Plasma Taurine Levels Research Articles

Reduction of plasma taurine level in children affected by Osteogenesis Imperfecta during bisphosphonate therapy

Osteogenesis Imperfecta (OI) is a heritable disease of connective tissue characterized by increased bone fragility. To date, bisphosphonates seem to be the most promising therapy, at least for children. In the last decade experimental and clinical studies indicate that several amino acids are implicated in bone mineralization. Particularly, taurine is localized in matrices of the bone and can regulate osteoblast metabolism with antiosteopenic effect. To investigate a possible interaction between pharmacological effects of bisphosphonates and amino acids involved in bone metabolism, we performed plasma and urine amino acids analysis in children affected by OI before and during treatment with bisphosphonates. Fourteen prepubertal children with moderate to severe types of OI, 8 males and 6 females, aged from 2 to 11 years (mean (SD) 6,9 ± 2,53) were enrolled in the study. Patients were treated with neridronate infusion (1 mg/Kg/body weight) every three months. Plasma and urine specimens for amino acid analysis were kept at baseline (T0) and three months after each infusion of four consecutive cycles (T1–T4). A significant decrease in respect to the pre-treatment levels (T0) was observed after the fourth infusion for taurine ( p < 0.01). In addition, urinary excretion of this amino acid showed a significant decrease after the fourth infusion. No significant correlations were found between plasma level or urinary excretion of hydroxyproline, taurine, arginine and lysine in respect to bone mineral density. The progressive reduction of plasma taurine found in our patients treated with bisphosphonates could be implicated in the action mechanism of this drug in OI and possibly in other disorders of bone metabolism. This knowledge could provide new opportunities to improve treatment with bisphosphonates and address novel strategies for the therapeutic approach to bone disorders.

Taurine status and response to intravenous taurine supplementation in adults with short-bowel syndrome undergoing long-term parenteral nutrition: a pilot study

Taurine deficiency in patients on long-term parenteral nutrition may be involved in cholestasis. We aimed to assess plasma taurine and tauro-conjugated bile acids in adults with short-bowel syndrome and their response to intravenous taurine. Thirty-two adult patients, who had been on taurine-free parenteral nutrition for a mean of 59 (SE 14) months for short-bowel syndrome, were studied retrospectively. In a second study, a subgroup of ten patients with chronic cholestasis received taurine-enriched (6.0 (SE 0.6) mg/kg per d) parenteral nutrition for 55 (SE 13) months. Post-absorptive plasma taurine and bile acid concentrations were measured and liver function tests routinely sampled. At baseline, plasma taurine was lower in patients with a jejunal length of less than 35 cm (group A, n 16) than in those with a jejunal length of 35 cm or more (group B, n 16): 43 (SE 3) v. 58 (SE 4) micromol/l (P=0.01). The groups were no different in terms of chronic cholestasis (12/16 v.13/16 patients), total bile acids (26 (SE 13) v.14 (SE 5) micromol/l) or the ratio of tauro-conjugated:glyco-conjugated bile acids (5 (SE 2) v.8(SE 4)%, usual range 30-60%). After supplementation, there was an increase in plasma taurine level (63 (SE 8) v. 43 (SE 4), P=0.007) but was no change in either total bile acids or the ratio of tauro-conjugated: glyco-conjugated bile acids. There was a significant decrease in aspartate aminotransferase level. Long-term parenteral nutrition for short-bowel syndrome is associated with an impaired tauro-conjugation of bile acids (enterohepatic pool), irrespective of plasma taurine level (systemic pool) and despite long-term taurine intravenous supplementation.

