Sulfur is an essential element for the entire biological kingdom because of its incorporation into amino acids, proteins and other biomolecules. Sulfur atoms are also important in the iron-containing flavoenzymes. Unlike humans, plants can use inorganic sulfur to synthesize sulfur-containing amino acids. Therefore, plants are an important source of sulfur for humans. Sulfur-containing compounds are found in all body cells and are indispensable for life. Some of sulfur-containing antioxidant compounds are, cysteine, methionine, taurine, glutathione, lipoic acid, mercaptopropionylglycine, N-acetylcysteine, and the three major organosulfur compounds of garlic oil, diallylsulfide, diallyldisulfide and diallyltrisulfide. In a comparison of the structure-function relationship among these sulfur-containing antioxidant compounds, dihydrolipoic acid (the reduced form of LA) is the most effective antioxidant. Dihydrolipoic acid contains two sulfhydryl groups and can undergo further oxidation reaction to form lipoic acid. The antioxidative activities of sulfur-containing compounds follow a general trend, the more highly reduced forms are stronger antioxidants and the number of sulfur atoms determine, at least in part, their modulatory activites on the glutathione related antioxidant enzymes. In this article, the antioxidant effects and the antioxidative activities, of sulfur-containing amino acids, are reviewed. In addition, the general antioxidant effects and the structure-function relationship of some sulfur-containing compounds are also reviewed.
Acetylcysteine/pharmacology ; Amino Acids, Sulfur/*pharmacology ; Antioxidants/*pharmacology ; Cysteine/pharmacology ; Glutathione/pharmacology ; Methionine/pharmacology ; Structure-Activity Relationship ; Taurine/pharmacology ; Thioctic Acid/pharmacology ; Thiopronine/pharmacology

AIMClinical studies stated that low molecular weight compounds (< 1.0 kd) extracted from the new born calf liver could effectively inhibit the proliferation of tumor cells. In this report, we observed inhibition effects and their regulative mechanisms of taurine, ornithine, carnosine on the proliferation of HL-60 cells.

METHODSThree active ingredients, i.e., taurine, ornithine and carnosine were separated by ion-exchange chromatographic column and identified from the low molecular weight filtrate of new born calf liver. MTT assay was used to test the survival rate of HL-60 cells and normal lymphocytes treated by the three ingredients. The various effects of the three compounds on HL-60 cells were respectively evaluated by agarose gel electrophoresis, ESR and immunohistochemical methods.

RESULTSThese compounds effectively inhibited the proliferation of HL-60 cells and induced apoptosis which was determined by apoptotic changes in morphology and nuclear DNA degradation. Whereas no inhibition effects on normal lymphocytes were observed. In addition, the results of ESR showed that the activity of oxygen radical within HL-60 cells treated with there compounds decreased to trace level. Furthermore, in the immunohistochemical experiments, we found that the level of p45/skp2 in HL-60 cells decreased while the level of p27/kip increased.

CONCLUSIONThe taurine, ornithine and carnosine compounds can selectively suppress tumor cells proliferation by regulating the level of cell cycle proteins.

Animals ; Animals, Newborn ; Apoptosis ; drug effects ; Carnosine ; pharmacology ; Cattle ; HL-60 Cells ; Humans ; Liver ; chemistry ; Ornithine ; pharmacology ; Taurine ; pharmacology

OBJECTIVE: To investigate the anti-oxidative effect of ethyl pyruvate (EP) and taurine (TAU) on the quality of red blood cells stored at 4±2 ℃, hemolysis, energy metabolism and lipid peroxidation of the red blood cells in the preservation solution were studied at different intervals. METHODS: At 4±2 ℃, the deleukocyte red blood cells were stored in the citrate-phosphate-dextrosesaline-adenine-1 (CPDA-1) preservation (control group), preservation solution with EP (EP-AS), and TAU (TAU-AS) for long-term preservation. The enzyme-linked immunoassay and automatic blood cell analyzer were used to detect hemolysis and erythrocyte parameters. Adenine nucleoside triphosphate (ATP), glycerol 2,3-diphosphate (2,3-DPG) and malondialdehyde (MDA) kits were used to test the ATP, 2,3-DPG and MDA concentration. RESULTS: During the preservation, the rate of red blood cell hemolysis in EP-AS and TAU-AS groups were significantly lower than that in CPDA-1 group (P<0.01). The MCV of EP-AS group was increased with the preservation time (r=0.71), while the MCV of the TAU-AS group was significantly lower than that in the other two groups (P<0.05). The concentration of ATP and MDA in EP-AS and TAU-AS groups were significantly higher than that in CPDA-1 group at the 14th day (P<0.01). The concentrations of 2,3-DPG in the EP-AS and TAU-AS groups were significantly higher than that in the CPDA-1 group from the 7th day (P<0.01). CONCLUSION EP and TAU can significantly reduce the red blood cell hemolysis rate, inhibit the lipid peroxidation level of red blood cells, and improve the energy metabolism of red blood cells during storage. The mechanism of EP and TAU may be related to their antioxidation and membrane protection effect, so as to improve the red blood cell quality and extend the preservation time.
2,3-Diphosphoglycerate/metabolism* ; Adenine ; Adenosine Triphosphate/metabolism* ; Blood Preservation ; Citrates/pharmacology* ; Erythrocytes/metabolism* ; Glucose/pharmacology* ; Hemolysis ; Humans ; Pyruvates ; Taurine/pharmacology*

