Cell H2O2 steady-state concentration and mitochondrial nitric oxide.
For many years, mitochondrial respiration was thought to follow an "all or nothing" paradigm supporting the notion that in the normal O2 concentration range, respiration is mainly controlled by tissue demands. However, nitric oxide produced by cytosol or mitochondrial nitric oxide synthases adapts respiration to different physiologic conditions and increases the mitochondrial production of O2 active species that contributes to NO clearance. Because mitochondrial NO utilization is sensitive to environmental or hormonal modulation, and because diffusible active species, like H2O2, are able to regulate genes related to proliferation, quiescence, and death, we surmised that the two mechanisms converge to elicit the different responses in cell physiology.
Carreras
Maria Cecilia
MC
Laboratory of Oxygen Metabolism, University Hospital and School of Pharmacy and Biochemistry, University of Buenos Aires, Argentina.
Clara Franco
Maria
M
P Converso
Daniela
D
Finocchieto
Paola
P
Galli
Soledad
S
José Poderoso
Juan
J
D000818:Animals; D002374:Catalase / Q000378:metabolism; D049109:Cell Proliferation; D004591:Electrophoresis, Polyacrylamide Gel; D005979:Glutathione Peroxidase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism*; D008928:Mitochondria / Q000201:enzymology / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D030421:Peroxynitrous Acid / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism
D013481:Superoxides; D030421:Peroxynitrous Acid; D009569:Nitric Oxide; D006861:Hydrogen Peroxide; D002374:Catalase; D005979:Glutathione Peroxidase; D019001:Nitric Oxide Synthase