CS0720

Sigma-Aldrich

Citrate Synthase Assay Kit

 kit sufficient for 100 reactions (using a 1 ml cuvette),  kit sufficient for 480 reactions (using 96 multiwell plates)

Pricing and availability is not currently available.

Quality Level

usage

 kit sufficient for 100 reactions (using a 1 ml cuvette)
 kit sufficient for 480 reactions (using 96 multiwell plates)

shipped in

dry ice

storage temp.

−20°C

Gene Information

human ... CS(1431)

General description

The Citrate Synthase Assay Kit contains all the required reagents (including a positive control enzyme) for a fast and simple measurement of citrate synthase activity in a whole cell extract or in isolated mitochondria. In addition, the kit enables testing of the intactness of the mitochondrial inner membrane.

Biochem/physiol Actions

Citrate synthase is the initial enzyme of the tricarboxylic acid (TCA) cycle. The enzyme catalyzes the reaction of 2 carbon acetyl CoA with 4 carbon oxaloacetate to form the 6 carbon citrate. This enzyme is an exclusive marker of the mitochondrial matrix.

Analysis Note

The activity of the enzyme is measured by following the color of TNB, which is generated from DTNB present in the reaction of citrate synthesis, and caused by the deacetylation of Acetyl-CoA. The overall reaction product, TNB, absorbs at 412 nm.

Kit Components Only

Product No.
Description

  • Assay buffer for citrate synthase 5x 25 mL

  • Bicine buffer 10 mL

  • CelLytic M Cell Lysis Reagent 10 mL

  • DTNB 5,5'-Dithiobis-(2-nitrobenzoic acid) 4 mg

  • Acetyl coenzyme A 25 mg

  • Oxaloacetic acid 1 g

  • Citrate synthase (positive control) .1 mL

Pictograms

Exclamation mark

Signal Word

Warning

Hazard Statements

Target Organs

Respiratory system

Hazard Codes

C

Risk Statement

34-37

Safety Statement

26-36/37/39-45

RIDADR

UN 3316 9

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificate of Analysis
Certificate of Origin
Stefan M Gehrig et al.
Experimental physiology, 93(11), 1190-1198 (2008-06-24)
Contraction-mediated injury is a major contributing factor to the pathophysiology of muscular dystrophy and therefore therapies that can attenuate this type of injury have clinical relevance. Systemic administration of insulin-like growth factor-I (IGF-I) has been shown to improve muscle function...
Postnatal PPARa Activation and Myostatin Inhibition Exert Distinct yet Complimentary Effects on the Metabolic Profile of Obese Insulin-Resistant Mice
Bernardo,B et al.
PLoS ONE, 5(6) (2010)
Sara Anjomani Virmouni et al.
Disease models & mechanisms, 8(3), 225-235 (2015-02-15)
Friedreich's ataxia (FRDA) is an autosomal recessive neurodegenerative disorder caused by a GAA repeat expansion mutation within intron 1 of the FXN gene, resulting in reduced levels of frataxin protein. We have previously reported the generation of human FXN yeast...
Alexander L Pendleton et al.
American journal of physiology. Endocrinology and metabolism, 319(1), E67-E80 (2020-05-13)
Fetal sheep with placental insufficiency-induced intrauterine growth restriction (IUGR) have lower hindlimb oxygen consumption rates (OCRs), indicating depressed mitochondrial oxidative phosphorylation capacity in their skeletal muscle. We hypothesized that OCRs are lower in skeletal muscle mitochondria from IUGR fetuses, due...
Jonathan Alcántar-Fernández et al.
PloS one, 14(12), e0226652-e0226652 (2019-12-18)
Glucose is an important nutrient that dictates the development, fertility and lifespan of all organisms. In humans, a deficit in its homeostatic control might lead to hyperglucemia and the development of obesity and type 2 diabetes, which show a decreased...

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