Hypertaurinemia in Bile Duct–Ligated Rats After Surgery: The Effect of Gut Endotoxin Restriction on Organ Fluxes and Oxidative Status

Surgery in obstructive jaundice is associated with complications related to gut-derived endotoxemia. The organs involved in these complications, including liver, kidneys, and gut, are important in the metabolism of taurine, which is implicated in bile acid conjugation and has antioxidative effects. Taurine organ metabolism and liver oxidative status were studied in bile duct-ligated rats (BDL) after laparotomy. Oral cholestyramine treatment inhibits gut-derived endotoxemia and was used to evaluate the role of endotoxin. In BDL rats, postoperative plasma taurine levels were higher compared with SHAM (p < .0001). Cholestyramine treatment reduced plasma taurine in BDL rats (p < .005), but levels remained higher compared with SHAM groups (p < .0001). In contrast to a liver uptake of taurine in SHAM rats, a release from livers of BDL rats was found (p < .005). Cholestyramine treatment in BDL rats resulted in a liver uptake of taurine (p < .05 vs BDL). A higher uptake of taurine by the kidneys was found in both BDL animals after surgery and SHAM controls (p < .005); however, cholestyramine had no effect. A release of taurine from the gut was found in the SHAM groups, which was reversed in both BDL groups (p < .01). Cholestyramine lowered the elevated levels of hepatic enzymes in BDL rats (ALT and AST: p < .05). Total liver glutathione levels were lower in BDL rats (p < .0001) compared with SHAM groups, and cholestyramine significantly attenuated this decrease (p < .01). Liver malondialdehyde levels were higher in BDL rats compared with SHAM (p < .01), whereas cholestyramine completely prevented this increase in lipid peroxidation (p < .0001). Hypertaurinemia in BDL rats after surgery is most likely explained by reduced bile acid conjugation and hepatocellular leakage. Cholestyramine treatment reduced hepatocellular damage by inhibiting gut-derived endotoxemia, and reversed the release of taurine from the jaundiced liver into an uptake and consequently lowered plasma taurine levels. This uptake may contribute to the improved antioxidant status in cholestyramine-treated BDL rats.

Relationship of taurine and other amino acids in plasma and in neutrophils of septic trauma patients

Recently, an interdependency of plasma taurine and other amino acids as well as metabolic and clinical variables implicating therapeutic options was reported. This result may be an indication that plasma taurine levels are directly related to intracellular levels. Therefore, the aim of this study was to analyse the possible relationship between taurine levels in plasma and in neutrophils, the relationship to other amino acids, and variables quantifying metabolic impairment and severity of sepsis in multiple trauma patients developing sepsis. After multiple trauma taurine decreased significantly in plasma in thirty-two patients as well as within the neutrophil and does not recover in sepsis. Lower individual levels in the neutrophil did not follow lower individual levels in plasma and no correlation of taurine in plasma and in the neutrophils could be observed. In sepsis, only plasma showed an interdependency of taurine, aspartate, and glutamate. No association between taurine plasma or intracellular levels and SOFA score as indicator for severity of sepsis or metabolic variables was observed. After multiple trauma and in sepsis, taurine uptake in cells (which is regulated in different ways), and intracellular taurine (which serves e.g. as an osmolyte) can be influenced. Therefore a prediction of the neutrophil taurine pool seems not fully possible from taurine plasma levels. Intracellular taurine has some unique properties explaining the missing interdependency despite some similarities in osmoregulation and metabolic interactions to other amino acids. The association of taurine, aspartate, and glutamate in plasma cannot be simply transferred to the neutrophils intracellular level. The clinical meaning of the plasma correlation remains unclear. A dependency of plasma and neutrophil taurine to severity of sepsis and to metabolic variables seems not possible because of the multifactorial pathophysiology of sepsis.

Effects of consecutive high-dose alcohol administration on the utilization of sulfur-containing amino acids by rats

