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D-Lactate dehydrogenase
(Leuconostoc mesenteroides)

D-Lactate dehydrogenase Leuconostoc mesenteroides E-DLDHLM
Product code: E-DLDHLM
€124.00

22,000 Units

Prices exclude VAT

Available for shipping

Content: 22,000 Units
Shipping Temperature: Ambient
Storage Temperature: 2-8oC
Formulation: In 3.2 M ammonium sulphate
Physical Form: Suspension
Stability: Minimum 1 year at 4oC. Check vial for details.
Enzyme Activity: Dehydrogenase
EC Number: 1.1.1.28 
CAS Number: 9028-36-8
Synonyms: D-lactate dehydrogenase; (R)-lactate:NAD+ oxidoreductase
Source: Leuconostoc mesenteroides
Molecular Weight: 36,455
Concentration: Supplied at ~ 20,000 U/mL
Expression: Recombinant from Leuconostoc mesenteroides
Specificity: Catalyses the reaction:
D-Lactate + NAD+ = pyruvate + NADH + H+
Specific Activity: ~ 1,500 U/mg (25oC, pH 7.0 on pyruvic acid)
Unit Definition: One Unit of D-lactate dehydrogenase is defined as the amount of enzyme required to produce one µmole of D-lactate from pyruvic acid (0.77 mM) per minute in the presence of NADH in sodium phosphate buffer (92 mM), pH 7.0 at 25oC.
Temperature Optima: 37oC
pH Optima: 7
Application examples: Applications for the measurement of D-lactic acid in the food, fermentation, wine, beverage and dairy industries.

High purity recombinant D-Lactate dehydrogenase (Leuconostoc mesenteroides) for use in research, biochemical enzyme assays and in vitro diagnostic analysis.

Display all analytical enzymes.

Documents
Certificate of Analysis
Safety Data Sheet
Booklet
Publications
Publication
Metabolic response of glioblastoma cells associated with glucose withdrawal and pyruvate substitution as revealed by GC-MS.

Oppermann, H., Ding, Y., Sharma, J., Paetz, M. B., Meixensberger, J., Gaunitz, F. & Birkemeyer, C. (2016). Nutrition & Metabolism, 13(1), 70.

Background: Tumor cells are highly dependent on glucose even in the presence of oxygen. This concept called the Warburg effect is a hallmark of cancer and strategies are considered to therapeutically exploit the phenomenon such as ketogenic diets. The success of such strategies is dependent on a profound understanding of tumor cell metabolism. With new techniques it is now possible to thoroughly analyze the metabolic responses to the withdrawal of substrates and their substitution by others. In the present study we used gas chromatography coupled to mass spectrometry (GC-MS) to analyze how glioblastoma brain tumor cells respond metabolically when glucose is withdrawn and substituted by pyruvate. Methods: Glioblastoma brain tumor cells were cultivated in medium with high (25 mM), medium (11 mM) or low (5.5 mM) glucose concentration or with pyruvate (5 mM). After 24 h GC-MS metabolite profiling was performed. Results: The abundances of most metabolites were dependent on the supply of glucose in tendency but not in a linear manner indicating saturation at high glucose. Noteworthy, a high level of sorbitol production and release was observed at high concentrations of glucose and high release of alanine, aspartate and citrate were observed when glucose was substituted by pyruvate. Intermediates of the TCA cycle were present under all nutritional conditions and evidence was found that cells may perform gluconeogenesis from pyruvate. Conclusions: Our experiments reveal a high plasticity of glioblastoma cells to changes in nutritional supply which has to be taken into account in clinical trials in which specific diets are considered for therapy.

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Precautionary Statements : Not Applicable
Safety Data Sheet
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