Taurine-treated Group Research Articles

Enhancement of astaxanthin production, recovery, and bio-accessibility in Haematococcus pluvialis through taurine-mediated inhibition of secondary cell wall formation under high light conditions

This study explored the use of taurine in enhancing the production and bio-accessibility of astaxanthin in Haematococcus pluvialis, which typically forms a secondary cell wall hindering astaxanthin extraction. The biomass of taurine-treated group significantly increased by 18%, and astaxanthin yield surged by 34% in comparison to the control group. Without cell disruption, astaxanthin recovery from thin-walled cells in the taurine-treated group, using dimethyl sulfoxide and ethanol as extraction reagents, was 97% and 75%, respectively, which were 30-fold higher than those of thick-walled cells in the control group. Additionally, the cell fragmentation rate increased by 86% in taurine-treated group relative to the control group. Comparative transcriptome analysis identified taurine-induced upregulation of genes involved in the astaxanthin biosynthesis pathway and downregulation of those associated with secondary cell wall synthesis. This study thus offers an innovative taurine-based strategy to enhance astaxanthin production and bio-accessibility while shedding light on the mechanisms driving this process.

Dose-dependent effects of taurine against testicular damage in a streptozotocin-induced type 1 diabetes mellitus rat model.

Testicular dysfunction has been associated with chronic hyperglycemia in diabetes mellitus patients. We investigated taurine's possible mechanisms and protective effects against testicular damage using a rat model of streptozotocin-induced diabetes. Wistar rats (N = 56) were divided into seven equal groups. Untreated control rats received saline, and treated control rats received taurine 50mg/kg orally. To induce diabetes, rats received a single dose of streptozotocin. Metformin-treated diabetic rats received metformin at a dose of 300mg/kg. Taurine-treated groups received 10, 25, or 50mg/kg. All treatments were provided orally once a day for 9weeks following the streptozotocin injection. Levels of blood glucose, serum insulin, cholesterol, testicular tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-1beta (IL-1β), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione (GSH), and catalase (CAT) were examined. Sperm count, progressive sperm motility, and sperm abnormalities were examined. Body and relative reproductive gland weights were assessed. Histopathological examinations of the testes and epididymis were performed. Metformin as well as taurine (in a dose-dependent manner) resulted in significant improvements in body and relative reproductive gland weights, blood glucose, serum cholesterol, and insulin levels, as well as cytokine and oxidative parameters. These findings were associated with significant improvement in sperm count, progressive sperm motility, sperm abnormalities, and histopathological lesions in the testes and epididymis. Taurine can potentially improve hyperglycemia, hypercholesterolemia, and testicular damage associated with diabetes mellitus, possibly by controlling inflammation and oxidative stress.

Taurine induces upregulation of p53 and Beclin1 and has antitumor effect in human nasopharyngeal carcinoma cells in vitro and in vivo

Taurine is an amino acid that has several physiological functions. Previously, we reported the apoptosis-inducing effect of taurine in human nasopharyngeal carcinoma (NPC) cells in vitro. However, the effect of taurine on NPC cell growth in vivo has not been elucidated. Autophagy plays an important role in cell metabolism and exhibits antitumor effects under certain conditions. In this study, we investigated the effects of taurine on apoptosis- and autophagy-related molecules in NPC cells in vitro and in vivo. In our in vitro study, NPC cells (HK1-EBV) were treated with taurine, and Western blot and immunocytochemical analyses revealed that taurine co-upregulated Beclin 1 and p53, with autophagy upregulation. In the in vivo study, we used a nude mouse model with subcutaneous xenografts of HK1-EBV cells. Once the tumors reached 2–3 mm in diameter, the mice were provided with distilled water (control group) or taurine dissolved in distilled water (taurine-treated group) ad libitum (day 1) and sacrificed on day 13. The volume and weight of the tumors were significantly lower in the taurine-treated group. Using immunohistochemistry (IHC), we confirmed that taurine treatment reduced the distinct cancer nest areas. IHC analyses also revealed that taurine promoted apoptosis, as evidenced by an increase in cleaved caspase-3, accompanied by upregulation of p53. Additionally, taurine increased LC3B and Beclin 1 expression, which are typical autophagy markers. The present study demonstrated taurine-mediated tumor growth suppression. Therefore, taurine may be a novel preventive strategy for NPC.

