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(L)-Sodium lactate Sale

(Synonyms: L-乳酸钠, Sodium L-Lactate) 目录号 : GC20111

L-乳酸钠((L)-Sodium lactate)是一种源自L-乳酸的有机酸,在无氧糖酵解过程中由丙酮酸通过乳酸盐脱氢酶产生。

(L)-Sodium lactate Chemical Structure

Cas No.:867-56-1

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Sample solution is provided at 25 µL, 10mM.

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实验参考方法

Cell experiment [1]:

Cell lines

Human SH-SY5Y cell line、astrocyte

Preparation Method

Cells were stimulated or not (untreated controls) with different concentrations of (L)-Sodium lactate (5, 10, and 25 mM) for 4 and 24 h.

Reaction Conditions

5, 10, 25 mM; 4, 24 h

Applications

SH-SY5Y cells respond with a dose-dependent increase of heat shock protein 70 kDa (HSP70) to treatment with (L)-Sodium lactate at 4 as well as at 24 h. However, astrocytes produced a significantly greater amount of HSP70 (an increase of approximately twofold).
Animal experiment [2]:

Animal models

Male C57BL/6 mice

Preparation Method

Male C57BL/6 mice aged 8 to 10 weeks were anaesthetized with 3% isoflurane. Then, mice were placed in the right lateral decubitus position. With the aid of surgical microscope, the left anterior descending artery (LAD) could be visualized and permanently ligated with a 7-0 silk suture at the site of 2 mm below the left appendix. (L)-Sodium lactate (2g/kg/day) or saline was treated intraperitoneally one day after operation. On day 3 or day 14 after treatment with sodium lactate or saline, myocardial infarction (MI) mice were anaesthetized and the hearts were exposed.

Dosage form

2g/kg/day; i.p.

Applications

(L)-Sodium lactate decreased cardiomyocyte apoptosis, restrained cardiac fibrosis, and increased new vessel density post-MI.

References:

[1]Coco M, Caggia S, Musumeci G, et al. Sodium L‐lactate differently affects brain‐derived neurothrophic factor, inducible nitric oxide synthase, and heat shock protein 70 kDa production in human astrocytes and SH‐SY5Y cultures[J]. Journal of neuroscience research, 2013, 91(2): 313-320.

[2]Zhang J, Huang F, Chen L, et al. Sodium lactate accelerates M2 macrophage polarization and improves cardiac function after myocardial infarction in mice[J]. Cardiovascular therapeutics, 2021, 2021(1): 5530541.

产品描述

(L)-Sodium lactate is an organic acid derived from L-lactic acid, which is produced from pyruvate by lactate dehydrogenase during anaerobic glycolysis[1]. (L)-Sodium lactate helps with pH regulation, acid-base balance and various physiological processes, and can be used as an antimicrobial agent, preservative, buffer and stabilizer, cell culture medium supplement and cellular fuel source[2]. (L)-Sodium lactate has neuroprotective effects and can prevent glutamate excitotoxicity[3].

In vitro, (L)-Sodium lactate (5, 10, 25 mM) treatment of human SH-SY5Y cell line and astrocytes for 4h and 24h dose-dependently increased the expression of heat shock protein 70 kDa (HSP70), brain-derived neurotrophic factor (BDNF) and inducible nitric oxide synthase (iNOS) in both cell lines, and also increased the release of nitric oxide (NO) through the Griess reaction [4]. Treatment of U937 cells with (L)-sodium lactate (0-12 mM) for 24 h enhanced the secretion of matrix metalloproteinase-1 (MMP-1), cytokines (IL-1β and IL-6), and the transcriptional activity of activator protein 1 (AP-1) and nuclear factor (NF-κB)[5].

In vivo, (L)-sodium lactate (2g/kg/day) was intraperitoneally injected into myocardial infarction (MI) mice for 14 days, which reduced cardiomyocyte apoptosis, inhibited cardiac fibrosis, and increased the density of neovascularization after MI, and increased the expression of arginine-1 (Arg-1) protein in the heart[6].

