Taurine Abstracts 7

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Taurine chloramine produced from taurine under inflammation provides anti-inflammatory and cytoprotective effects.
            (Kim and Cha, 2014) Download
Taurine is one of the most abundant non-essential amino acid in mammals and has many physiological functions in the nervous, cardiovascular, renal, endocrine, and immune systems. Upon inflammation, taurine undergoes halogenation in phagocytes and is converted to taurine chloramine (TauCl) and taurine bromamine. In the activated neutrophils, TauCl is produced by reaction with hypochlorite (HOCl) generated by the halide-dependent myeloperoxidase system. TauCl is released from activated neutrophils following their apoptosis and inhibits the production of inflammatory mediators such as, superoxide anion, nitric oxide, tumor necrosis factor-α, interleukins, and prostaglandins in inflammatory cells at inflammatory tissues. Furthermore, TauCl increases the expressions of antioxidant proteins, such as heme oxygenase 1, peroxiredoxin, thioredoxin, glutathione peroxidase, and catalase in macrophages. Thus, a central role of TauCl produced by activated neutrophils is to trigger the resolution of inflammation and protect macrophages and surrounding tissues from being damaged by cytotoxic reactive oxygen metabolites overproduced during inflammation. This is achieved by attenuating further production of proinflammatory cytokines and reactive oxygen metabolites and also by increasing the levels of antioxidant proteins that are able to scavenge and diminish the production of cytotoxic oxygen metabolites. These findings suggest that TauCl released from activated neutrophils may be involved in the recovery processes of cells affected by inflammatory oxidative stresses and thus TauCl could be used as a potential physiological agent to control pathogenic symptoms of chronic inflammatory diseases.

Taurine chloramine inhibits proliferation of rheumatoid arthritis synoviocytes by triggering a p53-dependent pathway.
            (Kontny et al., 2006) Download
OBJECTIVE AND DESIGN:  Taurine chloramine (Tau-Cl), originating from activated neutrophils, possesses antiinflammatory activities. Fibroblast-like synoviocytes (FLS) participate in the chronic synovitis and synovial membrane hyperplasia that are characteristic pathological features of rheumatoid arthritis (RA). The present study was conducted to investigate the mechanism of the Tau-Cl effect on the proliferation of these cells in culture. MATERIALS AND METHODS:  FLS were stimulated in vitro with platelet derived growth factor (PDGF) alone or together with Tau-Cl. Cell proliferation was evaluated by counting the total and dividing cell numbers and by measurement of (3)H-thymidine incorporation. Expression of the key cell-cycle regulators was evaluated at the protein (Western blotting) and/or mRNA (RT-PCR) levels. RESULTS:  Treatment of RA FLS with Tau-Cl (200-500 microM) resulted in an early nuclear accumulation of p53 tumor suppressor protein. Moreover, Tau-Cl inhibited PDGF-triggered cell proliferation (IC(50) value approximately 250-300 microM), accompanied by characteristic modulation of p53 transcriptional targets: down-regulation of proliferating cell nuclear antigen (PCNA) and survivin, and concomitant up-regulation of p21 mitotic inhibitor. CONCLUSION:  We propose that Tau-Cl inhibits proliferation of RA FLS by triggering a p53-dependent cell-cycle arrest and conclude that this compound suppresses pathways in FLS that are known to contribute to the pathology of RA.

