Taurine is a fundamental mediator of homeostasis that exerts multiple roles to confer protection against oxidant stress. The development of hypertension, muscle/neuro‑​associated disorders, hepatic cirrhosis, cardiac dysfunction and ischemia/reperfusion are examples of some injuries that are linked with oxidative stress. The present review gives a comprehensive description of all the underlying mechanisms of taurine, with the aim to explain its anti‑oxidant actions. Taurine is regarded as a cytoprotective molecule due to its ability to sustain normal electron transport chain, maintain glutathione stores, upregulate anti‑oxidant responses, increase membrane stability, eliminate inflammation and prevent calcium accumulation. In parallel, the synergistic effect of taurine with other potential therapeutic modalities in multiple disorders are highlighted. Apart from the results derived from research findings, the current review bridges the gap between bench and bedside, providing mechanistic insights into the biological activity of taurine that supports its potential therapeutic efficacy in clinic. In the future, further clinical studies are required to support the ameliorative effect of taurine against oxidative stress.

/pdf/protective-role-of-taurine-against-oxidative-stress-review-fysxic5or5.pdf

Protective role of taurine against oxidative stress (Review).

Taurine is a nonproteinogenic s-aminosulfonic acid. Important dietary sources of taurine are fish and seafood. Taurine interacts with ion channels, stabilizes membranes, and regulates the cell volume. These actions confirm its high concentrations in excitable tissues like retina, neurons, and muscles. Retinal degeneration, cardiomyopathy, as well as skeletal muscle malfunction are evident in taurine-deficient phenotypes. There is evidence that taurine counteracts lipid peroxidation and increases cellular antioxidant defense in response to inflammation. In activated neutrophils, taurine reacts with hypochloric acid to form taurine chloramine, which triggers the Kelch-like ECH-associated protein 1-nuclear factor E2-related factor 1 (Keap1-Nrf2) pathway. Consequently, Nrf2 target genes, such as heme oxygenase-1 and catalase, are induced. Furthermore, taurine may prevent an overload of reactive oxygen species (ROS) directly by an inhibition of ROS generation within the respiratory chain. Taurine affects mitochondrial bioenergetics and taurine-deficient mice exhibit an impaired exercise performance. Moreover, some studies demonstrate that taurine enhances the glycogen repletion in the postexercise recovery phase. In the case of taurine deficiency, many studies observed a phenotype known in muscle senescence and skeletal muscle disorders. Overall, taurine plays an important role in cellular redox homeostasis and skeletal muscle function.

Taurine: a regulator of cellular redox homeostasis and skeletal muscle function.

Glutathione (GSH) is a critical endogenous antioxidant found in all eukaryotic cells. Higher GSH concentrations protect against cellular damage, tissue degeneration, and disease progression in various models, so there is considerable interest in developing interventions that augment GSH biosynthesis. Oral GSH supplementation is not the most efficient option due to the enzymatic degradation of ingested GSH within the intestine by γ-glutamyltransferase, but supplementation of its component amino acids—cysteine, glycine, and glutamate—enhances tissue GSH synthesis. Furthermore, supplementation with some non-precursor amino acids and micronutrients appears to influence the redox status of GSH and related antioxidants, such as vitamins C and E, lowering systemic oxidative stress and slowing the rate of tissue deterioration. In this review, the effects of oral supplementation of amino acids and micronutrients on GSH metabolism are evaluated. And since specific dietary patterns and diets are being prescribed as first-line therapeutics for conditions such as hypertension and diabetes, the impact of overall diets on GSH homeostasis is also assessed.

https://www.mdpi.com/2072-6643/11/5/1056/pdf

Impact of Supplementary Amino Acids, Micronutrients, and Overall Diet on Glutathione Homeostasis

Oxidative stress contributes to the development of acute damage to the ischemia-reperfused heart and to ventricular remodeling ending in congestive heart failure, conditions associated with high mortality rates in man. There is evidence that taurine protects against these cardiovascular diseases, in part by limiting the degree of oxidative stress. Among other effects, oxidative stress disrupts myocardial Ca2+ handling, enhances cardiomyocyte loss and initiates a vicious cycle of reactive oxygen species (ROS) generation.

Role of ROS Production and Turnover in the Antioxidant Activity of Taurine.

The effects of oxidative stress occur as a result of peroxidative damage of the macromolecule and membranes of the cells and with the disruption of metabolic activities in the components of the cells in living organisms. Organ and tissue pathologies are known to occur when oxidative stress is excessive in the body. It is known that thiols are one of the main protective mechanisms of the body against oxidative stress. Thiols have been shown to play important roles in enzymatic reactions, apoptosis, detoxification and antioxidant protection in the body. Many studies have shown changes in thiol status and thiol/disulphide homeostasis in various diseases such as digestive system, respiratory system, reproductive system, urinary system, metabolic diseases and cancer. This also shows that the thiol state is very important in the pathogenesis of oxidative stress-mediated diseases. Therefore, it is thought that interventions that can improve thiol status may contribute to the prevention or treatment of oxidative stress-related diseases.

/pdf/thiols-role-in-oxidative-stress-related-disorders-esbrs9wnw7.pdf

Thiols: Role in Oxidative Stress-Related Disorders

The aim of the present study is to investigate the effects of oral administration of taurine on endogenous glutathione peroxidase (GPx) and Glutathione Reductase (GR) activities and reduced glutathione (GSH) level in normal rats. Normal saline (Group I) or 5% taurine in normal saline was administered in dose of 50 mg (Group II), 250 mg (Group III) or 500 mg kg(-1) of body weight (Group IV) through intragastric intubation for 60 days. GPx and GR enzyme activities and GSH and taurine levels were determined in liver, heart, stomach, kidney and plasma of normal Wistar rats. GPx activity showed an increase in liver, heart, stomach and plasma. GR activity increased in kidney and decreased in liver and plasma. GSH levels increased in liver, stomach and decreased in kidney. Liver showed an increase and heart, stomach and kidney a decrease in taurine level in taurine administered rats when compared to control rats. The results varied from organ to organ and the observed variations among organs might be related to their respective enzymatic, non-enzymatic antioxidant potential and its functions. From the present study it may be concluded that long term oral administration of taurine affects GPx, GR and GSH levels in normal rats.

Effects of taurine on glutathione peroxidase, glutathione reductase and reduced glutathione levels in rats.

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Effects of taurine on glutathione peroxidase, glutathione reductase and reduced glutathione levels in rats.