OBJECTIVETo explore the effects of taurine on the ultrastructure and P2X7 receptor protein expression in brain following traumatic brain injury (TBI) in rats.

METHODSForty male SD rats, were divided randomly into four groups that were sham-operated group, TBI group, TBI plus low-dose taurine group and TBI plus high-dose taurine group. The TBI model was established by Marmarou's method, the expression of P2X7 receptor protein in parietal cortex and hippocampus was detected by the immunohistochemical method, the ultrastructure of parietal cortex were observed by transmission electron microscope.

RESULTSCompared with sham-operated group, the positive expression cells of P2X7 receptor protein in parietal cortex and hippocampus of TBI group were significantly increased (P < 0.01). Compared with TBI group, the positive expression cells of P2X7 receptor protein in parietal cortex and hippocampus of TBI plus low-dose taurine group and TBI plus high-dose taurine group were significantly decreased (P <0.01 or P <0.05). Compared with TBI plus low-dose taurine group, the positive expression cells of P2X7 receptor protein in parietal cortex and hippocampus of TBI plus high-dose taurine group were significantly decreased (P < 0.05 or P < 0.01). The pathological damage of parietal cortex in the TBI plus high-dose taurine group was obviously lightened.

CONCLUSIONTaurine exerts the neuroprotective effect on TBI in rats, the protective mechanism might be associated with down-regulating the expression of P2X7 receptor protein in parietal cortex and hippocampus.

Animals ; Brain ; metabolism ; ultrastructure ; Brain Injuries ; metabolism ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, Purinergic P2X7 ; metabolism ; Taurine ; pharmacology

OBJECTIVETo track the translocation of water soluble taurine multi-wall carbon nanotubes (14C-tau-MWCNTs) in lungs of the Kunming mice and evaluate the acute lung toxicity of intratracheally instilled tau-MWCNTs in Kunming mice.

METHODSHealthy adult Kunming mice were randomly grouped by their body weight (5 mice in each group). The lungs of mice were intratracheally instilled with 0.125, 0.25, 0.5 and 1 mg/kg of water soluble tau-MWCNTs and phosphate-buffered saline (PBS) as negative control. After exposure of 1, 7, 14 and 28 days, the blood and lung tissue were collected. Blood were assessed by using biochemical biomarkers of alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and angiotensin converting enzyme (ACE). Lung tissues were assessed by histopathology. The intratracheal instillation of 14C-tau-MWCNTs was conducted in the same way, after 1, 3, 7, 14, 21, 28 days, 14C-activity of the samples was counted in several organs, tissues, blood and feces etc.

RESULTS14C-activities were detected only in lungs, and with the exposure time proceeding the radioactivity descending from (80 +/- 7.7)% of the 1st day to (22 +/- 6.9)% of the 28th day. Activity of all groups of ALP and LDH went to the highest level on the 7th day postexposure, and back to the control level on the 28th day post-exposure, but LDH of 1 mg/kg group[(14.18 +/- 1.70) micromol x s(-1) x L(-1)] was still higher than that of control [(10.95 +/- 3.51) micromol x s(-1) x L(-1)] after 28 days' exposure. There was no significant changes observed in the activity of ACE. Histopathology found that lungs of all groups presented significant increase in pulmonary inflammation, lung cell proliferation. Many tau-MWCNTs were clearly found in some alveolar macrophages and bronchial epithelial cells.

CONCLUSIONIntratracheal instillation of water soluble tau-MWCNTs could induce slight bio-effects on lungs of Kunming mice.

