Mitochondria

From Krebs cycle to the respiratory chain

Mitochondrial respiration is a fundamental metabolic closely linked and interdependent to oxidative metabolism. Oxidative stress often induces mitochondrial dysfunction, transient or not. This functional impairment can affect all functions mitochondrial, from Krebs cycle to the respiratory chain, impacting the basic cellular function. Conversely, impaired respiratory chain will generate a flow of electrons in the mitochondria and the cell, and cause oxidative stress.

 

For our scientists, the simultaneous analysis of these two metabolisms seem in many cases inseparable.

 

The role of mitochondrial dysfunction in the toxicity induced by drugs is increasingly clear. Of 38 drugs withdrawn from the market since 1994, most of them showed hepatotoxicity or cardiotoxicity, and in most cases of mitochondrial dysfunction. Among these drugs, several toxicities were documented, as troglitazone, cerivastatin or tolcapone.

 

The identification of this toxicity has been hampered by lack of access to technical markers clearly indicating that the drug induced dysfunction. Several markers were used (lactate, ratio lactate / pyruvate, measuring the activity of complex respiratory chain and ATP), but taken separately, they do draw a small fraction of mitochondrial activity. Indeed, there is no comprehensive approach to metabolic mitochondria with these methods.

 

To meet this need, we have concentrated our efforts on developing methods enabling the exploration of all of this metabolism. We've combined the exploration of its connections to surrounding metabolisms, such as oxidative stress, cell death, the energy status and inflammation.

 

Explore the Mitoxis test listing

 

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