Taurine Activates BMP-2/Wnt3a-Mediated Osteoblast Differentiation and Mineralization via Akt and MAPK Signaling

We aimed to elucidate the preventive effects of taurine against osteopenia in ovariectomized (OVX) rats and the mechanisms by which taurine regulates osteoblastogenesis in vitro and in vivo. The effects of the taurine on human osteoblast MG-63 cell differentiation and osteoblastogenesis effect in OVX rat were examined Konkuk University in 2018 by evaluating osteoblast differentiation, and expression of osteoblast-specific factors by western blotting analysis. Taurine supplementation significantly improved alkaline phosphatase (ALP) activity and mineralization in a concentration-dependent manner. Further, taurine induced the expression of osteogenic growth factors such as bone morphogenetic protein-2 (BMP-2), runt-related transcription factor 2 (RUNX2), small mothers against decapentaplegic 1/5/8 (SMAD1/5/8), wingless-type MMTV integration site family member 3A (Wnt3a), and collagen type 1 (COL-1) via mitogen-activated protein kinase (MAPK) and serine/threonine protein kinase (Akt). Moreover, the RUNX2 activity of the taurine-treated group was enhanced by protein-protein interactions such as Wnt3a-induced p-AKT/RUNX2 and BMP-mediated SMADs/MAPK/RUNX2 interactions. Our in vitro and in vivo results suggested that taurine can be considered as a potential therapeutic candidate agent for preventing bone loss in postmenopausal osteoporosis.

Histopathological and biochemical studies on the effect of curcumin and taurine against bisphenol A toxicity in male rats.

Bisphenol A (BPA) is a chemical found in environmental xenoestrogen. In the present study, olive oil, curcumin, taurine, BPA, curcumin plus BPA, and taurine plus BPA were exposed to rats for 4weeks via gavage. Content of malondialdehyde and activities of antioxidant enzymes (GPx, GST, SOD, CAT) and also histopathological and cytopathological changes of heart were studied. No significant changes in all studied parameters were seen between control, olive oil, curcumin, and taurine-treated groups. However, there were significant differences in levels of malondialdehyde and activities of antioxidant enzymes in BPA-exposed rats and some histo/cytopathological changes determined. In curcumin plus BPA-exposed and taurine plus BPA-exposed groups, we measured the preventive effects on some parameters but not exactly. As a result, curcumin and taurine significantly minimized BPA-induced cardiotoxicity in rats.

Oxidative Stress Alterations in the Bladder of a Short-period Type 2 Diabetes Rat Model: Antioxidant Treatment Can Be Beneficial for the Bladder.

A short-period type 2 diabetes model was established in order to identify changes in oxidative stress in the bladder at the initiation of the disease. The effect of antioxidant treatment was examined. Diabetes was induced in adult male Wistar rats with a single dose of streptozotocin (40 mg/kg; i.p.). Diabetic animals were then randomly separated into three groups: No treatment (DM), resveratrol treatment, and taurine treatment, and fed with a high-fat diet. Age-matched non-diabetic animals were used and fed with normal diet (control). Two weeks later, animals were sacrificed and bladders were processed for histological evaluation, and further analysis for oxidative stress markers. The body weight of all diabetic animals was significantly lower compared to the controls. The DM group demonstrated a significantly higher bladder weight to body weight ratio compared to the control. The bladder in the DM group demonstrated abruption of the mucosa from the muscularis and edema in the transitional epithelium. Bladders from the resveratrol-, and taurine-treated groups did not demonstrate these histological alterations. The level of malondialdehyde (MDA) in the bladder was significantly higher in the DM group compared to all other groups. Immunohistochemistry showed that diabetes induced a moderate to strong expression of oxidative stress markers MDA and 4-hydroxynonenal, and DNA oxidative stress marker 8-deoxyguanosine in the DM group compared to the other groups. Prompt diagnosis and treatment of diabetes is crucial in regard to disease progression. Specifically, in the bladder it appears that both mild damage at the structural level, as well as oxidative damage at the molecular level may be prevented by antioxidant treatment.

Antioxidant and Anti-Stress Effects of Taurine Against Electric Foot-Shock-Induced Acute Stress in Rats.