References:
[1] Dhup S, Kumar Dadhich R, Ettore Porporato P, et al. Multiple biological activities of lactic acid in cancer: influences on tumor growth, angiogenesis and metastasis[J]. Current pharmaceutical design, 2012, 18(10): 1319-1330.
[2] Langa R L S. Optimisation of cell growth and shelf life stability of Megasphaera elsdenii NCIMB 41125[M]. University of Pretoria (South Africa), 2010.
[3] Castillo X, Rosafio K, Wyss M T, et al. A probable dual mode of action for both L-and D-lactate neuroprotection in cerebral ischemia[J]. Journal of Cerebral Blood Flow & Metabolism, 2015, 35(10): 1561-1569.
[4] Coco M, Caggia S, Musumeci G, et al. Sodium L‐lactate differently affects brain‐derived neurothrophic factor, inducible nitric oxide synthase, and heat shock protein 70 kDa production in human astrocytes and SH‐SY5Y cultures[J]. Journal of neuroscience research, 2013, 91(2): 313-320.
[5] Nareika A, He L, Game B A, et al. Sodium lactate increases LPS-stimulated MMP and cytokine expression in U937 histiocytes by enhancing AP-1 and NF-κB transcriptional activities[J]. American Journal of Physiology-Endocrinology and Metabolism, 2005, 289(4): E534-E542.
[6] Zhang J, Huang F, Chen L, et al. Sodium lactate accelerates M2 macrophage polarization and improves cardiac function after myocardial infarction in mice[J]. Cardiovascular therapeutics, 2021, 2021(1): 5530541.

L-乳酸钠((L)-Sodium lactate)是一种源自L-乳酸的有机酸,在无氧糖酵解过程中由丙酮酸通过乳酸盐脱氢酶产生[1]。(L)-Sodium lactate有助于pH调节、酸碱平衡和各种生理过程,可以用作抗菌剂、防腐剂、缓冲剂和稳定剂,细胞培养基补充剂和细胞燃料来源[2]。(L)-Sodium lactate具有神经保护作用,可以防止谷氨酸兴奋性毒性[3]

在体外,(L)-Sodium lactate(5, 10, 25 mM)处理人类SH-SY5Y细胞系和星形胶质细胞4h和24h,剂量依赖性地增加了两种细胞的热休克蛋白70 kDa(HSP70)、脑源性神经营养因子(BDNF)和诱导型一氧化氮合酶(iNOS)的表达,还增加了通过格里斯反应释放的一氧化氮(NO[4]。(L)-Sodium lactate(0-12 mM)处理U937细胞24h,增强了基质金属蛋白酶-1(MMP-1)、细胞因子(IL-1β和IL-6)的分泌,增强了激活蛋白1(AP-1)和核转录因子(NF-κB)的转录活性[5]

在体内,(L)-Sodium lactate(2g/kg/day)通过腹腔注射治疗心肌梗死(MI)小鼠14天,减少了心肌细胞凋亡、抑制心脏纤维化并增加心肌梗死后新生血管密度,增加了心脏中精氨酸-1(Arg-1)蛋白的表达[6]

Chemical Properties

Cas No. 867-56-1 SDF
别名 L-乳酸钠, Sodium L-Lactate
分子式 C3H5NaO3 分子量 112.06
溶解度 DMSO: 196.3 mM 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 8.9238 mL 44.619 mL 89.2379 mL
5 mM 1.7848 mL 8.9238 mL 17.8476 mL
10 mM 0.8924 mL 4.4619 mL 8.9238 mL
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Research Update

Comparison of the kinetics and utilisation of D(-)-and L(+)-Sodium lactate in normal man

Ann Nutr Metab 1983;27(6):481-7.PMID:6651225DOI:10.1159/000176723.