In this study, we attempted to evaluate changes in sulfur-containing amino acid (SCAA) metabolism after short-term high-dose alcohol ingestion. At the beginning of the study, six animals were sacrificed as the baseline group and then other animals in the experiment were consecutively gavaged with alcohol (30%, 3 g/kg) for 7 days. Animals ( n=6 each) were subsequently sacrificed at the time points of Days 1 (Group E1), 3 (Group E3) and 7 (Group E7). Blood samples and selected tissues were collected at each time interval. SCAA, pyridoxal phosphate (PLP) and glutathione (GSH) levels were analyzed. Results showed that taurine levels of tissues (brain, liver, heart and kidneys) all declined after the ethanol intervention and continued to decrease in selected tissues except the brain during the experiment. Furthermore, the trends of plasma taurine and PLP contents were highly correlated ( r=.98, P=.045). A similar utilization pattern of plasma taurine and PLP indicated that transsulfuration preferred taurine production to GSH synthesis. The trend of plasma taurine levels being positively correlated with PLP levels reveals that dramatic transsulfuration occurred to meet the urgent demand for taurine by brain cells. In conclusion, we reported that continual alcohol ingestion alters SCAA utilization, especially by depletion of taurine and hypotaurine and by elevation of S-adenosyl homocysteine in the selected organs.

Effects of betaine supplementation on hepatic metabolism of sulfur-containing amino acids in mice

We previously reported that acute betaine treatment induced significant changes in the hepatic glutathione and cysteine levels in mice and rats. The present study was aimed to determine the effects of dietary betaine on the metabolism of sulfur-containing amino acids. Male mice were supplemented with betaine (1%) in drinking water for up to 3 weeks. Changes in hepatic levels of major sulfur amino acid metabolites and products were stabilized after 2 weeks of betaine supplementation. Betaine intake increased methionine, S-adenosylmethionine, and S-adenosylhomocysteine levels significantly, but homocysteine and cystathionine were reduced. Methionine adenosyltransferase activity was elevated to three-fold of control. Cysteine catabolism to taurine was inhibited as evidenced by a decrease in cysteine dioxygenase activity and taurine levels in liver and plasma. Despite the significant changes in the transsulfuration reactions, neither hepatic cysteine nor glutathione was altered. Betaine supplementation decreased the hepatotoxicity induced by chloroform (0.5 ml/kg, ip) significantly. Betaine supplementation enhances recycling of homocysteine for the generation of methionine and S-adenosylmethionine while reducing its utilization for the synthesis of cystathionine and cysteine. However, the hepatic levels of cysteine or glutathione are not affected, most probably due to the depression of taurine generation from cysteine.

Effect of a swim training on homocysteine and cysteine levels in rats

The purpose of this study was to investigate the effects of a 8-week of swim training on total plasma homocysteine and cysteine levels in 16 male Sprague-Dawley rats aged 17 weeks. We also evaluated the activity of hepatic cystathionine beta-synthase (CBS), an enzyme involved in the metabolism of Hcy, the concentration of plasma glutathione, taurine, and a fraction of vitamin B6: the pyridoxal 5-phosphate (PLP). After one week of acclimatization, rats were randomly divided into two groups: 8 non-trained (NTR) and 8 trained rats (TR). Following the training period, body weight gain was lower in TR than in NTR. Plasma homocysteine did not differ among groups while significantly lower plasma cysteine and taurine levels were found in TR (157.83 +/- 8.6 micromol/L; 133.01 +/- 9.32 micromol/L; P < 0.05) compared with data of NTR (176.19 +/- 4.9 micromol/L; 162.57 +/- 8.16 micromol/L; P < 0.05). No significant changes in hepatic CBS activity were observed in TR compared with NTR. Moreover, values for plasma glutathione and PLP concentrations were not affected by training.These results indicate that training reduces plasma cysteine and taurine levels whereas it does not modify other studied parameters. Thus, physical training may regulate cysteine metabolism.

Infantile dilated cardiomyopathy in Portuguese water dogs: Correlation of the autosomal recessive trait with low plasma taurine at infancy

Infantile dilated cardiomyopathy (IDCM) in Portuguese water dogs (PWD) involves an autosomal recessive trait. Based on our previous studies we have tested the hypothesis that this disorder may be correlated with taurine deficiency. The plasma taurine levels of 249 puppies from 36 litters obtained from breeders at six and nine weeks of age, an early stage when usually the clinical symptoms are not manifested, were analyzed. Additional samples were collected from sixteen puppies that we raised from four litters. These litters were born to a dam that had low plasma taurine as a puppy and two known carrier sires. From the random samples obtained from the breeders, forty-eight pups from fourteen litters and twenty-nine pups from seven litters had low plasma taurine at least at one and at two time points, respectively. Also several puppies showing low plasma taurine died due to IDCM. Furthermore, from the sixteen pups we raised, fifteen had at least low taurine level at one and seven had at two time points. Considered together, these results strongly support the view that IDCM in PWD is associated with abnormal taurine metabolism that leads to low plasma taurine at early stages before the clinical symptoms appear.