In the present study, we evaluated the antioxidant and anti-stress activities of taurine in electric foot-shock stress model rats. Taurine supplementation markedly increased the hepatic glutathione (GSH) levels, compared to the levels in the stress group. In addition, activities of antioxidant enzymes such as catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) were improved in the taurine-treated group. Plasma cortisol and dehydroepiandrosterone-sulfate (DHEA-S) levels were significantly reduced in the taurine-supplemented group compared to those in the stress group. In contrast, the levels of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were markedly increased in the taurine or betaine-treated group compared to those in the stress group. It may be concluded that taurine produces beneficial effects in the form of antioxidant status and biochemical alterations in foot-shock-induced acute stress in rats.

Effects of Taurine Administration on Carbohydrate Metabolism in Skeletal Muscle during the Post-Exercise Phase.

We previously reported that taurine (2-aminoethanesulfonic acid; dose: 0.5 mg/g body weight) administration after treadmill running at 25 m/min for 90 min increased the glycogen concentration in the skeletal muscle of ICR mice at 120 min after the exercise (Takahashi et al. 2014). In the current study, we further investigated the effects of taurine administration on glycogen repletion and carbohydrate metabolism in the tibialis anterior muscle after endurance exercise. The metabolomic profiles of the tibialis anterior muscle at 120 min after the exercise were analyzed by a capillary electrophoresis-time-of-flight mass spectrometry (n=6). Fructose-1,6-bisphosphate (F1,6P), a glycogenolytic/glycolytic intermediate produced by phosphofructokinase, was significantly lower in the taurine-treated group than that in the control group (p<0.01). Dihydroxyacetonephosphate (DHAP), a downstream product of F1,6P was lower (p=0.05) and glycerol 3-phosphate, a downstream product of F1,6P and DHAP, tended to be lower (p=0.09) in the taurine-treated group than in the controls. At that time, phosphorylated Ser293 on the E1α subunit of pyruvate dehydrogenase (PDH) tended to be higher in the taurine-treated mice than in the controls (p=0.09, n=5). There was a positive correlation between phosphorylation of the PDH E1α subunit at Ser293 and glycogen concentration (r=0.73, p<0.05). Our results showed that the enhanced glycogen repletion in skeletal muscle by taurine treatment during the post-exercise phase was accompanied by the lower levels of glycogenolytic/glycolytic intermediates.

Effects of taurine on the expression of neurons SCF mRNA of focal cerebral ischemia in rat

Objective To investigate the effects of taurine on the expression of stem cell factor mRNA of the focal cerebral ischemia in rat.Methods 63 adult male rats were randomly divided into taurine-treated group (Taurine, 80 mg/kg, began at the day of MCAO and continuously intravenous injection for 10 min, daily for 7 days) and controlled group (0.9% normal saline, 1 ml, continuously intravenous injection for 10 min daily for 7 days). The rats received right middle cerebral artery occlusion at 2h and different hours of reperfusion. Expression of SCF was detected by in situ hybridization in the rats subjected to2h,24h,3d,7d, 14 d of reperfusion and sham-operated group (n=3). Results Low level SCF mRNA expressions were found in cortex, striatum and extraventricular zone in sham-operated group. The expression of SCF mRNA in ischemic hemisphere of controlled group increased markedly compared with sham-operated group (t=2.16~25.19, P＜ 0.05), besides that of 2 h in cortex, 2 h in striatum, 2h and 14d in extraventricular zone. SCF mRNA expression in the treatment group increased markedly in cortex,striatum and extraventricular zone at 3d and 7d(t=5.19~ 26.17,P＜0.05). Conclusion Taurine increased the SCF mRNA expression in MCAO rats, therefore it might promote the creation of neural stem cell. Key words: Taurine; Neurons; Neural stem cell factor; Ischmia reperfusion injury

Differential effects of taurine treatment and taurine deficiency on the outcome of renal ischemia reperfusion injury