Maternal taurine supplementation attenuates maternal fructose-induced metabolic and inflammatory dysregulation and partially reverses adverse metabolic programming in offspring.
            (Li et al., 2015) Download
Excessive fructose consumption is associated with insulin resistance (IR) and nonalcoholic fatty liver disease (NAFLD), and high fructose intake during pregnancy can lead to compromised fetal development in the rat. Evidence suggests that the amino acid taurine can ameliorate fructose-induced IR and NAFLD in nonpregnant animals. This study investigated the efficacy of taurine supplementation on maternal fructose-induced metabolic dysfunction and neonatal health. Time-mated Wistar rats were randomized to four groups during pregnancy and lactation: (a) control diet (CON), (b) CON supplemented with 1.5% taurine in drinking water (CT), (c) CON supplemented with fructose solution (F) and (d) F supplemented with taurine (FT). Maternal and neonatal weights, plasma cytokines and hepatic gene expression were analyzed. Maternal hyperinsulinemia, increased homeostasis model assessment of IR indices and elevated proinflammatory cytokines were observed in F group and normalized in FT group. Maternal fructose-induced hepatic steatosis accompanied with increased liver weight was ameliorated with taurine supplementation. Maternal hepatic sterol regulatory element-binding protein-1c and fatty acid synthase expression was significantly increased in the F group compared to the CON, CT and FT groups. Neonatal hepatic phosphoenolpyruvate carboxykinase expression was increased in male F neonates compared to the CON, CT and FT groups and was increased in female F and FT neonates compared to CON and CT. Interleukin-1β expression was decreased in male CT and FT neonates compared to other male groups. Hepatic tumour necrosis factor receptor-1 was lower in the male FT group than the F group. These results demonstrate that maternal taurine supplementation can partially reverse fructose-induced maternal metabolic dysfunction and may ameliorate adverse developmental programming effects in offspring in a sex-specific manner.

Taurine improves obesity-induced inflammatory responses and modulates the unbalanced phenotype of adipose tissue macrophages.
            (Lin et al., 2013) Download
SCOPE:  It is increasingly accepted that chronic inflammation is a feature of obesity. Obesity-induced inflammation triggers enhanced recruitment of macrophages into the adipose tissue. Depending on their phenotype, macrophages can be designated either as pro-inflammatory M1 macrophages or anti-inflammatory M2 macrophages. We have therefore investigated the effects of taurine, a sulfated amino acid that is abundant in seafood, on obesity-related inflammation. METHODS AND RESULTS:  In high-fat diet fed C57BL/6J mice, taurine treatment reduced the infiltration of macrophages and promoted an M2-like phenotype of macrophages in adipose tissues. In addition, taurine decreased the production of inflammatory cytokines, and suppressed the development of hyperglycemia in diet-induced obese mice. Moreover, in vitro experiments that involved bone marrow derived macrophages indicated that taurine treatment induced alternative M2 macrophage activation, and its chloride, taurine chloramines, inhibited classical M1 macrophage activation. CONCLUSION:  Our findings indicate that taurine treatment attenuates the infiltration of adipose tissue by macrophages and modulates the phenotype of macrophages, which suggest that taurine is a valuable food constituent with a potential to attenuate chronic inflammation in adipose tissue and improve obesity-related insulin resistance.

Taurine Attenuates Hepatic Inflammation in Chronic Alcohol-Fed Rats Through Inhibition of TLR4/MyD88 Signaling.
            (Lin et al., 2015) Download
Accumulating evidence indicates that overconsumption of ethanol contributes in many ways to the pathogenesis of hepatic injury. Although studies indicate that taurine decreases lipogenesis, oxidative stress, and inflammatory cytokines, the protective effect of taurine against alcohol-induced liver injury is still unclear. To clarify the precise signaling involved in the beneficial effect of taurine on alcohol-induced liver injury, rats were randomly divided into four treatment groups: (1) control (Ctl), (2) alcohol (Alc), (3) Alc+taurine (Tau), and (4) Alc+silymarin (Sil). The Tau and Sil groups had lower lymphocyte infiltration and significantly lower TLR-4/MyD88 and IκB/NFκB compared to the Alc group. The inducible nitric oxide synthase (iNOS), C-reactive protein (CRP), tumor necrosis factors (TNF)-α, interleukin (IL)-6, and IL-1β were also significantly lower in the Tau and Sil groups than in the Alc group. The experimental results indicated that hepatoprotection against alcohol-induced inflammation may be mediated by decreased TLR-4/MyD88 signaling.

