Bouillaud 2012 Abstract Bioblast
|Bouillaud F (2012) Sulfide - a remarkable mitochondrial substrate. Mitochondr Physiol Network 17.12.|
Bouillaud F (2012)
Event: Bioblast 2012
Mitochondria show a high affinity for sulfide and its oxidation usually takes priority over ongoing mitochondrial oxidation processes. Something that is mandatory to ensure efficient sulfide disposal in presence of largely greater intracellular concentrations of other substrates. Extracellular sulfide is therefore a remarkable substrate: it could be used at nanomolar concentrations, its gaseous nature allows fast transfer to mitochondria without transporters, it is directly usable to reduce quinone without metabolic processing (including for example initial ATP consuming steps). This metabolic role of sulfide and its reductant properties contrast sharply with the other two gazotransmitters and particularly with NO which is pro-oxidant. There are still uncertainties about the lowest concentration of sulfide that SQR would detect but, in physiological conditions, the overlap between bioenergetically relevant and signaling concentrations appears even more likely with sulfide than with NO or CO.
Colonocytes are adapted to high sulfide exposure. In these cells reverse bioenergetic reactions including reverse electron flux in Complex I are taking place to ensure continuation of a fast sulfide oxidation even if CIV is inhibited.
• Keywords: Sulfide, Gasotransmitters, CHO cells, Colonocytes
• O2k-Network Lab: FR Paris Bouillaud F
Labels: MiParea: Respiration
Organism: Human Tissue;cell: CHO
Enzyme: Complex I, Complex IV;cytochrome c oxidase Regulation: Coupling efficiency;uncoupling, Inhibitor
Pathway: N, CIV, Other combinations HRR: Oxygraph-2k, TIP2k
Mitochondries, bioenergetique, metabolisme et signalisation - Institut Cochin, INSERM U567, CNRS UMR 8104 - Universite Paris Descartes, Departement d'Endocrinologie, Métabolisme et Cancer 24, Rue du Faubourg Saint-Jacques 75 014 Paris, FRANCE; E-mail: firstname.lastname@example.org
The oxygen consumption (JO2) of CHO cells in suspension is recorded, the background rate (black) and in presence of rotenone inhibition of mitochondrial Complex I (red) are shown. Sulfide additions are indicated in blue. Addition of the same amount of sulfide (+53 nmol in 2 ml) has different consequences when it is infused (blue bars) at a rate that matches with the sulfide oxidation capacities of cells (66), exceeds it (166) or added as a single injection (+26 µM). Note that the maximal sulfide flux (66) compares well with the initial background JO2 (100). The increase in JO2 is figured with vertical bars (red/black) with the red repeated side to the black for comparison. The ratio (increase in JO2) / (sulfide injection rate) provides an indication of the stoichiometry oxygen / sulfide. This value is close to the theorical value of 0.75 in presence of rotenone but close to 0.5 for background. This suggests that electrons from sulfide replaced electrons previously provided to quinone by Complex I (priority of sulfide oxidation over other substrates). In contrast, when inhibition by sulfide takes place (+26 µM) the length of the horizontal red/black bars (= time to oxidize sulfide) indicates that under these conditions Complex I becomes an opponent to sulfide oxidation probably because of the change in its reduction state.