Taurine possesses membrane stabilization, osmoregulatory and antioxidant properties, aspects of relevance to ischemic injury. We tested the hypothesis that body taurine status is a determinant of renal ischemic injury. Accordingly, renal function and structure were examined in control (C), taurine-treated (TT) and taurine deficient (TD) rats that were subjected to bilateral renal ischemia (60 min) followed by reperfusion (IR); sham operated rats served as controls. Baseline urine osmolality was greater in the TD group than in the control and the TT groups, an effect associated with increased renal aquaporin 2 level. The IR insult reduced urine osmolality (i.e., day-1 post insult); the TD/IR group displayed a more marked recovery in urine osmolality by day-6 post insult than the other two groups. Fluid and sodium excretions were lower in the TD/IR group, suggesting propensity to retention. Histopathological examination revealed the presence of tubular necrotic foci in the C/IR group than sham controls. While renal architecture of the TD/IR group showed features resembling sham controls, the TT/IR group showed dilated tubules, which lacked immunostaining for aquaporin 2, but not 1, suggestive of proximal tubule origin. Finally, assessment of cell proliferation and apoptosis revealed lower proliferation but higher apoptotic foci in the TT/IR group than other IR groups. Collectively, the results indicate that body taurine status is a major determinant of renal IR injury.

Taurine exerts neuroprotective effects via anti-apoptosis in hypoxic-ischemic brain injury in neonatal rats

= Abstract = Purpose : Taurine (2-aminoethanesulfonic acid) is a simple sulfur-containing amino acid. It is abundantly present in tissues such as brain, retina, heart, and skeletal muscles. Current studies have demonstrated the neuroprotective effects of taurine, but limited data are available for such effects during neonatal period. The aim of this study was to determine whether taurine could reduce hypoxic-ischemic (HI) cerebral injury via anti-apoptosis mechanism. Methods : Embryonic cortical neurons isolated from Sprague-Dawley (SD) rats at 18 days gestation were cultured in vitro. The cells were divided into hypoxia group, taurine-treated group before hypoxic insult, and taurine-treated group after HI insult. In the in vivo model, left carotid artery ligation was performed in 7-day-old SD rat pups. The pups were exposed to hypoxia, administered an injection of 30 mg/kg of taurine, and killed at 1 day, 3 days, 1 week, 2 weeks, and 4 weeks after the hypoxic insult. We compared the expressions of Bcl-2, Bax, and caspase-3 among the 3 groups by using real- time polymerase chain reaction (PCR) and western blotting. Results : The cells in the taurine-treated group before hypoxic insult, although similar in appearance to those in the nor- moxia group, were lesser in number. In the taurine-treated group, Bcl-2 expression increased, whereas Bax and caspase-3 expressions reduced. Conclusion : Taurine exerts neuroprotective effects onperinatal HI brain injury due to its anti-apoptotic effect. The neuro- protective effect was maximal at 1-2 weeks after the hypoxic injury. (Korean J Pediatr 2009;52:1337-1347)

Antioxidant Treatment with Taurine Ameliorates Chronic Pancreatitis in an Experimental Rat Model

Based on the results of recent studies that reported depleted antioxidant capacity in patients with chronic pancreatitis (CP), prevention of free radical production has gained importance in antifibrotic treatment strategies in CP. The aim of this study was to investigate the effects of taurine on oxidative capacity and fibrosis in experimental chronic rat pancreatic fibrosis. CP was induced in male Sprague-Dawley rats by intraductal trinitrobenzene sulfonic acid (TNBS) dissolved in ethanol. Taurine was given intraperitoneally at a concentration of 1000 mg/kg. The treatment groups were as follows: group 1, TNBS plus normal saline (NS); group 2, TNBS plus taurine; group 3, ethanol plus NS; and group 4, NS plus NS. Each group contained 15 animals. Treatment was started after established CP. After 4 weeks of treatment, markers of oxidative stress and the degree of pancreatic fibrosis were determined. The amount of weight loss was significantly lower in the taurine-treated group with CP (P < 0.002). Tissue malondialdehyde levels increased and superoxide dismutase and glutathione peroxidase activities decreased significantly after treatment as well (P < 0.001). Histopathologic scores were also lower in taurine-treated animals with CP (P < 0.005). Taurine treatment improved the degree of oxidative stress and fibrosis in rat CP. Antioxidant treatment might be considered a novel option to alleviate the fibrotic process in CP.