Lipoic Acid and Ascorbic Acid Affect Plasma Free Amino Acids Selectively in the Teleost Fish Pacu (Piaractus mesopotamicus)

Most studies on the antioxidants, lipoic acid (LA) and ascorbic acid (AA), focused on species that, unlike teleost fish, are not scurvy-prone, and are able to synthesize AA. The antioxidant properties of LA may make it useful in aquaculture nutrition, but several effects must first be investigated, and we address here plasma free amino acids (FAA). In mammals, LA and AA in high doses were claimed to alter plasma FAA profile; to our knowledge, however, no data are available in fish. We therefore studied the effects of dietary LA and AA on plasma FAA in the South American teleost fish pacu, which is being used increasingly in aquaculture. LA treatment decreased concentrations of 18 of 23 individual FAA; specifically, dispensable and total FAA were significantly affected. Ornithine was elevated (+26%) in LA-treated fish and significantly decreased ratios of plasma [Arg]/[Orn] and other individual [FAA]/[Orn] were observed. LA and AA both affected sulfur FAA concentrations. Plasma cystine levels were significantly increased in the LA-supplemented groups. AA had little effect on most amino acids, and no interaction with LA was detected. AA supplementation did, however, significantly lower taurine (-42%) and cystathionine (-31%) levels in plasma. No effect on the branched chain:aromatic amino acid ratios was observed. The data indicate that at the dietary level studied, LA and AA independently affect selected plasma FAA in pacu, and suggest that any use of LA in particular as a dietary supplement should take into account an altered plasma FAA profile.

Sub-optimal taurine status may promote platelet hyperaggregability in vegetarians

Although vegan diets typically have a very favorable effect on a range of vascular risk factors, several independent groups have reported that the platelets of vegetarians are more sensitive to pro-aggregatory agonists than are those of omnivores. In light of clear and convincing evidence that platelet function has an important impact on risk for thromboembolic events, it is important to clarify the basis of platelet hyperaggregability in vegetarians. A dietary deficit of long-chain ω-3 fatty acids is not likely to explain this phenomenon, since most omnivore diets do not include enough of these fats to discernibly influence platelet function. A more plausible possibility is that relatively poor taurine status – a function of the facts that plants are devoid of taurine and the human capacity for taurine synthesis is limited – is responsible. Plasma taurine levels are lower, and urinary taurine excretion is substantially lower, in vegetarians than in omnivores. Platelets are rich in taurine, which functions physiologically to dampen the calcium influx evoked by aggregating agonists – thereby down-regulating platelet aggregation. Supplemental intakes of taurine as low as 400 mg daily have been reported to markedly decrease the sensitivity of platelets to aggregating agonists ex vivo. Although the average daily intake of taurine from omnivore diets may be only about 150 mg, it is credible to speculate that a supplemental intake of this magnitude could normalize the platelet function of vegetarians in the long term; in any case, this thesis is readily testable clinically. Taurine is just one of a number of nutrients found almost solely in animal products – “carninutrients” – which are rational candidates for supplementation in vegans.

Plasma taurine and cysteine levels following an oral methionine load: relationship with coronary heart disease.

