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硝酸钠 BioXtra, ≥99.0%; CAS Number: 7631-99-4; EC Number: 231-554-3; Synonyms: 智利硝石; find Sigma-Aldrich-S8170 MSDS, related peer-reviewed papers, technical documents, similar products & more at Sigma-Aldrich

硝酸钠 BioXtra, ≥99.0% | Sigma-Aldrich

硝酸钠

Quantification of Chlorophyll as a Proxy for Biofilm Formation in the Cyanobacterium Synechococcus elongatus

Methylglyoxal evokes acute Ca2+ transients in distinct cell types and increases agonist-evoked Ca2+ entry in endothelial cells via CRAC channels

Inorganic nitrate as a treatment for acute heart failure: a protocol for a single center, randomized, double-blind, placebo-controlled pilot and feasibility study

Re-evaluation of sodium nitrate (E 251) and potassium nitrate (E 252) as food additives

Cytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver

Two-step concentration of complex water samples for the detection of viruses

Testicular torsion, a common urologic emergency, is primarily caused by ischemia/reperfusion (I/R) injury of the testis. Nitric oxide (NO)-derived from nitrite (NO2-) has been reported to have prominent therapeutic effects on I/R injury in the heart, liver, and brain; however, its effects on testicular I/R injury have not been evaluated. This study, therefore, investigated whether NO from NO2- is beneficial in a rat model of testicular I/R injury which eventually results in impaired spermatogenesis. Male Sprague-Dawley rats were assigned to the following seven groups: group A, sham-operated control group; Group B, I/R with no treatment; Groups C, D, and E, I/R followed by treatment with three different doses of NO2-; Group F, I/R followed by administration of NO2- and NO scavenger (2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt [C-PTIO]); and Group G, I/R followed by administration of nitrate (NO3-). NO2-, NO3-, and C-PTIO were intravenously administered. Histological examination of the testes and the western blot analysis of caspase-3 were performed. Levels of antioxidant enzymes and lipid peroxidation were measured. Germ cell apoptosis, oxidative stress, antioxidant enzymatic function, and lipid peroxidation in Group B were significantly higher than those in Group A. Group B exhibited an abnormal testicular morphology and impaired spermatogenesis. In contrast, testicular damages were attenuated in the NO2- treatment groups, which were caused by reduction in superoxide and peroxynitrite levels and an inhibition of caspase-3-dependent apoptosis. The results of this study suggest NO2- to be a promising therapeutic agent with anti-oxidant and anti-apoptotic properties in testicular I/R injury.

Sodium nitrite-derived nitric oxide protects rat testes against ischemia/reperfusion injury.

One of the most important requirements for non-viral gene delivery systems is the ability to mediate high levels of gene expression with low toxicity. After the DNA/vector complexes are taken up by cells through endocytosis, DNA is typically contained within the endocytic compartments and rapidly degraded due to the low pH and hydrolytic enzymes within endosomes and lysosomes, limiting its accessibility to the cytosol and ultimately to the nucleus. In this study, the endosomolytic protein listeriolysin O (LLO) from the intracellular pathogen Listeria monocytogenes was conjugated with polyethylenimine (PEI) of average molecular weight 25 kDa (PEI25) via a reversible disulfide bond (LLO-s-s-PEI), and incorporated into plasmid DNA condensed with disulfide-crosslinked low molecular weight PEI 1.8 kDa (PEI1.8). We have investigated and demonstrated that high gene transfection efficiency, which is comparable to that by the most commonly used PEI25, can be achieved by reversibly crosslinking low molecular weight PEI (PEI1.8) using disulfide bonds, with greatly reduced cytotoxicity of the PEI. The reversible incorporation of LLO into the DNA condensates of PEI, through the use of the synthesized LLO-s-s-PEI conjugate, further enhances the transfection efficiency beyond that of DNA condensates with disulfide-crosslinked PEI1.8 alone.

Enhanced gene delivery using disulfide-crosslinked low molecular weight polyethylenimine with listeriolysin o-polyethylenimine disulfide conjugate.