Taurine inhibits ischemia/reperfusion-induced compartment syndrome in rabbits1

To investigate effects of taurine on ischemia/reperfusion (I/R)-induced compartment syndrome in rabbit hind limbs. Rabbits underwent femoral artery occlusion after ligation of branches from terminal aorta to femoral artery. After a 7-h ischemia, reperfusion was established with the use of heparinized polyethylene shunts. Rabbits received taurine (1g/kg) or normal saline (control) by iv infusion 10 min before shunt placement. During reperfusion, anterior compartment pressure (ACP) was monitored continuously in the left lower extremity. Gastrocnemius muscle triphenyltetrazolium chloride (TTC) level, taurine content and myeloperoxidase activity were assayed. Oxidative stress was induced in the in vitro gastrocnemius muscle slices by free radical generating systems (FRGS), and the malondialdehyde content was measured in presence or absence of taurine. After 7 h of ischemia, none of the parameters that we measured were different from those before ischemia, except that TTC reduction decreased by 80%. In the control group, after 2 h of reperfusion, ACP increased 4.5-fold, and gastrocnemius muscle taurine content was reduced by 33%. In taurine-treated animals, at 2h reperfusion, the mean arterial blood pressure and heart rate were increased, by 6% and 10%. ACP decreased by 39%, muscle edema decreased by 16%, TTC reduction increased by 150%, and lactate dehydrogenase decreased by 36% compared to control group. Plasma and muscle taurine content increased by 70% and 88%, respectively. In the taurine-treated group, at 2 h reperfusion, plasma malondialdehyde and conjugated diene content were decreased by 38% and 23%, respectively, and muscle malondialdehyde and conjugated diene content decreased by 22% and 30%, respectively compared to the control group. At 2 h reperfusion, myeloperoxidase activity was increased 3.5-fold in control animals. In the in vitro study, taurine decreased malondialdehyde content in muscle slices incubated with hypochlorous acid in a dose-dependent manner, but there was no change when incubated with hydrogen peroxide and xanthine oxidase. Treatment with taurine inhibited I/R-induced compartment syndrome by at least in part attenuating oxidative stress injury induced by I/R, suggesting clinical application of taurine might be a new strategy for the prevention and treatment of compartment syndrome.

Taurine protects against methotrexate-induced toxicity and inhibits leukocyte death

The efficacy of methotrexate (MTX), a widely used cytotoxic chemotherapeutic agent, is often limited by severe side effects and toxic sequelae. Regarding the mechanisms of these side effects, several hypotheses have been put forward, among which oxidative stress is noticeable. The present study was undertaken to determine whether taurine, a potent free radical scavenger, could ameliorate MTX-induced oxidative injury and modulate immune response. Following a single dose of methotrexate (20 mg/kg), either saline or taurine (50 mg/kg) was administered for 5 days. After decapitation of the rats, trunk blood was obtained and the ileum, liver, and kidney were removed to measure malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen content, as well as histological examination. Our results showed that MTX administration increased the MDA, MPO activity, and collagen contents and decreased GSH levels in all tissues ( P < 0.001), while these alterations were reversed in taurine-treated group ( P < 0.05–0.01). Elevated ( P < 0.001) TNF-α level observed following MTX treatment was depressed with taurine ( P < 0.01). Oxidative burst of neutrophils stimulated by phorbol myristate acetate was reduced in saline-treated MTX group ( P < 0.001), while taurine abolished this effect. Similarly, flow cytometric measurements revealed that leukocyte apoptosis and cell death were increased in MTX-treated animals, while taurine reversed these effects ( P < 0.05). Reduced cellularity in bone marrow samples of MTX-treated group ( P < 0.01) was reversed back to control levels in taurine-treated rats. Severe degeneration of the intestinal mucosa, liver parenchyma, glomerular, and tubular epithelium observed in saline-treated group was improved by taurine treatment. In conclusion, it appears that taurine protects against methotrexate-induced oxidant organ injury and inhibits leukocyte apoptosis and may be of therapeutic potential in alleviating the systemic side effects of chemotherapeutics.