Taurine prevents the neurotoxicity of beta-amyloid and glutamate receptor agonists: activation of GABA receptors and possible implications for Alzheimer's disease and other neurological disorders.
            (Louzada et al., 2004) Download
Alzheimer's disease (AD) and several other neurological disorders have been linked to the overactivation of glutamatergic transmission and excitotoxicity as a common pathway of neuronal injury. The beta-amyloid peptide (Abeta) is centrally related to the pathogenesis of AD, and previous reports have demonstrated that the blockade of glutamate receptors prevents Abeta-induced neuronal death. We show that taurine, a beta-amino acid found at high concentrations in the brain, protects chick retinal neurons in culture against the neurotoxicity of Abeta and glutamate receptor agonists. The protective effect of taurine is not mediated by interaction with glutamate receptors, as demonstrated by binding studies using radiolabeled glutamate receptor ligands. The neuroprotective action of taurine is blocked by picrotoxin, an antagonist of GABA(A) receptors. GABA and the GABA(A) receptor agonists phenobarbital and melatonin also protect neurons against Abeta-induced neurotoxicity. These results suggest that activation of GABA receptors decreases neuronal vulnerability to excitotoxic damage and that pharmacological manipulation of the excitatory and inhibitory neurotransmitter tonus may protect neurons against a variety of insults. GABAergic transmission may represent a promising target for the treatment of AD and other neurological disorders in which excitotoxicity plays a relevant role.

Taurine improves the spatial learning and memory ability impaired by sub-chronic manganese exposure.
            (Lu et al., 2014) Download
BACKGROUND:  Excessive manganese exposure induced cognitive deficit. Several lines of evidence have demonstrated that taurine improves cognitive impairment induced by numerous neurotoxins. However, the role of taurine on manganese-induced damages in learning and memory is still elusive. This goal of this study was to investigate the beneficial effect of taurine on learning and memory capacity impairment by manganese exposure in an animal model. RESULTS:  The escape latency in the Morris Water Maze test was significantly longer in the rats injected with manganese than that in the rats received both taurine and manganese. Similarly, the probe trial showed that the annulus crossings were significantly greater in the taurine plus manganese treated rats than those in the manganese-treated rats. However, the blood level of manganese was not altered by the taurine treatment. Interestingly, the exposure of manganese led to a significant increase in the acetylcholinesterase activity and an evidently decrease in the choline acetyltransferase activity, which were partially restored by the addition of taurine. Additionally, we identified 9 differentially expressed proteins between the rat hippocampus treated by manganese and the control or the manganese plus taurine in the proteomic analysis using the 2-dimensional gel electrophoresis followed by the tandem mass spectrometry (MS/MS). Most of these proteins play a role in energy metabolism, oxidative stress, inflammation, and neuron synapse. CONCLUSIONS:  In summary, taurine restores the activity of AChE and ChAT, which are critical for the regulation of acetylcholine. We have identified seven differentially expressed proteins specifically induced by manganese and two proteins induced by taurine from the rat hippocampus. Our results support that taurine improves the impaired learning and memory ability caused by excessive exposure of manganese.