In the present study, a new approach which uses immunoaffinity column clean-up combined with dispersive liquid-liquid microextraction (DLLME) is proposed for the preconcentration of ultra trace amounts of aflatoxins (B₁, B₂, G₁ and G₂). The aflatoxins are then determined using a high-performance liquid chromatography coupled with fluorescent detector. Samples are extracted by immunoaffinity column (IAC) clean-up, and their eluents are used as dispersants of the subsequent DLLME, for further enrichment of aflatoxins. Various parameters (the type of elution solvent, the type and volume of extraction solvent and disperser solvent, extraction time, and centrifugation time) that affect the efficiency of the two steps are optimized. Under the optimum conditions (extraction solvent: 120 μL of chloroform, disperser solvent: 500 μL of acetonitrile, sample pH: 7.4, centrifugation time: 3 min), the calibration for B₁, B₂, G₁ and G₂ was found to be linear with coefficient of estimation (R²) of 0.9994, 0.9976, 0.9989, 0.9973 respectively and the limit of detection (LOD) was between 1.1 × 10⁻⁴ to 5.3 × 10⁻³ ng mL⁻¹ (3σ(b)/m, n=9). The recoveries at the two spiked levels ranged from 96.0 to 110.0% and the relative standard deviation (RSD) was less than 7.8% (n=9). The results show that dispersive liquid-liquid microextraction combined with HPLC is a selective, simple, sensitive, and effective analytical method for the preconcentration and determination of ultra trace amounts of aflatoxins. The proposed method was applied for preconcentration and determination of B₁, B₂, G₁ and G₂ aflatoxin in edible oils. Analysis of aflatoxins in FAPAS test material showed that the proposed method has good accuracy.

A novel method for high preconcentration of ultra trace amounts of B₁, B₂, G₁ and G₂ aflatoxins in edible oils by dispersive liquid-liquid microextraction after immunoaffinity column clean-up.

Supplementation with inorganic nitrate has been suggested to be an ergogenic aid for athletes as nitric oxide donor. The purpose of this study was to determine whether ingestion of inorganic sodium nitrate benefits well-trained athletes performing a 40-min exercise test in laboratory conditions. In addition, we investigated the effect of this supplement on plasma levels of endothelin-1 (ET-1) and in nitrated proteins. Thirteen trained athletes participated in this randomized, double-blind, crossover study. They performed a 40-min cycle ergometer distance-trial test after two 3-d periods of dietary supplementation with sodium nitrate (10 mg·kg of body mass) or placebo. Concentration of plasma nitrate (256 ± 35 μM) and nitrite (334 ± 86 nM) increased significantly (P < 0.05) after nitrate supplementation compared with placebo (nitrate: 44 ± 11 μM; nitrite: 187 ± 43 nM). In terms of exercise performance, there were no differences in either the mean distance (nitrate: 26.4 ± 1.1 km; placebo: 26.3 ± 1.2 km; P = 0.61) or mean power output (nitrate: 258 ± 28 W; placebo: 257 ± 28 W; P = 0.89) between treatments. Plasma ET-1 increased significantly (P < 0.05) just after exercise in nitrate (4.0 ± 0.8 pg·mL) and placebo (2.4 ± 0.4 pg·mL) conditions. This increase was significantly greater (P < 0.05) in the nitrate group. Levels of nitrated proteins did not differ between treatments (nitrate: preexercise, 91% ± 23%; postexercise, 81% ± 23%; placebo: preexercise, 95% ± 20%; postexercise, 99% ± 19%). Sodium nitrate supplementation did not improve a 40-min distance-trial performance in endurance athletes. In addition, concentration of plasma ET-1 increased significantly after exercise after supplementation with sodium nitrate.

Sodium nitrate supplementation does not enhance performance of endurance athletes.

