Template:SUIT text D111: Difference between revisions

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After the addition of mitochondria in the absence of fuel substrates and ADP, [[Ren|''Ren'']], respiration due to oxidation of endogenous substrates remaining after mitochondrial isolation is measured. The titration of a small concentration of ADP stimulates the depletion of the endogenous substrates, leading to a decrease in mitochondria respiration.  
After the addition of mitochondria in the absence of fuel substrates and ADP, [[Ren|''Ren'']], respiration due to oxidation of endogenous substrates remaining after mitochondrial isolation is measured. The titration of a small concentration of ADP stimulates the depletion of the endogenous substrates, leading to a decrease in mitochondria respiration.  


The addition complex III inhibitor myxothiazol allows the measurement of [[ROX|''Rox'']].
The addition of the complex III inhibitor myxothiazol allows the measurement of [[ROX|''Rox'']].

Latest revision as of 10:46, 12 January 2024

SUIT-034 O2 mt D111 is used as a control protocol for SUIT-034 NADH mt D082, allowing for cytochrome c test and the evaluation of mitochondrial respiration in OXPHOS and ET in the N-pathway. In the absence of ATPases in the sample, LEAK state can also be evaluated. In order to measure LEAK in the presence of ATPases, this protocol should be performed in parallel to SUIT-006 02 mt D108.

After the addition of mitochondria in the absence of fuel substrates and ADP, Ren, respiration due to oxidation of endogenous substrates remaining after mitochondrial isolation is measured. The titration of a small concentration of ADP stimulates the depletion of the endogenous substrates, leading to a decrease in mitochondria respiration.

The addition of the complex III inhibitor myxothiazol allows the measurement of Rox.

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