Taurine ameliorates cholesterol metabolism by stimulating bile acid production in high-cholesterol-fed rats.
            (Murakami et al., 2016) Download
This study was designed to investigate the effects of dietary taurine on cholesterol metabolism in high-cholesterol-fed rats. Male Sprague-Dawley rats were randomly divided into two dietary groups (n = 6 in each group): a high-cholesterol diet containing 0.5% cholesterol and 0.15% sodium cholate, and a high-cholesterol diet with 5% (w/w) taurine. The experimental diets were given for 2 weeks. Taurine supplementation reduced the serum and hepatic cholesterol levels by 37% and 32%, respectively. Faecal excretion of bile acids was significantly increased in taurine-treated rats, compared with untreated rats. Biliary bile acid concentrations were also increased by taurine. Taurine supplementation increased taurine-conjugated bile acids by 61% and decreased glycine-conjugated bile acids by 53%, resulting in a significant decrease in the glycine/taurine (G/T) ratio. Among the taurine-conjugated bile acids, cholic acid and deoxycholic acid were significantly increased. In the liver, taurine supplementation increased the mRNA expression and enzymatic activity of hepatic cholesterol 7α-hydroxylase (CYP7A1), the rate-limiting enzyme for bile acid synthesis, by three- and two-fold, respectively. Taurine also decreased the enzymatic activity of acyl-CoA:cholesterol acyltransferase (ACAT) and microsomal triglyceride transfer protein (MTP). These observations suggest that taurine supplementation increases the synthesis and excretion of taurine-conjugated bile acids and stimulates the catabolism of cholesterol to bile acid by elevating the expression and activity of CYP7A1. This may reduce cholesterol esterification and lipoprotein assembly for very low density lipoprotein (VLDL) secretion, leading to reductions in the serum and hepatic cholesterol levels.

Protective effects of taurine on doxorubicin-induced acute hepatotoxicity through suppression of oxidative stress and apoptotic responses.
            (Nagai et al., 2016) Download
The organ toxicity of doxorubicin (DOX), an anthracycline antineoplastic agent, narrows the therapeutic window despite its clinical usefulness. In the present study, we determined whether taurine protected against DOX-induced hepatic injury, and explored the molecular mechanisms underlying the suppressive effects of taurine in terms of alterations in oxidative stress and apoptotic responses. DOX-induced body weight loss was completely suppressed by taurine treatment. Elevations in the serum activity levels of lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase by DOX were also dose-dependently attenuated by a concurrent treatment with taurine. Superoxide dismutase activity and reduced glutathione content in the liver were decreased following the administration of DOX, whereas these changes were suppressed when 10 mg/kg taurine was given in combination with DOX. Taurine attenuated the increased expression of mRNAs for Fas and Bax after DOX exposure. Furthermore, the formation of cleaved caspase-3 protein in the group given DOX with taurine was lower than that in the group treated with DOX alone. Our results suggest that taurine can protect against DOX-induced acute hepatic damage, the underlying mechanism of which is attributable to the suppression of oxidative stress and apoptotic responses.

Activation of glycine and extrasynaptic GABA(A) receptors by taurine on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis.
            (Nguyen et al., 2013) Download
The substantia gelatinosa (SG) of the trigeminal subnucleus caudalis (Vc) has been known for the processing and transmission of orofacial nociceptive information. Taurine, one of the most plentiful free amino-acids in humans, has proved to be involved in pain modulation. In this study, using whole-cell patch clamp technique, we investigated the direct membrane effects of taurine and the action mechanism behind taurine-mediated responses on the SG neurons of the Vc. Taurine showed non-desensitizing and repeatable membrane depolarizations and inward currents which remained in the presence of amino-acid receptors blocking cocktail (AARBC) with tetrodotoxin, indicating that taurine acts directly on the postsynaptic SG neurons. Further, application of taurine at different doses (10  μM to 3 mM) showed a concentration dependent depolarizations and inward currents with the EC50 of 84.3  μM and 723  μM, respectively. Taurine-mediated responses were partially blocked by picrotoxin (50  μM) and almost completely blocked by strychnine (2  μM), suggesting that taurine-mediated responses are via glycine receptor (GlyR) activation. In addition, taurine (1 mM) activated extrasynaptic GABA(A) receptor (GABA(A)R)-mediated currents. Taken together, our results indicate that taurine can be a target molecule for orofacial pain modulation through the activation of GlyRs and/or extrasynaptic GABA(A)Rs on the SG neurons.