Animals ; Instillation, Drug ; Lung ; drug effects ; Male ; Mice ; Mice, Inbred Strains ; Nanotubes, Carbon ; Taurine ; administration & dosage ; pharmacokinetics ; pharmacology ; Trachea

The function for cardiac vascular system of taurine is extensive, and the mechanism is complicated. Taurine protects the cells from the cell injury caused by ischemia etc. Through repressing apoptosis, prevents endothelial dysfunction caused by hyperglycemia, hypercholesterolemia, smoking and homocysteine; suppresses the proliferation and calcification in vascular smooth muscle cells, promotes metabolization and excretion of cholesterol in the animal models of hyperlipemia, and confers the resistance to an oxidant, hypochlorous acid, produced by neutrophil on cells, and taurine chrolamine to inhibit activation of NF-kappaB, which might be associated with anti-atherosclerotic effect. Taurine mainly acts inside the cell. However, taurine transport system becomes aberrant in pathological myocardial and vascular tissue. In addition, taurine improves cardiovascular function in fructose-induced hypertension and an iron-overload murine animal models.
Animals ; Antioxidants ; pharmacology ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Humans ; Lipid Metabolism ; drug effects ; Materia Medica ; pharmacology ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Cardiac ; pathology ; Taurine ; pharmacology

OBJECTIVES: To investigate the effect of taurine magnesium coordination compound (TMCC) on torsades de pointes (TdP) in isolated guinea pig hearts. METHODS: Healthy male guinea pigs weighting 250~300 g were randomly divided into 4 groups:①TdP model group (=7):Isolated hearts were perfused by normal K-H solution 20 minutes, then perfused by slowly activated delayed rectifier potassium current(IKs) blocker 10mol/L Chromanol 293B under hypokalemic solution(1.8 mmol/L) to establish TdP model;②~④ TdP model + TMCC group (=6):Isolated hearts were perfused by normal K-H solution for 20 minutes, then perfused by IKs blocker 10mol/L Chromanol 293B under hypokalemic solution(1.8 mmol/L) for 60 minutes, at the same time TMCC which concentration was 1, 2, 4 mmol/L was administered respectively by Langendorff retrograde aortic perfusion method. Cardiac surface electrocardiogram of guinea pigs was collected and recorded by Biopac electrophysiological recorder. Incidence of TdP, transmural dispersion of repolarization (TDR), instability of QT interval were acquired from Lead Ⅱ electrocardiograph (ECG) wave forms to describe the effect of TMCC on TdP model. Datas were acquired at the time of 20 min and pre-TdP, in case there was no TdP observed, a value of 60 min was entered for calculation purpose. RESULTS: Incidence of TdP in TdP model group was 6/7. TdP incidence could be decreased significantly by 1, 2, 4 mmol/L TMCC, and was 5/6, 1/6, 0/6 respectively. Compared with the pre-drug, Chromanol 293B under hypokalemic solution in TdP model group increased TDR(corrected) evidently(<0.01). Compared with the pre-drug, 1, 2, 4 mmol/L TMCC in TdP model + TMCC group could decrease the increased TDR(corrected) induced by Chromanol 293B under hypokalemic solution(>0.05). Compared with the TdP model group, 2, 4 mmol/L TMCC could evidently decrease the instability of QT interval induced by Chromanol 293B under hypokalemic solution(<0.05). During the establishment of TdP model, P waves in more than one cardiac cycle continuously were disappeared in ECG. However, P wave could always be seen independent in ECG acquired from TdP model + TMCC group. CONCLUSIONS TMCC can play the role against TdP through decreasing TDR and instability of QT interval, and inhibiting early after depolarization(EAD).
Animals ; Anti-Arrhythmia Agents ; pharmacology ; Electrocardiography ; Guinea Pigs ; In Vitro Techniques ; Long QT Syndrome ; Magnesium ; pharmacology ; Male ; Random Allocation ; Taurine ; pharmacology ; Torsades de Pointes ; drug therapy

OBJECTIVETo investigate the vasorelaxant effect of taurine (Tau) in rat aortic rings and the mechanism.

METHODThe isolated thoracic aortic rings of male Wistar rats were mounted on the organ bath. The effect of Tau 10, 20, 40, 80 mmol x L(-1) on the rings with endothelium intact or endothelium denuded precontracted by the phenylephrine (1 micromol x L(-1)) or KCl (60 mmol x L(-1)), and the effect of Tau on the vessel reaction induced by various drugs were recorded with biological signal analytical system.

RESULTTaurine completely relaxed the contractions induced by KCl and phenylephrine in a concentration-dependent manner in endothelium-intact and endothelium-denuded rat aorta. Taurine attenuated the contraction to PE both in the absence and presence of calcium, but had no significant effect on the contraction induced by caffeine. The relaxant effect of taurine was significantly inhibited by pretreatment of endothelium-denuded aorta with potassium channel antagonists glibenclamide and tetraethylamine but not by BaCl2 or 4-aminopyridine.

CONCLUSIONTaurine induces an endothelium-independent relaxation in rat aortic rings. The mechanisms may involve the reduction in Ca2+-influx and Ca2+-release and the participation of the potassium channels (KATP and KCa, but not Kir or KV).

