Taurine in the central nervous system and the mammalian actions of taurine

Intense exercise is thought to increase oxidative stress and damage muscle tissue. Taurine is present in high concentration in skeletal muscle and may play a role in cellular defenses against free radical-mediated damage. The aim of this study was to determine if manipulating muscle levels of taurine would alter markers of free radical damage after exercise-induced injury. Adult male Sprague-Dawley rats were supplemented via the drinking water with either 3% (w/v) taurine (n = 10) or the competitive taurine transport inhibitor, β-alanine (n = 10), for one month. Controls (n = 20) drank tap water containing 0.02% taurine and all rats were placed on a taurine free diet. All the rats except one group of sedentary controls (n = 10) were subjected to 90 minutes of downhill treadmill running. Markers of cellular injury and free radical damage were determined along with tissue amino acid content. The 3% taurine treatment raised plasma levels about 2-fold and 3% β-alanine reduced plasma taurine levels about 50%. Taurine supplementation (TS) significantly increased plasma glutamate levels in exercised rats. Exercise reduced plasma methionine levels and taurine prevented its decline. Taurine supplementation increased muscle taurine content significantly in all muscles except the soleus. β-alanine decreased muscle taurine content about 50% in all the muscles examined. Lipid peroxidation (TBARS) was significantly increased by exercise in the extensor digitorium longus (EDL) and gastrocnemius (GAST) muscles. Both taurine and β-alanine completely blocked the increase in TBARs in the EDL, but had no effect in the GAST. Muscle content of the cytosolic enzyme, lactate dehydrogenase (LDH) was significantly decreased by exercise in the GAST muscle and this effect was attenuated by both taurine and β-alanine. Muscle myeloperoxidase (MPO) activity was significantly elevated in the gastrocnemius muscle, but diet had no effect. MPO activity was significantly increased by exercise in the liver and both taurine and β-alanine blocked this effect. There was no effect of either exercise or the diets on MPO activity in the lung or spleen. Running performance as assessed by a subjective rating scale was improved by taurine supplementation and there was a significant loss in body weight in the β-alanine-treated rats 24 hours after exercise. In summary, taurine supplementation or taurine depletion had measurable cytoprotective actions to attenuate exercise-induced injury.

The cytoprotective role of taurine in exercise-induced muscle injury.

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.510260102

Cytotoxicity of bile salts against biliary epithelium: A study in isolated bile ductule fragments and isolated perfused rat liver

Taurine (2-aminoethylsulfonic acid) has many physiological and pharmacological functions in most tissues. It is abundantly maintained in the liver by both endogenous biosynthesis and exogenous transport, but is decreased in liver diseases. In the hepatic lobule, there are heterogeneous differences in metabolism between the pericentral (PC) and periportal regions, and the distributions of the biosynthesis capacity and specific taurine transporter expression are predominantly in the PC region. In cases of depletion of hepatic taurine level, serious liver damages were observed in the PC region. Taurine has protective effects against xenobiotics-induced liver damages in the PC region, but not xenobiotics-induced PP region damages. The xenobiotics that injure the PC region are mainly catabolized by NADPH-dependent cytochrome P450 2E1 that is also predominantly expressed in the PC region. Taurine treatment seems to be a useful agent for CYP2E1-related liver diseases with predominant damages in the PC region.

Taurine and liver diseases: a focus on the heterogeneous protective properties of taurine

Rats fed a reduced sulfur amino acid diet (LTD) or a high-taurine diet (HTD) demonstrate a renal adaptive response The LTD results in hypotaurinuria and enhanced brush border membrane vesicle (BBMV) accumulation of taurine The HTD causes hypertaurinuria and reduced BBMV uptake This adaptation may relate to changes in plasma or renal cortex taurine concentration Rats were fed a normal-taurine diet (NTD), LTD, or HTD for 14 d or they underwent: (a) 3% beta-alanine for the last 8 d of each diet; (b) 3 d of fasting; or (c) a combination of 3% beta-alanine added for 8 d and 3 d of fasting Each maneuver lowered the cortex taurine concentration, but did not significantly lower plasma taurine values compared with controls Increased BBMV taurine uptake occurred after each manipulation Feeding 3% glycine did not alter the plasma, renal cortex, or urinary taurine concentrations, or BBMV uptake of taurine Feeding 3% methionine raised plasma and urinary taurine excretion but renal tissue taurine was unchanged, as was initial BBMV uptake Hence, nonsulfur-containing alpha-amino acids did not change beta-amino acid transport The increase in BBMV uptake correlates with the decline in renal cortex and plasma taurine content However, since 3% methionine changed plasma taurine without altering BBMV uptake, it is more likely that the change in BBMV uptake and the adaptive response expressed at the brush border surface relate to changes in renal cortex taurine concentrations Finally, despite changes in urine and renal cortex taurine content, brain taurine values were unchanged, which suggests that this renal adaptive response maintains stable taurine concentrations where taurine serves as a neuromodulator

https://dm5migu4zj3pb.cloudfront.net/manuscripts/112000/112230/JCI85112230.pdf

Renal cortex taurine content regulates renal adaptive response to altered dietary intake of sulfur amino acids.

Taurine mobilizing effects of beta alanine and other inhibitors of taurine transport

Although high levels of taurine occur in heart and other tissues of a wide variety of species (Jacobsen and Smith, 1968; Kocsis et al., 1976), the function(s) of taurine in these extrahepatic tissues is not well established. Development of methods to reduce tissue taurine levels should prove useful in determining the functional roles of tissue (intracellular) as opposed to plasma (extracellular) taurine. A basis for developing such a method is the use of structural analogues of taurine that inhibit taurine transport. Among analogues known to inhibit taurine transport in vitro are beta-alanine, the carboxylic acid analogue of taurine; γ-aminobutyric acid (GABA), the homologue of beta-alanine; and taurocyamine, the guanidino analogue of taurine (Goldman and Scriver, 1967; Gaut and Nauss, 1976; Grosso et al., 1978). Beta-alanine has been shown to greatly increase the urinary excretion of taurine in mice (Gilbert et al., 1960) and rats (Kocsis and Kostos, 1963; Shaffer and Kocsis, 1978). The hypertaurinuria induced by such taurine analogues measures their ability to mobilize tissue taurine, since taurine displayed from tissue into plasma is not reabsorbed as efficiently by the renal tubules as other amino acids (Goldman and Scriver, 1967).

Methods of Reducing Tissue Taurine Levels

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Taurine mobilizing effects of beta alanine and other inhibitors of taurine transport

Methods of Reducing Tissue Taurine Levels