Taurine and epilepsy.
            (Oja and Saransaari, 2013) Download
Dysfunction of excitatory and inhibitory neurotransmitters or neuromodulators is thought to underlie epileptic symptoms. Taurine, 2-aminoethanesulfonate, is a ubiquitous free amino acid abounding in the brain of humans and most animal species. It hyperpolarizes neurons and inhibits their firing. It may be a participating factor in certain subpopulations of epilepsy patients but its deficiency is not a universal prerequisite for seizures. Here, the participation of taurine in animal seizure models and human epilepsy patients is reviewed.

Potential protection of taurine on antioxidant system and ATPase in brain and blood of rats exposed to aluminum.
            (Qiao et al., 2015) Download
OBJECTIVES:  Taurine (Tau) is used in clinical treatments but its protection of brains against aluminum-induced oxidative damage has been explored for the first time. The positive effect of Tau was studied on the activities of antioxidant enzymes and ATPase. RESULTS:  Aluminum (Al) intake caused significant increasement of malondialdehyde (MDA) but reduction of the activities of superoxide dismutase, glutathione peroxidase (GSH-Px), Na(+)K(+)-ATPase and Mg(2+)-ATPase in brain compared to control group (P < 0.05). Tau administration, however, significantly reduced the MDA content, and increased the activities of aforementioned enzymes (P < 0.05). The MDA content was higher and the activities of GSH-Px, Ca(2+)-ATPase and Mg(2+)-ATPase lower in the blood of the Al-treated group' (P < 0.05), while Tau markedly decreased MDA content and improved the activities of GSH-Px and Ca(2+)-ATPase (P < 0.05). CONCLUSIONS:  Tau may play a crucial role in the protection of antioxidant system and ATPase against Al-induced toxicity in brain and blood of rats.

Inflammation after trauma: microglial activation and traumatic brain injury.
            (Ramlackhansingh et al., 2011) Download
OBJECTIVE:  Patient outcome after traumatic brain injury (TBI) is highly variable. The underlying pathophysiology of this is poorly understood, but inflammation is potentially an important factor. Microglia orchestrate many aspects of this response. Their activation can be studied in vivo using the positron emission tomography (PET) ligand [11C](R)PK11195 (PK). In this study, we investigate whether an inflammatory response to TBI persists, and whether this response relates to structural brain abnormalities and cognitive function. METHODS:  Ten patients, studied at least 11 months after moderate to severe TBI, underwent PK PET and structural magnetic resonance imaging (including diffusion tensor imaging). PK binding potentials were calculated in and around the site of focal brain damage, and in selected distant and subcortical brain regions. Standardized neuropsychological tests were administered. RESULTS:  PK binding was significantly raised in the thalami, putamen, occipital cortices, and posterior limb of the internal capsules after TBI. There was no increase in PK binding at the original site of focal brain injury. High PK binding in the thalamus was associated with more severe cognitive impairment, although binding was not correlated with either the time since the injury or the extent of structural brain damage. INTERPRETATION:  We demonstrate that increased microglial activation can be present up to 17 years after TBI. This suggests that TBI triggers a chronic inflammatory response particularly in subcortical regions. This highlights the importance of considering the response to TBI as evolving over time and suggests interventions may be beneficial for longer intervals after trauma than previously assumed.

Taurine supplementation enhances nutrient-induced insulin secretion in pancreatic mice islets.
            (Ribeiro et al., 2009) Download
BACKGROUND:  Taurine (TAU), a naturally occurring sulfur-containing amino acid, is found at high concentrations in plasma and mammalian tissues and regulates osmolarity, ion channel activity, and glucose homeostasis. Several reports have shown that physiological plasma TAU levels seem to be important for adequate beta (beta)-cell function and insulin action, since low concentrations of TAU in the plasma have been reported in the pre-diabetic and diabetic states. METHODS:  Glucose tolerance and insulin sensitivity were investigated in mice supplemented with 2% (w/v) TAU in their drinking water for 30 days, as well as the insulin secretion from isolated islets stimulated by glucose or L-leucine. RESULTS:  TAU-supplemented mice demonstrated improved glucose tolerance and higher insulin sensitivity, compared to controls (CTL). In addition, their islets secreted more insulin in response to high concentrations of glucose and L-leucine. L-[U-(14)C]leucine oxidation was higher in TAU than in CTL islets, whereas D-[U-(14)C]glucose oxidation, ATP levels, glucose transporter (GLUT) 2 and glucokinase (GCK) protein expressions were similar in both types of islets. The L-type beta(2) subunit voltage-sensitive Ca(2+) channel protein, as well as (45)Ca uptake, were significantly higher in TAU-supplemented than CTL islets. In addition, islets from TAU-supplemented mice secreted more glucagon than CTL islets at low glucose. CONCLUSIONS:  TAU supplementation improves glucose tolerance and insulin sensitivity in mice, as well as insulin secretion from isolated islets. The latter effect seems to be, at least in part, dependent on a better Ca(2+) handling by the islets.