Animals ; Aorta ; drug effects ; physiology ; Endothelium, Vascular ; drug effects ; physiology ; Male ; Models, Animal ; Muscle Relaxation ; drug effects ; Rats ; Rats, Wistar ; Taurine ; pharmacology ; Vasodilation ; drug effects ; Vasodilator Agents ; pharmacology

OBJECTIVETo explore the possible mechanism(s) of taurine-inhibiting the proliferation of hepatic stellate cells (HSC), this study investigated the effect of taurine on the HSC cell cycle and its regulatory protein expression.

METHODSCell proliferation was assessed by MTT assay. Cell cycle was analyzed by flow cytometry. Cell cycle regulatory protein Cyclin D1 and P21waf1 expression were determined by immunocytochemistry and image-analysis system, and real-time quantitative PCR.

RESULTSHSC proliferation was markedly inhibited when HSC were treated with taurine at concentrations of 5, 10, 20, 30, 40 and 50 mmol/L for 48 hours, and the inhibition rates were 6.7%, 14.4%, 23.3%, 32.2%, 36.7% and 45.6% respectively (P < 0.05-0.01). In the flow cytometry analysis, it was found that taurine could block HSC in the G0/G1 phase from entering the S phase, resulting in more cells in the G0/G1 phase and fewer in the S phase. The percentage of the cells in the G0/G1 phase and the S phase at the dosage of 40 mmol/L were 68.2%+/-1.4% and 26.2+/-1.3% respectively, which was significantly different in comparison to the controls (56.2%+/-1.7% and 38.5%+/-0.8% respectively, P < 0.01). HSC expressed cyclin D1 and P21waf1. Taurine inhibited cyclin D1 expression and induced P21waf1 expression. The cyclin D1 protein and mRNA in the HSC treated with 40 mmol/L taurine were significantly reduced compared with the controls [protein (optical density value): 0.13+/-0.02 versus 0.18+/-0.02, P < 0.01; mRNA: 5776.7+/-3345.0 versus 18,400.6+/-1374.8 copies/10(6) GAPDH, P < 0.01]; and the P21waf1 protein and mRNA were markedly increased compared with the controls [protein (optical density value): 0.19+/-0.02 versus 0.14+/-0.01, P < 0.01; mRNA: 44,866.7+/-3910.7 versus 16,933.3+/-960.9 copies/10(6) GAPDH, P less than 0.05].

CONCLUSIONSCyclin D1 and P21waf1 were cell cycle regulatory proteins in HSC, and taurine can inhibit the HSC cyclin D1 expression and stimulate P21waf1 expression, facilitate arresting cells in G0/G1 phase, and suppress cell proliferation.

Animals ; Cell Cycle Proteins ; biosynthesis ; genetics ; Cell Line ; Cell Proliferation ; Cyclin D1 ; biosynthesis ; genetics ; Cyclin-Dependent Kinase Inhibitor p21 ; biosynthesis ; genetics ; Depression, Chemical ; Hepatocytes ; cytology ; Rats ; Taurine ; pharmacology

AIMTo investigate the effect of taurine on nitric oxide synthase (NOS) activity and nitric oxide products (NO2 /NO3 ) content in myocardium and plasma during shock resuscitation.

METHODSTwenty-four rabbits were divided randomly into 3 groups (n=8): control group, shock group, taurine group. The model of hemorrhagic shock resuscitation was used. The activities of nitric oxide synthase (NOS), lactate dehydrogenase (LDH) and the contents of nitric oxide products (NO2- /NO3-) in plasma were observed before shock and shock 1.5 hours, after resuscitation 1 hour, 2 hours and 3 hours. The activities of NOS and the contents of NO2-/NO3- in myocardium homogenate were measured after resuscitation 3 hours. Meanwhile, pathologic samples treated routinely.

RESULTS(1) During resuscitation, the activities of NOS, LDH and the contents of NO2- /NO3- in plasma of shock group were significantly higher than that of before shock and shock 1.5 hours (P < 0.01). (2) After resuscitation 3 hours, the activity of NOS and the contents of NO2- / NO3 in myocardium of shock group were significantly higher than that of control group (P < 0.01). The cardiac myocyte appeared edema, fatty degeneration. (3) All the changes of above mentioned could be attenuated by intravenous injection taurine (40 mg/kg) (P < 0.01).

CONCLUSIONThese results suggest that the NOS activation and NO release may mediated myocardium injury induced by shock resuscitation, taurine can ameliorate the myocardium injury, which may be related to decreasing the generation of NO.

Animals ; Myocardium ; metabolism ; pathology ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Plasma ; metabolism ; Rabbits ; Resuscitation ; Shock, Hemorrhagic ; blood ; metabolism ; Taurine ; pharmacology