After infusion of sodium D(-)L(+)-lactate in healthy man the clearance of the D(-)-isomer from blood was 70% of that of the L(+)-isomer. Utilisation of L(+)-lactate may have been inhibited by the presence of the D(-)-isomer. The changes in blood pyruvate concentration and ketone body ratio were compatible with mitochondrial oxidation of D(-)-lactate to pyruvate. After infusion of a D(-)L(+)-lactate racemic mixture, the renal excretion of the D(-)-isomer was much greater than that of the L(+)-isomer, although peak blood concentrations of the L(+) were higher than those of the D(-)-isomer. After infusion of sodium L(+)-lactate, the renal excretion of D(-)-lactate increased 7 times, although no D(-)-lactate could be detected in the blood or in the sodium L(+)-lactate infused.

Sodium lactate and hypertonic sodium chloride induce equivalent panic incidence, panic symptoms, and hypernatremia in panic disorder

Biol Psychiatry 1998 Nov 15;44(10):1007-16.PMID:9821565DOI:10.1016/s0006-3223(98)00053-5.

Background: Although experimental induction of panic by infusion of 0.5 mol/L sodium lactate in persons with panic disorder was described three decades ago, the mechanism underlying this observation remains unclear. Here we asked if the rapid administration of the large sodium load contained in the 0.5-mol/L sodium lactate infusion might be involved in panic induction. Methods: We compared in panic disorder and healthy subjects behavioral, electrolyte, endocrine, and acid-base responses to three double-blind randomly ordered equal volume 20-min infusions: 0.5 mol/L sodium lactate, hypertonic saline (3% sodium chloride), and normal saline placebo. Results: Sodium lactate (0.5 mol/L) and hypertonic saline produced the same high incidence of panic and equivalent increases in panic symptoms, serum sodium, and plasma vasopressin in the panic disorder subjects. Neither hypertonic infusion increased cortisol or adrenocorticotropin. No normal subject experienced panic in any condition. The 0.5-mol/L sodium lactate infusion induced alkalosis, whereas hypertonic saline and normal saline induced a mild acidosis. Conclusions: Hypertonic sodium solution containing either chloride or lactate anion induces panic in panic disorder. The large sodium loads delivered by hypertonic saline and 0.5 mol/L sodium lactate may be involved in the mechanism of panic induction.

MRS detection of whole brain lactate rise during 1 M sodium lactate infusion in rats

Biol Psychiatry 1992 Nov 15;32(10):913-21.PMID:1467376DOI:10.1016/0006-3223(92)90180-8.

Proton magnetic resonance spectroscopy (1H MRS) performed in vivo on nine Sprague Dawley rats detected a threefold increase in whole brain lactate during intravenous 1 mol/L sodium lactate infusion. Significant increases in whole brain lactate were detected within 5 min after starting lactate infusion, progressively rose to a maximum level estimated at 3.2 +/- 1.5 mmol/L (all values +/- SD) immediately postinfusion, then decreased towards baseline levels during the next hr. Venous lactate concentration, increasing from 2.3 +/- 2.4 mmol/L to 43.0 +/- 8.0 mmol/L during the infusion, exhibited a steeper rise and then decreased more rapidly in comparison to changes in whole brain lactate. These data suggest MRS can be used in vivo to study acute changes in brain lactate associated with increasing blood lactate concentrations.

Seasonal and maternal effects on acid-base, l-lactate, electrolyte, and hematological status of 205 dairy calves born to eutocic dams

J Dairy Sci 2017 Sep;100(9):7534-7543.PMID:28711257DOI:10.3168/jds.2017-12543.