Serum level of taurine would be associated with the amelioration of minimal hepatic encephalopathy in cirrhotic patients.
            (Saito et al., 2016) Download
AIM:  A variety of treatment modalities including L-carnitine have been tried for cirrhotic patients with minimal hepatic encephalopathy (MHE), which improved MHE for some patients, but were not effective for the other patients. We aimed to identify pre-therapeutic independent factors to predict the amelioration of MHE after L-carnitine treatment. METHODS:  We performed a prospective cohort study on a total of 64 consecutive outpatients of cirrhotic patients who underwent blood biochemical examinations and neuropsychiatric (NP) test at Kobe University Hospital. MHE patients diagnosed by the NP test were p.o. administrated L-carnitine for 3 months. The patients with and without MHE amelioration were compared, and the independent factors were statistically examined. Predictive scoring systems of the amelioration of MHE were established using multivariate logistic regression. RESULTS:  The amelioration of MHE was found in 45.8% of MHE patients. Serum taurine before the treatment was the best predictive factor of the amelioration of MHE (P = 0.046). The predictive model using serum taurine discriminated well between patients with and without the amelioration of MHE (area under the receiver-operator curve, 0.748; 95% confidence interval, 0.531-0.901). The predictive scores of the amelioration of MHE enable the patient-specific probability to be easily looked up. CONCLUSION:  Serum taurine before L-carnitine treatment was shown to be an independent factor associated with the amelioration of MHE 3 months after the treatment. The easy pre-therapeutic prediction of MHE amelioration after L-carnitine treatment would help in improving awareness of the selection of MHE patients with good response to L-carnitine, thus being beneficial from a financial perspective.

Impaired energy metabolism of the taurine‑deficient heart.
            (Schaffer et al., 2016) Download
Taurine is a β-amino acid found in high concentrations in excitable tissues, including the heart. A significant reduction in myocardial taurine content leads to the development of a unique dilated, atrophic cardiomyopathy. One of the major functions of taurine in the heart is the regulation of the respiratory chain. Hence, we tested the hypothesis that taurine deficiency-mediated defects in respiratory chain function lead to impaired energy metabolism and reduced ATP generation. We found that while the rate of glycolysis was significantly enhanced in the taurine-deficient heart, glucose oxidation was diminished. The major site of reduced glucose oxidation was pyruvate dehydrogenase, an enzyme whose activity is reduced by the increase in the NADH/NAD+ ratio and by decreased availability of pyruvate for oxidation to acetyl CoA and changes in [Mg2+]i. Also diminished in the taurine-deficient heart was the oxidation of two other precursors of acetyl CoA, endogenous fatty acids and exogenous acetate. In the taurine-deficient heart, impaired citric acid cycle activity decreased both acetate oxidation and endogenous fatty acid oxidation, but reductions in the activity of the mitochondrial transporter, carnitine palmitoyl transferase, appeared to also contribute to the reduction in fatty acid oxidation. These changes diminished the rate of ATP production, causing a decline in the phosphocreatine/ATP ratio, a sign of reduced energy status. The findings support the hypothesis that the taurine-deficient heart is energy starved primarily because of impaired respiratory chain function, an increase in the NADH/NAD+ ratio and diminished long chain fatty acid uptake by the mitochondria. The results suggest that improved energy metabolism contributes to the beneficial effect of taurine therapy in patients suffering from heart failure.