Necrotizing enterocolitis (NEC) is a devastating disease of premature infants characterized by severe intestinal necrosis and for which breast milk represents the most effective protective strategy. Previous studies have revealed a critical role for the lipopolysaccharide receptor toll-like receptor 4 (TLR4) in NEC development through its induction of mucosal injury, yet the reasons for which intestinal ischemia in NEC occurs in the first place remain unknown. We hypothesize that TLR4 signaling within the endothelium plays an essential role in NEC development by regulating perfusion to the small intestine via the vasodilatory molecule endothelial nitric oxide synthase (eNOS). Using a unique mouse system in which we selectively deleted TLR4 from the endothelium, we now show that endothelial TLR4 activation is required for NEC development and that endothelial TLR4 activation impairs intestinal perfusion without effects on other organs and reduces eNOS expression via activation of myeloid differentiation primary response gene 88. NEC severity was significantly increased in eNOS(-/-) mice and decreased upon administration of the phosphodiesterase inhibitor sildenafil, which augments eNOS function. Strikingly, compared with formula, human and mouse breast milk were enriched in sodium nitrate--a precursor for enteral generation of nitrite and nitric oxide--and repletion of formula with sodium nitrate/nitrite restored intestinal perfusion, reversed the deleterious effects of endothelial TLR4 signaling, and reduced NEC severity. These data identify that endothelial TLR4 critically regulates intestinal perfusion leading to NEC and reveal that the protective properties of breast milk involve enhanced intestinal microcirculatory integrity via augmentation of nitrate-nitrite-NO signaling.

Endothelial TLR4 activation impairs intestinal microcirculatory perfusion in necrotizing enterocolitis via eNOS-NO-nitrite signaling.

Nitrate, which is an inorganic anion abundant in vegetables, increases the efficiency of isolated human mitochondria. Such an effect might be reflected in changes in the resting metabolic rate (RMR) and formation of reactive oxygen species. The bioactivation of nitrate involves its active accumulation in saliva followed by a sequential reduction to nitrite, nitric oxide, and other reactive nitrogen species. We studied effects of inorganic nitrate, in amounts that represented a diet rich in vegetables, on the RMR in healthy volunteers. In a randomized, double-blind, crossover study, we measured the RMR by using indirect calorimetry in 13 healthy volunteers after a 3-d dietary intervention with sodium nitrate (NaNO₃) or a placebo (NaCl). The nitrate dose (0.1 mmol · kg⁻¹ · d⁻¹) corresponded to the amount in 200-300 g spinach, beetroot, lettuce, or other vegetable that was rich in nitrate. Effects of direct nitrite exposure on cell respiration were studied in cultured human primary myotubes. The RMR was 4.2% lower after nitrate compared with placebo administration, and the change correlated strongly to the degree of nitrate accumulation in saliva (r² = 0.71). The thyroid hormone status, insulin sensitivity, glucose uptake, plasma concentration of isoprostanes, and total antioxidant capacity were unaffected by nitrate. The administration of nitrite to human primary myotubes acutely inhibited respiration. Dietary inorganic nitrate reduces the RMR. This effect may have implications for the regulation of metabolic function in health and disease.

Dietary nitrate reduces resting metabolic rate: a randomized, crossover study in humans.

Nitrite anion has been demonstrated to be a prodrug of nitric oxide (NO) with positive effects on tissue ischemia/reperfusion injury, cytoprotection, and vasodilation. However, effects of nitrite anion therapy for ischemic tissue vascular remodeling during diabetes remain unknown. We examined whether sodium nitrite therapy altered ischemic revascularization in BKS-Lepr(db/db) mice subjected to permanent unilateral femoral artery ligation. Sodium nitrite therapy completely restored ischemic hind limb blood flow compared with nitrate or PBS therapy. Importantly, delayed nitrite therapy 5 days after ischemia restored ischemic limb blood flow in aged diabetic mice. Restoration of blood flow was associated with increases in ischemic tissue angiogenesis activity and cell proliferation. Moreover, nitrite but not nitrate therapy significantly prevented ischemia-mediated tissue necrosis in aged mice. Nitrite therapy significantly increased ischemic tissue vascular endothelial growth factor (VEGF) protein expression that was essential for nitrite-mediated reperfusion of ischemic hind limbs. Nitrite significantly increased ischemic tissue NO bioavailability along with concomitant reduction of superoxide formation. Lastly, nitrite treatment also significantly stimulated hypoxic endothelial cell proliferation and migration in the presence of high glucose in an NO/VEGF-dependent manner. These results demonstrate that nitrite therapy effectively stimulates ischemic tissue vascular remodeling in the setting of metabolic dysfunction that may be clinically useful.