Effects of taurine on the expression of nitric oxide synthase in lung of rats exposed to silica

To evaluate the effects of taurine in diet on the expression of inducible nitric oxide synthase (iNOS) in rat lung induced by silica. Wistar rats were established by direct tracheal instillation of silica into rat lungs exposed surgically, and the animals of taurine-treated group were silica-instilled with a diet containing taurine. The taurine concentration of serum was analyzed by means of HPLC. The expression of iNOS protein in paraffin-embedded lung sections with Streptavidin/peroxidase (SP) immunohistochemistry on tissue microarray was measured by Image-Pro Plus. The concentration of taurine in serum of taurine-treated group was significantly higher than those in saline-treated and silica-treated groups (P < 0.05). The activities of total NOS and iNOS in BALF supernatant and iNOS positive area percentage of rat lung in silica-treated group were at the peak on 14th day, which were 1.84 U/ml, 1.12 U/ml and 5.42% more respectively than those in saline-treated group (P < 0.05). There were no significant differences between taurine-treated group and silica-treated group in total NOS and iNOS activities of BALF supernatant, and iNOS positive area of the lung (P > 0.05). Treatment with taurine hardly influences on the increase in expression of nitric oxide synthase in rat lung induced by silica dust.

The effect of taurine treatment on oxidative stress in experimental liver fibrosis.

Oxidative stress is important in pathogenesis of liver fibrosis, which is the result of deposition of excessive ECM proteins produced by activated hepatic stellate cells (HSCs). Reducing reactive oxygen species (ROS) production decreases collagen accumulation in liver. We investigated the benefits of antioxidant therapy in liver fibrosis and its association with HSC apoptosis. Forty-five male Spraque-Dawley rats were subdivided into three groups. Group I was treated with CCl(4) plus taurine, Group II with CCl(4) plus saline, and Group III with saline for 12 weeks. Erythrocyte and liver malondialdehyde (MDA) levels, superoxide dismutase (SOD) activities, Glutathione peroxidase (GSHpx) activities, and serum and liver TIMP-1 and MMP-13 levels were measured. Histopathological examinations were performed. Activated and total HSCs were quantified immunohistochemically. Apoptotic HSCs were detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. Taurine decreased histopathological injury scores and oxidative stress parameters significantly. The number of activated HSCs was significantly higher in taurine untreated group ( [Formula: see text] ). Serum and tissue MMP-13 levels were significantly higher and TIMP-1 levels were significantly lower in taurine-treated group ( [Formula: see text] and [Formula: see text], respectively). The number of apoptotic activated hepatic stellate cells was significantly higher with taurine treatment ( [Formula: see text] ). Preventing the production of reactive oxygen species is effective in inhibiting fibrogenesis in experimental rat model. Inhibitory activity of this agent on HSCs' activation, apoptosis, and further fibrogenic events should be clearly identified.

Islet Cryopreservation: Improved Recovery following Taurine Pretreatment

Simple and efficient freezing methods with maximal postthawing recovery form the basis of ideal cryopreservation. Taurine (2-amino ethanesulfonic acid), an end-product of sulphur amino acid metabolism, is one of the most abundant free amino acids in the body. The membrane stabilizing, free radical scavenging, and osmoregulatory roles of taurine have been well documented. We studied the effect of physiological and supra-physiological concentrations (0.3 and 3.0 mM) of taurine on islet cryopreservation. Islet viability on cryopreservation was significantly improved in both the taurine-treated groups (91.9 +/- 2.3% in 0.3 mM and 94.6 +/- 1.58% in 3.0 mM group, p < 0.05) compared with the controls (85.7 +/- 3.4%). Loss of peripheral islet cells was highly reduced in the taurine group, as examined under phase contrast and quantified by islet morphometric analysis (p < 0.05) using a digital image analysis system. Taurine-treated islets showed significant reduction in lipid peroxidation (0.905 and 0.848 nM MDA/microg protein for 0.3 and 3.0 mM taurine, respectively, p < 0.05) compared with control (1.307 nM MDA/microg protein) islets. In all, 500 islet equivalents (IE) of treated or control group islets were transplanted to BALB/c mice rendered diabetic with STZ. All animals showed a normal glucose clearance following a glucose load. Graft functionality was confirmed by normoglycemia (fasting plasma glucose: fpg < 150 mg/dl) after transplantation and reappearing hyperglycemia (fpg > 200 mg/dl) following removal of the graft. Suboptimal islet transplantation using 250 IE suggests that the grafted islet mass was inadequate for diabetes reversal. In addition, no significant differences were observed in the islet insulin content between the three groups following cryopreservation of the islets at -196 degrees C. Our studies indicate that taurine pretreatment and its continued presence during islet cryopreservation improves the postthawing viable recovery of islets.

