Effects and Mechanisms of Taurine as a Therapeutic Agent

Stephen Schaffer, Ha Won Kim, Stephen Schaffer, Ha Won Kim

Abstract

Taurine is an abundant, β-amino acid with diverse cytoprotective activity. 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. These findings have spurred interest in the potential use of taurine as a therapeutic agent. 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. 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 present review summarizes studies supporting a role of taurine in the treatment of diseases of muscle, the central nervous system, and the cardiovascular system. 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 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.

Keywords: Antioxidation; Cytoprotection; ER stress; MELAS; Neurodegenerative diseases; Taurine.

Figures

Fig. 1.
Fig. 1.
Taurine-mediated protection against pathology and disease. High concentrations of taurine in most cells regulate physiological function of excitable tissues and mitochondria. Taurine protects CNS by decreasing ER stress and antagonizing neurotransmitter receptors of GABAA, glycine and NMDA. Protection of the cardiovascular system by taurine occurs through regulation of cell signaling, such as Ca2+ transport, ROS generation and protein phosphorylation. Supplementation of taurine ameliorates symptoms of MELAS and diabetes mellitus. 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. Taurine depletion or taurine transporter KO leads to cardiac and skeletal muscle dysfunction. Taurine prevents sarcopenia in aged person by minimizing gradual muscle loss. CNS: central nervous system; FXS: fragile X syndrome; SSDD: succinic semialdehyde dehydrogenase deficiency; MELAS: mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes.
Fig. 2.
Fig. 2.
Comparison of MELAS and taurine deficiency in mitochondria. The mitochondrial disease, MELAS, is caused by specific point mutations in mitochondrial DNA (mtDNA) that codes for tRNALeu(UUR). Most of the point mutations of MELAS with 80% frequency occur at A3243G while mutations at T3271C exist with 10% frequency. In mtDNA, ND genes are shown in red color and tRNA genes are depicted as blue circles. The gene of tRNALeu(UUR) responsible for MELAS is located adjacent to ND1. The mutation in MELAS alters the structure of the tRNALeu(UUR) preventing the conjugation of taurine with the uridine base of the UAA anti-codon from forming 5-taurinomethyluridine (τm5U). MELAS patients also show reduced aminoacylation of taurine deficient tRNALeu(UUR) by leucine catalyzed by aminoacyl-tRNA synthetase (AS). Both reduced aminoacylation of tRNALeu(UUR) by leucine and formation of the taurine conjugate of τm5UAA-tRNALeu(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. On the other hand, taurine deficiency has normal aminoacylation of tRNALeu(UUR) by leucine, but exhibits reduced formation of the taurine conjugate of τm5UAA-tRNALeu(UUR), which also prevents decoding of mitochondrial ND6 mRNA, resulting in increased superoxide generation and reduced ATP generation. 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.

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