To test the hypothesis that endogenous synthesis of taurine from methionine is impaired in people with coronary heart disease (CHD). Nested case-control. Indian Asian and white European males aged 35-60 y. Both racial group included patients with CHD and healthy controls. Samples from 20 subjects in each of the four groups were selected at random. Fasting blood samples were taken before and 6 h after consumption of methionine (100 mg/kg body weight) Plasma concentrations of taurine, cysteine, pyridoxal-5-phosphate and 4-pyridoxic acid. Fasting plasma taurine values were higher in Indian Asian cases than controls, but not significantly different between European cases and controls. Postload taurine values were higher in cases than controls in both racial groups (P=0.002). Fasting plasma cysteine was higher in cases than controls (P=0.002) and higher in Indian Asians than Europeans (0.007), but there were no significant differences between any of the groups in postload cysteine values, nor in plasma pyridoxal-5-phosphate or 4-pyridoxic acid. Taurine production from methionine was not impaired in patients with CHD, but fasting plasma cysteine was higher in CHD cases than controls.

Co-variation of plasma sodium, taurine and other amino acid levels in critical illness

This study investigates the relationship between changes in plasma sodium and changes in amino acid levels in a patient with post-traumatic sepsis and prolonged critical illness. Ninety-two consecutive measurements were performed at regular intervals over a period of many weeks; these consisted in the determination of full amino-acidograms, plasma sodium and complementary variables. A unique, highly significant inverse correlation between taurine and plasma sodium was found (r(2) = 0.48, p < 0.001). All other amino acids were unrelated, or much more weakly related, to sodium. Taurine was also strongly and directly related to phosphoethanolamine, glutamate and aspartate. Changes in sodium and in levels of these amino acids explained up to 86% of the variability of taurine. Besides, levels of these amino acids maintained a high degree of co-variation, remaining reciprocally related one to each other, directly, with r(2) ranging between 0.33 and 0.59 (p < 0.001 for all). There were similar findings for beta-alanine, which however was measured inconsistently. These data provide gross clinical evidence of a specific link binding plasma sodium and taurine levels, and may be consistent with occurrence of opposite and interdependent shifts of sodium and taurine between intravascular and extravascular space, to maintain osmoregulation. Co-variation of taurine with the other amino acids may be related to the same phenomenon, and/or to similarities in transport systems and chemical structure, or true metabolic interactions.

Ischemia/reperfusion injury of skeletal muscle: Plasma taurine as a measure of tissue damage

Background. Cell membrane rupture by oxygen-derived free radicals is a systematic feature of ischemia/reperfusion (I/R) injury. High taurine concentration gradients in skeletal muscle prompted us to evaluate whether plasma taurine levels (pTau) are a useful marker of I/R injury after different periods of ischemia. Methods. Rabbits were randomly assigned to either 1 or 2.5 hours of hind-limb ischemia followed by 2 hours of reperfusion (groups IR1 [n = 12] and IR2.5 [n = 13], respectively). Corresponding sham groups (SHAM1 [n = 8] and SHAM2.5 [n = 9]) were used as controls. Analyzed parameters included histomorphometry and electron microscopy of skeletal muscle biopsies, pTau, and plasma level of malondialdehyde. Skeletal muscle function was assessed 3 weeks after I/R injury. Results. No significant morphologic changes were detectable at the end of ischemia. After reperfusion, mild interstitial edema with intact muscle cell membranes developed in IR1 group; pTau was not increased. IR2.5 group, by contrast, showed severe interstitial edema formation (interfiber area increased by 112%, P <.005), microvascular constriction (microvessel area decreased by 33%, P <.0005), and damage to the muscle cell membranes that was confirmed by the increased plasma malondialdehyde. pTau was higher than in the SHAM2.5 group (P <.0005). Pronounced cell damage in IR2.5 group resulted in impaired muscle function (maximal tetanic tension was reduced 2 times, P <.005) but not in IR1 group. Conclusion. Skeletal muscle tolerates 1 h/2 h but not 2.5 h/2 h of I/R, the latter resulting in interstitial edema formation, microvascular constriction, and a late muscle dysfunction. Cell membrane rupture through stimulated lipid peroxidation promotes leakage of intracellular taurine, leading to increased pTau after reperfusion and may be considered as prognostically unfavorable in terms of organ function reversibility. In the rabbit model, pTau seems to be a sensitive marker of I/R injury to skeletal muscle. (Surgery 2003;133:91-100.)

Effect of the obesity index on plasma taurine levels in Korean female adolescents.

