treatment of diseases of muscle, the central nervous system, and the cardiovascular system. Today, taurine has been approved for the treatment of congestive heart failure in Japan and shows promise in the treatment of several other diseases. The discovery that taurine is an effective therapy against congestive heart failure led to the study of taurine as a therapeutic agent against other disease conditions. These findings have spurred interest in the potential use of taurine as a therapeutic agent. In some species, taurine is an essential nutrient but in man it is considered a semi-essential nutrient, although cells lacking taurine show major pathology. Taurine is an abundant, β-amino acid with diverse cytoprotective activity.
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