In this study, we used linear mixed models to determine the effects of season, time of sampling relative to birth (factors), duration of the delivery process, duration of maternal grooming, calf body weight (BW) at birth, and time of day (covariates) on values of venous blood gas, acid-base and electrolyte parameters, and l-lactate concentrations in dairy calves born to eutocic dams in summer (SUM, n = 101) and winter (WIN, n = 104). Neonatal vitality was assessed at 0, 1, and 24 h after delivery in a linear scoring system using muscle tone, erection of the head, muscle reflexes, heart rate, and sucking drive as criteria. Simultaneously with vitality scoring, venous blood samples were collected by jugular venipuncture. Blood was tested for pH, partial pressure of CO2 (pCO2; mmHg) and oxygen (pO2; mmHg), l-lactate (mmol/L), hemoglobin (Hb; g/L), ionized calcium (Ca2+; mmol/L), sodium (Na+; mmol/L), potassium (K+; mmol/L) and chloride (Cl-; mmol/L). Bicarbonate (HCO3-; mmol/L), base excess (BE; mmol/L), total carbon dioxide (TCO2; mmol/L), and anion gap (mmol/L) were calculated. Electrolyte parameters were affected by none of the factors or covariates. Time of day at birth did not affect any of the parameters of interest. Vitality score tended to increase over time and it showed higher values in WIN calves than in SUM calves. Concentrations of HCO3-, BE, and l-lactate indicated a higher degree of metabolic acidosis in SUM calves; however, pH was not affected by season. Concentrations of Hb were higher in SUM calves than in WIN calves; however, covariates did not affect Hb concentrations. Blood pH, concentrations of pO2, HCO3-, and BE decreased, whereas l-lactate concentrations and values of pCO2, TCO2, and anion gap increased with longer duration of delivery. A shift in acid-base balance was also linked to BW of the calf at birth, with lower values of blood pH, HCO3-, and BE in calves with higher BW compared with those with lower BW at birth, whereas TCO2 and l-lactate concentrations increased with higher calf BW at birth. Values of pO2 increased and pCO2 decreased with longer duration of maternal grooming. Blood pH, HCO3-, and BE increased, whereas l-lactate concentrations and anion gap decreased with longer duration of licking the calf. Our results indicate that prolonged delivery can impair acid-base status and can cause slight lactic acidosis, even in calves born from spontaneous or eutocic calvings, and that high BW at birth predisposes calves to acidosis. The positive effect of maternal grooming on neonatal acid-base status should be considered in parturition management. Season, duration of the delivery process, calf BW at birth, and duration of maternal grooming are recommended for consideration in future studies on blood gas and acid-base parameters in dairy calves in the immediate neonatal period.

Hematology and Plasma Chemistry Reference Values in Nursehound Shark ( Scyliorhinus Stellaris) Maintained Under Human Care

Front Vet Sci 2022 Jul 11;9:909834.PMID:35898538DOI:10.3389/fvets.2022.909834.

Studies determining baseline hematological reference intervals (RI) in elasmobranchs are very limited. In this study, blood samples were collected from 94 clinically healthy Nursehound Shark (Scyliorhinus stellaris) maintained under human care. Median (RI) in major leukocyte types were similar to other Carcharhinid sharks as lymphocytes were the predominant leukocyte with 38.0 (28.2-53.5)%, followed by coarse eosinophilic granulocytes with 20.0 (12.2-31.7)%, fine eosinophilic granulocytes with 6.0 (1.2-12.8) %, monocytes with 2.0 (0.0-6.0)%, and neutrophils with 2.0 (0.0-6.0)%. Nursehound Shark produced granulated thrombocytes, which were classified as granulocytes and represented 28.5 (12.4-39.7)% of all leukocytes. Median (RI) manual red blood cell and white blood cell counts were 177.50 (132.50-210.00) x 109 cells/L and 8.26 (5.24-14.23) x 109 cells/L, respectively. Median (RI) plasma chemistry values showed alkaline phosphatase 7.7 (4.2-13.0) U/L, aspartate aminotransferase 7.6 (3.3-17.1) U/L, blood urea nitrogen 281.6 (261.2-305.0) mmol/L, calcium 3.97 (3.59-4.47) mmol/L, total cholesterol 2.04 (1.02-3.91) mmol/L, chloride 233.0 (215.2-259.0) mmol/L, iron 3.79 (1.74-6.93) μmol/L, glucose 0.87 (0.47-1.44 mmol/L), potassium 3.8 (2.9-4.6) mmol/L, sodium 243.0 (227.7-271.0) mmol/L, phosphorus 1.58 (1.13-2.10) mmol/L, total protein 24.0 (20.0-35.0) g/L, and triglycerides 0.97 (0.49-3.35) mmol/L. Creatine kinase, gamma glutamyl transferase, and lactate dehydrogenase levels were below the instrument reading range.