Obesity is currently an increasing disease that affects many countries in the world including the United States where this condition is responsible for 300,000 deaths annually1. Adolescent obesity has rapidly increased in recent years in Korea due to westernized lifestyle2.

Effects of Taurine Deficiency and Chronic Methanol Administration on Rat Retina, Optic Nerve and Brain Amino Acids and Monoamines

A chronic methanol (MeOH) intoxication scheme (2 g/kg/day ip for 2 weeks) was carried out in Sprague-Dawley rats, previously depleted of folates with methotrexate (MTX). β-Alanine (β-Ala), 5%, was also administered to some animals in the drinking water. Amino acids were determined in plasma, retina, optic nerve, hippocampus and posterior cortex by HPLC with fluorescence detection and monoamines in retina, hippocampus and posterior cortex by electrochemical detection. β-Ala administration reduced taurine (Tau) levels in plasma, hippocampus and posterior cortex, but not in retina and optic nerve. Aspartate (Asp) concentration in the optic nerve was increased in MTX-MeOH treated animals, and the administration of β-Ala did not modify this elevation. The association of β-Ala with MTX-MeOH produced an increase of threonine, and a decrease of 5-hydroxytryptamine (5-HT) in the retina without modifying 5-hydroxyindoleacetic acid, whereas in the hippocampus an elevation of asparagine was observed. We conclude that, in the retina, β-Ala in combination with MTX-MeOH increased serotonin and decreased dopamine (DA) turnover rate, and resulted in changes in the amino acid balance, that could affect glycinergic activity. On the other hand, in the hippocampus, Asp metabolism could be affected by Tau depletion with β-Ala.

Plasma sulfur amino acids in relation to cardiovascular disease, nutritional status, and diabetes mellitus in patients with chronic renal failure at start of dialysis therapy

Sulfur amino acids (sAAs) are potential candidates as risk factors for cardiovascular disease (CVD). However, we recently reported that chronic hemodialysis patients with CVD had a greater prevalence of malnutrition, hypoalbuminemia, and lower plasma total homocysteine (tHcy) levels than those without CVD. In this cross-sectional study, we examined the relationship of plasma sAAs to CVD and nutritional status in 151 patients with chronic renal failure (CRF) close to the start of regular dialysis treatment (33 ± 7 days before the first dialysis treatment). Clinical signs of CVD were present in 32% of patients with CRF, 41% had malnutrition assessed by subjective global nutritional assessment (SGNA) score, and 26% had diabetes mellitus (DM). Plasma tHcy levels were high in 91% of patients, as were plasma total cysteine (tCys) levels, whereas plasma methionine (Met) and taurine (Tau) levels were normal. Patients with CRF who had CVD were older, more often malnourished, and had lower tHcy and serum albumin (s-albumin) levels and a greater frequency of DM than those without CVD. Plasma tCys, Met, and Tau levels did not differ between patients with CRF with and without CVD. The tCys-tHcy ratio was higher in patients with CVD and related to SGNA score and DM. Moreover, this ratio, but not tHcy or tCys level, correlated with age and triglyceride, total cholesterol, and apolipoprotein B levels. Malnutrition and hypoalbuminemia were associated with low plasma sAA levels (tHcy, Met, and Tau); tCys was related to s-albumin level, but not SGNA score. Among patients with diabetes, sAA levels did not differ between patients with and without CVD or between malnourished and well-nourished patients. In conclusion, patients with CRF at the start of dialysis treatment with CVD were more often diabetic, malnourished, and had lower s-albumin and tHcy levels and a higher tCys-tHcy ratio than patients with no CVD. tCys-tHcy ratio, but not tHcy or tCys levels per se, was related to cardiovascular risk factors, suggesting that cysteine may have a role in the development of CVD. Malnutrition, hypoalbuminemia, and DM in patients with CRF influence sAA levels, mainly plasma tHcy, which should be considered when evaluating hyperhomocysteinemia as a cardiovascular risk factor. © 2002 by the National Kidney Foundation, Inc.