Nitrite anion therapy protects against chronic ischemic tissue injury in db/db diabetic mice in a NO/VEGF-dependent manner.

Nitric oxide (NO) deficiency mediates oxidative stress in the kidney and is involved in the development of hypertension. NO synthesis occurs via 2 pathways: nitric oxide synthase (NOS) dependent and NOS-independent. We tested whether the development of hypertension is prevented by restoration of NO by dietary l-citrulline or nitrate supplementation in young spontaneously hypertensive rats (SHRs). Male SHRs and normotensive Wistar Kyoto control rats (WKYs)s age 4 weeks were assigned to 4 groups: untreated SHRs and WKYs, and SHRs and WKYs that received 0.25% l-citrulline for 8 weeks. In our second series of studies, we replaced l-citrulline with 1 mmol/kg/d sodium nitrate. All rats were sacrificed at age 12 weeks. We found an increase in the blood pressure of SHRs was prevented by dietary supplementation of l-citrulline or nitrate. Both treatments restored NO bioavailability and reduced oxidative stress in SHR kidneys. l-Citrulline therapy reduced levels of l-arginine and asymmetric dimethylarginine (ADMA)-an endogenous inhibitor of NOS-and increased the l-arginine-to-ADMA ratio in SHR kidneys. Nitrate treatment reduced plasma levels of l-arginine and ADMA concurrently in SHRs. Our findings suggest that both NOS-dependent and -independent approaches in the prehypertensive stage toward augmentation of NO can prevent the development of hypertension in young SHRs.

Two different approaches to restore renal nitric oxide and prevent hypertension in young spontaneously hypertensive rats: l-citrulline and nitrate.

Reverse osmosis concentrate from wastewater reclamation contains biorefractory trace organic contaminants that may pose environmental or health hazard. Due to its high conductivity, electrochemical oxidation of brine requires low voltage which is energetically favourable. However, the presence of chloride ions may lead to the formation of chlorinated by-products, which are likely to exert an increased toxicity and persistence to further oxidation than their non-chlorinated analogues. Here, the performance of Ti/Pt-IrO(2), Ti/SnO(2)-Sb and Si/BDD anodes was evaluated for the electrochemical oxidation of ROC in the presence of chloride, nitrate or sulfate ions (0.05 M sodium salts). In order to investigate the electrooxidation of ROC with nitrate and sulfate ions as dominant ion mediators, chloride ion concentration was decreased 10 times by electrodialytic pretreatment. The highest Coulombic efficiency for chemical oxygen demand (COD) removal was observed in the presence of high chloride ions concentration for all anodes tested (8.3-15.9%). Electrooxidation of the electrodialysed concentrate at Ti/SnO(2)-Sb and Ti/Pt-IrO(2) electrodes exhibited low dissolved organic carbon (DOC) (i.e. 23 and 12%, respectively) and COD removal (i.e. 37-43 and 6-22%, respectively), indicating that for these electrodes chlorine-mediated oxidation was the main oxidation mechanism, particularly in the latter case. In contrast, DOC removal for the electrodialysed concentrate stream was enhanced at Si/BDD anode in the presence of SO(4)(2-) (i.e. 51%) compared to NO(3)(2-) electrolyte (i.e. 41%), likely due to the contribution of SO(4)(·-) and S(2)O(8)(2-) species to the oxidative degradation. Furthermore, decreased concentration of chloride ions lead to a lower formation of haloacetic acids and trihalomethanes at all three electrodes tested.

