Metabolism assays

Mitochondrial function and metabolism are linked with numerous regulatory mechanisms of the cell. Abnormal metabolic functioning is involved in many human diseases including atherosclerosis, ischemia reperfusion injury, and neurodegenerative disorders.

Assays that can monitor the metabolic profile are essential for understanding and assessing the impact of candidate compounds that have either a protective or diminishing effect on cell metabolism.

Ncardia offers a variety of assays that relate with several features of metabolism and mitochondrial activity.

Horizon 2020This project has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No 737978.


Oxygen Consumption Rate (OCR) assay

OCR is a very good indicator of mitochondrial function. The oxidative phosphorylation capabilities of cells can be evaluated with this assay.


Extracellular Acidification Rate (ECAR) assay

ECAR is a good measure of the glycolytic activity in cells. By recording lactate production via the acidification rate, this assay can monitor the glycolytic activity of cells.


Intracellular Oxygen Concentration Assay

The Intracellular Oxygen Concentration Assay can quantify real-time cellular oxygenation under hypoxic conditions and upon drug treatment. It is a great assay to investigate the interplay between cellular oxygenation & metabolism in research including hypoxia, cancer metabolism, and oxidative stress.


TMRE Mitochondrial Membrane Potential Assay

The TMRE assay allows monitoring of the mitochondrial membrane potential in whole cells, which is also a good indicator of mitochondrial function.


MitoSOX assay

Reactive oxygen species (ROS) production is increased with oxidative stress, resulting in oxidative damage. With the MitoSOX assay the superoxide concentration inside the mitochondria can be assessed, providing an indication of ROS toxicity.

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Ischemia reperfusion injury

During myocardial infarction the supply of oxygen in the parts of the heart is decreased or stopped by reduced or arrested blood flow. The condition of reduced oxygen concentration in a tissue is called ischemia. During the ischemic period the heart has to adopt its metabolism and is forced to generate ATP through anaerobic processes, which is mainly cytosolic glycolysis. This adoption prevents the heart from major damage. Most of the damage/cell death caused by the myocardial infarction develops during the so-called reperfusion when the blood flow is suddenly re-established and oxygen is again supplied to the former ischemic tissue.

Ischemia reperfusion like processes can be modeled in cardiomyocytes incubated in an atmospheric control unit (ACU) that can rapidly reduce the oxygen levels (infarction phase), maintain oxygen at low levels (ischemic phase) and rapidly increase oxygen levels (reperfusion phase).


An example of how real time consumption of intracellular oxygen occurs in cells with different metabolic states: Cell oxygenation traces from cardiomyocytes that are respiring and consume intracellular oxygen (light red) and from cardiomyocytes that are not respiring (dark red). The black trace represents the oxygen level inside the plate reader chamber.

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