 


References

Kim, C and YN Cha (2014), ‘Taurine chloramine produced from taurine under inflammation provides anti-inflammatory and cytoprotective effects.’, Amino Acids, 46 (1), 89-100. PubMed: 23933994
Kontny, E, et al. (2006), ‘Taurine chloramine inhibits proliferation of rheumatoid arthritis synoviocytes by triggering a p53-dependent pathway.’, Inflamm Res, 55 (10), 446-55. PubMed: 17109072
Li, M, et al. (2015), ‘Maternal taurine supplementation attenuates maternal fructose-induced metabolic and inflammatory dysregulation and partially reverses adverse metabolic programming in offspring.’, J Nutr Biochem, 26 (3), 267-76. PubMed: 25576095
Lin, CJ, et al. (2015), ‘Taurine Attenuates Hepatic Inflammation in Chronic Alcohol-Fed Rats Through Inhibition of TLR4/MyD88 Signaling.’, J Med Food, 18 (12), 1291-98. PubMed: 26090712
Lin, S, et al. (2013), ‘Taurine improves obesity-induced inflammatory responses and modulates the unbalanced phenotype of adipose tissue macrophages.’, Mol Nutr Food Res, 57 (12), 2155-65. PubMed: 23939816
Louzada, PR, et al. (2004), ‘Taurine prevents the neurotoxicity of beta-amyloid and glutamate receptor agonists: activation of GABA receptors and possible implications for Alzheimer’s disease and other neurological disorders.’, FASEB J, 18 (3), 511-18. PubMed: 15003996
Lu, CL, et al. (2014), ‘Taurine improves the spatial learning and memory ability impaired by sub-chronic manganese exposure.’, J Biomed Sci, 21 51. PubMed: 24885898
Murakami, S, et al. (2016), ‘Taurine ameliorates cholesterol metabolism by stimulating bile acid production in high-cholesterol-fed rats.’, Clin Exp Pharmacol Physiol, 43 (3), 372-78. PubMed: 26710098
Nagai, K, et al. (2016), ‘Protective effects of taurine on doxorubicin-induced acute hepatotoxicity through suppression of oxidative stress and apoptotic responses.’, Anticancer Drugs, 27 (1), 17-23. PubMed: 26426519
Nguyen, TT, et al. (2013), ‘Activation of glycine and extrasynaptic GABA(A) receptors by taurine on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis.’, Neural Plast, 2013 740581. PubMed: 24379976
Oja, SS and P Saransaari (2013), ‘Taurine and epilepsy.’, Epilepsy Res, 104 (3), 187-94. PubMed: 23410665
Qiao, M, et al. (2015), ‘Potential protection of taurine on antioxidant system and ATPase in brain and blood of rats exposed to aluminum.’, Biotechnol Lett, 37 (8), 1579-84. PubMed: 25967032
Ramlackhansingh, AF, et al. (2011), ‘Inflammation after trauma: microglial activation and traumatic brain injury.’, Ann Neurol, 70 (3), 374-83. PubMed: 21710619
Ribeiro, RA, et al. (2009), ‘Taurine supplementation enhances nutrient-induced insulin secretion in pancreatic mice islets.’, Diabetes Metab Res Rev, 25 (4), 370-79. PubMed: 19405082
Saito, M, et al. (2016), ‘Serum level of taurine would be associated with the amelioration of minimal hepatic encephalopathy in cirrhotic patients.’, Hepatol Res, 46 (2), 215-24. PubMed: 26224109
Schaffer, SW, et al. (2016), ‘Impaired energy metabolism of the taurine‑deficient heart.’, Amino Acids, 48 (2), 549-58. PubMed: 26475290