Electrochemical oxidation of electrodialysed reverse osmosis concentrate on Ti/Pt-IrO2, Ti/SnO2-Sb and boron-doped diamond electrodes.

Dietary nitrate supplementation has been shown to reduce O2 cost of submaximal exercise, improve exercise tolerance, and enhance performance in moderately trained individuals. In contrast, data have been provided that elite athletes do not benefit from nitrate supplementation. The aim of this study was to evaluate the effects of short-term nitrate supplementation on endurance performance in subjects with different levels of aerobic fitness. Twenty-one subjects (mean age, 22.7 ± 1.8 yr) with different aerobic fitness level (V˙O2peak value ranging from 28.2 to 81.7 mL·kg·min) participated in a crossover double-blind placebo-controlled study. Subjects were tested after 6 d of supplementation with either 0.5 l per day of nitrate (5.5 mmol)-containing water (NITR) or nitrate-free water (PLA). Participants performed an incremental running test until exhaustion and four repetitions of 6-min submaximal (approximately 80% of gas exchange threshold) constant load exercise on a motorized treadmill. Moreover, subjects performed a 3-km running time trial on the field. After NITR, a negative correlation between reduction of O2 cost of submaximal exercise and individual aerobic fitness level was observed (r = 0.80; P < 0.0001). A significant inverse correlation was also found between aerobic fitness level and improvement in performance for 3-km time trial after NITR (r = 0.76; P < 0.0001). Additionally, subjects responded differently to dietary nitrate supplementation according to aerobic fitness level with higher-fit subjects showing a lower increase in plasma [NO3] (r = 0.86; P < 0.0001) and [NO2] (r = 0.75; P < 0.0001). The results of the present study suggest that the individual aerobic fitness level affects the ergogenic benefits induced by dietary nitrate supplementation. The optimal nitrate loading regimen required to elevate plasma [NO2] and to enhance performance in elite athletes is different from that of low-fit subjects and requires further studies.

Aerobic Fitness Affects the Exercise Performance Responses to Nitrate Supplementation.

Imatinib is a principal therapeutic agent for targeting colorectal tumours. However, mono-targeting by imatinib does not always achieve complete cancer eradication. Selenite, a well-known chemopreventive agent, is commonly used in cancer patients. In this study, we aimed to explore whether selenite can modulate imatinib cytotoxicity in colorectal cancer cells. HCT116 cells were treated with different concentrations of imatinib and/or selenite for 24, 48 and 72 hr. Imatinib-selenite interaction was analysed using isobologram equation. As indicators of apoptosis, DNA fragmentation, caspase-3 activity, Bcl-2 expression were explored. Autophagic machinery was also checked by visualizing acidic vesicular organelles and measuring Beclin-1 expression. Furthermore, reactive oxygen and nitrogen species were also examined. This study demonstrated that selenite synergistically augmented imatinib cytotoxicity in HCT116 cells as demonstrated by combination and dose reduction indices. Supranutritional dose of selenite when combined with imatinib induced apoptotic machinery by decreasing Bcl-2 expression, increasing caspase-3 activity and subsequently fragmenting DNA and blunted cytoprotective autophagy by decreasing Beclin-1 expression and autophagosomes formation. Moreover, their combination induced cell cycle S-phase block, increased total thiol content and reduced nitric oxide levels. In conclusion, selenite synergizes imatinib cytotoxicity through multi-barrelled molecular targeting, providing a novel therapeutic approach for colorectal cancer.

Modulation of imatinib cytotoxicity by selenite in HCT116 colorectal cancer cells.