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

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, beta-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% beta-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. beta-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 beta-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 beta-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 beta-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 beta-alanine-treated rats 24 hours after exercise. In summary, taurine supplementation or taurine depletion had measurable cytoprotective actions to attenuate exercise-induced injury.

The possible role of taurine and GABA as endogenous cryogens in the rabbit: changes in CSF levels in heat-stress.

We investigated whether heat-stress induced hyperthermia could enhance release of both endogenous taurine and GABA from nerve cells into the extracellular compartment, thus acting like endogenous cryogens. Conscious rabbits were exposed for 1 hr to 40 degrees C (heat stress) while cerebrospinal fluid (CSF) and plasma osmolality and the CSF concentrations of some cations, proteins as well as those of taurine and GABA were determined. Heat stress-induced hyperthermia was accompanied by a significant rise in CSF and plasma osmolality, CSF calcium, taurine and GABA levels. It is suggested that during heat stress taurine and GABA are released in the extracellular space of brain tissues in higher amounts, as compared to control conditions, to counteract the resulting hyperthermia, thus acting as cryogenic agents.

Alteration of excitation‐contraction coupling mechanism in extensor digitorum longus muscle fibres of dystrophic mdx mouse and potential efficacy of taurine

No clear data is available about functional alterations in the calcium-dependent excitation-contraction (e-c) coupling mechanism of dystrophin-deficient muscle of mdx mice. By means of the intracellular microelectrode "point" voltage clamp method, we measured the voltage threshold for contraction (mechanical threshold; MT) in intact extensor digitorum longus (EDL) muscle fibres of dystrophic mdx mouse of two different ages: 8 - 12 weeks, during the active regeneration of hind limb muscles, and 6 - 8 months, when regeneration is complete. The EDL muscle fibres of 8 - 12-week-old wildtype animals had a more negative rheobase voltage (potential of equilibrium for contraction- and relaxation-related calcium movements) with respect to control mice of 6 - 8 months. However, at both ages, the EDL muscle fibres of mdx mice contracted at more negative potentials with respect to age-matched controls and had markedly slower time constants to reach the rheobase. The in vitro application of 60 mM taurine, whose normally high intracellular muscle levels play a role in e-c coupling, was without effect on 6 - 8-month-old wildtype EDL muscle, while it significantly ameliorated the MT of mdx mouse. HPLC determination of taurine content at 6 - 8 months showed a significant 140% rise of plasma taurine levels and a clear trend toward a decrease in amino acid levels in hind limb muscles, brain and heart, suggesting a tissue difficulty in retaining appropriate levels of the amino acid. The data is consistent with a permanent alteration of e-c coupling in mdx EDL muscle fibres. The alteration could be related to the proposed increase in intracellular calcium, and can be ameliorated by taurine, suggesting a potential therapeutic role of the amino acid.

Low taurine, gamma-aminobutyric acid and carnosine levels in plasma of diabetic pregnant rats: consequences for the offspring.

Gestational diabetes compromises fetal development and induces a diabetogenic effect in the offspring, including the development of gestational diabetes and the transmission of the effect to the next generation. Changes are not limited to glucose and insulin metabolism, and appear to be modulated by alterations at the hypothalamo-hypophyseal axis. In the present work, serum concentrations are given for the non-protein amino-acids taurine and gamma-aminobutyric acid (GABA), both neurotransmitters essential for normal brain development, and for the endogenous neuroprotector carnosine, a known anti-oxydans. Taurine levels are significantly below normal values in mildly diabetic mothers, in their fetal and adult offspring, virgin and pregnant, and in the fetuses of these pregnant offspring. GABA and carnosine levels are at the limit of detection in the diabetic mothers and their offspring at every stage. It is concluded that the low taurine, GABA and carnosine levels in diabetic mothers and their fetuses might compromise the normal structural and functional development of the fetal brain. When adult, these offspring present a deficiency of the circulating levels of these neurotransmitters involved in the hypothalamo-hypophyseal regulation of insulin secretion. This might contribute to the development of impaired glucose tolerance and gestational diabetes, thereby transmitting the effect to the next generation.