Response of cats with dilated cardiomyopathy to taurine supplementation

Summary Between October 1986 and September 1988, 37 cats with moderate to severe idiopathic myocardial failure (dilated cardiomyopathy) were evaluated. Clinical management of these cats was similar to that described in the literature, except that it also included administration of 500 or 1,000 mg of the sulfur amino acid, taurine per day. Early death (death within the first 30 days of treatment) occurred in 14 (38%) cats. One cat was lost to follow-up evaluation. Twenty-two cats (59%) had marked clinical and echocardiographic improvement and survived longer than 240 days. In all but 1 cat, the observed improvement in echocardiographic measurements persisted. Hypothermia and thromboembolism were positively associated with an increased risk of early death. Administration of digoxin did not significantly affect survival. All 22 cats that survived &gt; 30 days remained clinically stable despite withdrawal of all medications except taurine. Administration of taurine was eventually discontinued in 20 of the 22 cats and adequate taurine intake was thereafter provided for in the food. The clinical response and 1-year survival rate of 58% (21 of 36 cats with a known outcome) in the taurine-treated group represents a marked improvement, compared with a 1-year survival rate of 13% (4 of 31 cats with a known outcome) in a retrospectively evaluated population of 33 cats with dilated cardiomyopathy.

Effect of intravenous taurine supplementation on plasma, blood cell, and urine taurine concentrations in adults undergoing long-term parenteral nutrition

Thirty-four adults undergoing long-term parenteral nutrition (TPN) were treated either with or without intravenous taurine for less than or equal to 24 mo. Statistical comparisons were carried out in eight patients randomly assigned to receive intravenous taurine, usually 10 mg.kg-1.d-1, and 10 patients not receiving taurine. Compared with normal adults, baseline plasma taurine and urine taurine-creatinine ratios were decreased in both groups and platelet taurine was reduced in the taurine-treated group. During taurine treatment the mean of the mean values for taurine became normal in plasma and platelets and remained normal in erythrocytes, granulocytes, and lymphocytes; urine taurine-creatinine ratios rose to approximately five times normal. During follow-up, patients not given taurine had plasma, erythrocyte, and granulocyte taurine and urine taurine-creatinine ratios below normal values and the concentrations of taurine-treated patients. Their platelet taurine was also subnormal. Thus, 10 mg taurine.kg-1.d-1 intravenously normalizes plasma and blood cell taurine concentrations in long-term TPN patients.

Membrane perturbations and mediation of gap junction formation in response to taurine treatment in normal and injured alveolar epithelia.

Nitrogen dioxide is an air pollutant that causes pulmonary alterations. Employing light and transmission electron microscopy, we examined plastic sections and freeze-fracture replicas of alveolar epithelium of groups of hamsters exposed to nitrogen for 24 h to determine taurine-induced changes in intercellular junctions. Prior to exposure, one group of hamsters was given 0.5% taurine in their drinking water for 2 weeks. A second group of hamsters was given taurine-free water. The taurine-treated group was divided into three subgroups. The first subgroup was exposed to nitrogen dioxide at a concentration of 7 ppm for 24 h, the second subgroup was exposed to nitrogen dioxide at a concentration of 30 ppm for 24 h, and the third subgroup was exposed to normal room air for 24 h. The nontaurine-treated animals were similarly divided into three subgroups and treated as described above. The lungs of the hamsters exposed to nitrogen dioxide without the taurine pretreatment exhibited extensive inflammatory cell infiltration in the walls of the terminal bronchioles, alveolar ducts, and peribronchiolar alveoli. The degree of infiltration was proportional to the degree of nitrogen dioxide concentration. The taurine-treated animals exposed to nitrogen dioxide and the nontaurine-treated animals exposed to room aid did not show any inflammatory infiltrate. Freeze-fracture replicas of the tight junctional regions of the type I and type II pneumocytes revealed significant fragmentation in the nitrogen dioxide-exposed lungs. It was also observed that the tight junctions between the type I pneumocytes of the taurine-treated groups, whether exposed or not, revealed gap junction-like aggregates among the tight junction fibrils. The 30-ppm nitrogen dioxide exposed group exhibited larger and more frequent gap junctions between the pneumocytes than those observed in the 7-ppm nitrogen dioxide exposed group. The evidence suggests that taurine may have an effect on plasma membranes and intercellular communications. Changes in intercellular communication may contribute to decreased susceptibility to injury and increased pneumocyte survival.