Diets including food products rich in inorganic nitrate are associated with lower blood pressure (BP). The evidence for the BP-lowering effects of inorganic nitrate and beetroot in randomized clinical trials has not been systematically assessed. The objective was to conduct a systematic review and meta-analysis of randomized clinical trials that examined the effects of inorganic nitrate and beetroot supplementation on BP. Medline, EMBASE, and Scopus databases were searched from inception to February 2013. The specific inclusion criteria were: 1) randomized clinical trials; 2) trials reporting effects on systolic or diastolic BP or both; and 3) trials comparing inorganic nitrate or beetroot juice supplementation with placebo control groups. Random-effects models were used to assess the pooled BP effect sizes. Sixteen trials met the eligibility criteria for the systematic review. All studies had a crossover study design. The trials were conducted between 2006 and 2012 and included a total of 254 participants with 7-30 participants/study. The duration of each intervention ranged from 2 h to 15 d. Inorganic nitrate and beetroot juice consumption were associated with greater changes in systolic BP [-4.4 mm Hg (95% CI: -5.9, -2.8); P < 0.001] than diastolic BP [-1.1 mm Hg (95% CI: -2.2, 0.1); P = 0.06]. The meta-regression showed an association between daily dose of inorganic nitrate and changes in systolic BP (P < 0.05). Inorganic nitrate and beetroot juice supplementation was associated with a significant reduction in systolic BP. These findings need to be tested in long-term trials and in individuals at greater cardiovascular risk.

Inorganic nitrate and beetroot juice supplementation reduces blood pressure in adults: a systematic review and meta-analysis.

Graphene is a promising material capable of driving technological advancement. It is, however, a challenge to obtain pristine graphene in large quantities given the limitation of current synthetic methods. Among the numerous methods available, the chemical approach provides an optimistic outlook and has garnered much interest within the graphene community as a potential alternative. One of the most crucial steps of the chemical approach is the chemical reduction of graphene oxide as this dictates the final quality of the graphene sheets. In recent years, much of the focus has shifted to the usage of established reducing agents or oxygen removal reagents, frequently applied in organic chemistry, onto a graphene oxide platform. Herein, the selective removal of epoxide groups and subsequent regeneration of disrupted conjugated sp(2) system is highlighted, based on the synergistic effect of indium and indium(I) chloride. The morphological, structural, and electrical properties of the resulting graphene were fully characterized with X-ray photoelectron, Fourier transform IR, solid-state (13)C NMR, and Raman spectroscopy; thermogravimetric analysis; scanning electron microscopy; and conductivity measurements. The as-prepared graphene showed a tenfold increase in conductivity against conventional graphene treated with hydrazine reducing agent and demonstrated a high dispersion stability in ethanol. Moreover, the selective defunctionalization of the epoxide groups provides opportunities for potential tailoring of graphene properties for prospective applications.

Regeneration of a conjugated sp² graphene system through selective defunctionalization of epoxides by using a proven synthetic chemistry mechanism.

With an objective to develop optical probes for biologically important anions and neutral molecules, we synthesized three novel NIR absorbing aza-BODIPY derivatives, 3a-3c, and have systematically tuned their photophysical properties by changing the peripheral substitution. A profound red-shift was observed in the absorption and fluorescence spectra of the aza-BODIPY dyes with the change in substitution from azido (3a) to amino (3b) to dimethylamino (3c) groups. Theoretical calculations of 3a-3c showed a consistent decrease in bandgap, which supports the observed spectral changes. The study of their interactions with various analytes revealed that the azido-aza-BODIPY 3a selectively interacts with hydrogen sulfide (H2S) when compared to other molecules. Uniquely, the detection of H2S can be visualized through a change in color from bright blue to purple with a detection limit of 0.5 ppm. The sensitivity of the probe was observed to be ~20-fold higher than the allowed exposure limits of H2S as defined by EPA (10 ppm). The aza-BODIPY derivative 3b, on the other hand, exhibited selective interactions with nitrite ions (NO2(-)) and nitric oxide (NO) in aqueous medium through a visible color change from blue to green with a sensitivity of 20 and 0.15 ppb, respectively. In contrast, the dimethylamino-aza-BODIPY derivative, 3c, showed negligible affinity for the anions and neutral molecules tested. By tuning the photophysical properties through the judicious functionalization, the aza-BODIPY dyes thus synthesized can be utilized for the sensitive on-site detection and analysis of H2S, NO2(-), and NO in the aqueous medium.

硝酸钠

BioXtra, ≥99.0%

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