Difference between revisions of "Masci 2008 Biochim Biophys Acta"
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{{Publication | {{Publication | ||
|title=Masci A, Mastronicola D, Arese M, Piane M, De Amicis A, Blanck TJ, Chessa L, Sarti P (2008) Control of cell respiration by nitric oxide in Ataxia Telangiectasia lymphoblastoid cells. Biochim Biophys Acta 1777: 66-73. | |title=Masci A, Mastronicola D, Arese M, Piane M, De Amicis A, Blanck TJ, Chessa L, Sarti P (2008) Control of cell respiration by nitric oxide in Ataxia Telangiectasia lymphoblastoid cells. Biochim Biophys Acta 1777:66-73. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/18047827 PMID: 18047827] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/18047827 PMID: 18047827 Open Access] | ||
|authors=Masci A, Mastronicola D, Arese M, Piane M, De Amicis A, Blanck TJ, Chessa L, Sarti P | |authors=Masci A, Mastronicola D, Arese M, Piane M, De Amicis A, Blanck TJ, Chessa L, Sarti P | ||
|year=2008 | |year=2008 | ||
|journal=Biochim | |journal=Biochim Biophys Acta | ||
|abstract=Ataxia Telangiectasia (AT) patients are particularly sensitive to oxidative–nitrosative stress. Nitric oxide (NO) controls mitochondrial respiration via the reversible inhibition of complex IV. The mitochondrial response to NO of AT lymphoblastoid cells was investigated. Cells isolated from three patients and three intrafamilial healthy controls were selected showing within each group a normal diploid karyotype and homogeneous telomere length. Different complex IV NO-inhibition patterns were induced by varying the electron flux through the respiratory chain, using exogenous cell membrane permeable electron donors. Under conditions of high electron flux the mitochondrial NO inhibition of respiration was greater in AT than in control cells (P ≤ 0.05). This property appears peculiar to AT, and correlates well to the higher concentration of cytochrome c detected in the AT cells. This finding is discussed on the basis of the proposed mechanism of reaction of NO with complex IV. It is suggested that the peculiar response of AT mitochondria to NO stress may be relevant to the mitochondrial metabolism of AT patients. | |abstract=Ataxia Telangiectasia (AT) patients are particularly sensitive to oxidative–nitrosative stress. Nitric oxide (NO) controls mitochondrial respiration via the reversible inhibition of complex IV. The mitochondrial response to NO of AT lymphoblastoid cells was investigated. Cells isolated from three patients and three intrafamilial healthy controls were selected showing within each group a normal diploid karyotype and homogeneous telomere length. Different complex IV NO-inhibition patterns were induced by varying the electron flux through the respiratory chain, using exogenous cell membrane permeable electron donors. Under conditions of high electron flux the mitochondrial NO inhibition of respiration was greater in AT than in control cells (P ≤ 0.05). This property appears peculiar to AT, and correlates well to the higher concentration of cytochrome c detected in the AT cells. This finding is discussed on the basis of the proposed mechanism of reaction of NO with complex IV. It is suggested that the peculiar response of AT mitochondria to NO stress may be relevant to the mitochondrial metabolism of AT patients. | ||
|keywords=Nitrosative stress, Bioenergetics, Cytochrome c oxidase, Genetic disease, Reaction mechanism, Respiratory chain | |keywords=Nitrosative stress, Bioenergetics, Cytochrome c oxidase, Genetic disease, Reaction mechanism, Respiratory chain | ||
|mipnetlab=IT Rome Sarti P | |||
|discipline=Mitochondrial Physiology, Biomedicine | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|injuries=Oxidative stress;RONS | |||
|organism=Human | |||
|tissues=Nervous system | |||
|preparations=Intact cells | |||
|enzymes=Complex IV;cytochrome c oxidase | |||
|topics=Ion;substrate transport, Redox state | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k, NO | |||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} |
Latest revision as of 11:20, 21 January 2020
Masci A, Mastronicola D, Arese M, Piane M, De Amicis A, Blanck TJ, Chessa L, Sarti P (2008) Control of cell respiration by nitric oxide in Ataxia Telangiectasia lymphoblastoid cells. Biochim Biophys Acta 1777:66-73. |
Masci A, Mastronicola D, Arese M, Piane M, De Amicis A, Blanck TJ, Chessa L, Sarti P (2008) Biochim Biophys Acta
Abstract: Ataxia Telangiectasia (AT) patients are particularly sensitive to oxidative–nitrosative stress. Nitric oxide (NO) controls mitochondrial respiration via the reversible inhibition of complex IV. The mitochondrial response to NO of AT lymphoblastoid cells was investigated. Cells isolated from three patients and three intrafamilial healthy controls were selected showing within each group a normal diploid karyotype and homogeneous telomere length. Different complex IV NO-inhibition patterns were induced by varying the electron flux through the respiratory chain, using exogenous cell membrane permeable electron donors. Under conditions of high electron flux the mitochondrial NO inhibition of respiration was greater in AT than in control cells (P ≤ 0.05). This property appears peculiar to AT, and correlates well to the higher concentration of cytochrome c detected in the AT cells. This finding is discussed on the basis of the proposed mechanism of reaction of NO with complex IV. It is suggested that the peculiar response of AT mitochondria to NO stress may be relevant to the mitochondrial metabolism of AT patients. • Keywords: Nitrosative stress, Bioenergetics, Cytochrome c oxidase, Genetic disease, Reaction mechanism, Respiratory chain
• O2k-Network Lab: IT Rome Sarti P
Labels:
Stress:Oxidative stress;RONS Organism: Human Tissue;cell: Nervous system Preparation: Intact cells Enzyme: Complex IV;cytochrome c oxidase Regulation: Ion;substrate transport, Redox state Coupling state: OXPHOS
HRR: Oxygraph-2k, NO