EPR characterization of molecular targets for NO in mammalian cells and organelles

Henry, Y.; Lepoivre, Michel; Drapier, Jean‐Claude; Ducrocq, Claire; Boucher, Jean‐Luc; Guissani, Annie

doi:10.1096/fasebj.7.12.8397130

Cited by 366 publications

(170 citation statements)

References 59 publications

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“…5 NO has multiple intracellular targets that could potentially affect cell growth. [15][16][17] These include protein tyrosine nitration by generating peroxynitrite, nitrosylation of thiol residues, ADP-ribosylation, ribonucleotide reductase inhibition, and the induction of DNA strand breaks. In the current work, we show that NO induces apoptosis in HL-60 and U937 cells in a dose-dependent fashion, with the rank order of effectiveness for apoptosis and for inhibiting cell growth in liquid and semisolid media being comparable.…”

Section: Discussionmentioning

confidence: 99%

Schedule and concentration-dependent induction of apoptosis in leukemia cells by nitric oxide

1998

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Nitric oxide (NO) has potent antiproliferative properties. In previous work we have shown that NO inhibits growth, induces differentiation and modulates gene expression in acute nonlymphocytic leukemia (ANLL) cells. The goal of this work was to determine whether the rate of NO delivery affected its growth inhibition of ANLL cells. We also wanted to determine whether the NO inhibition of ANLL cell growth is associated with the induction of apoptosis. We treated HL-60 and U937 cells with three compounds that generate the same amount of NO but at different rates. MAMA-NO, PAPA-NO and DETA-NO have halflives of NO delivery of 2 and 30 min, and 20 h, respectively. The compound with the longest t . of NO delivery (DETA-NO) was the most potent inhibitor of leukemia cell and colony growth. Furthermore, the NO-induced growth inhibition was associated with apoptosis in a rate and concentration-dependent fashion.

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Section: Discussionmentioning

confidence: 99%

Schedule and concentration-dependent induction of apoptosis in leukemia cells by nitric oxide

1998

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“…[3][4][5][6] The increased hydrogen peroxide, and also the acidosis induced by ischemia can release iron from its binding proteins leading to an increased concentration of non-protein-bound iron (NPBI) in plasma. [7][8][9] Iron delocalization or misregulation of iron metabolism may play a critical role in brain injury. [10][11][12] As a powerful pro-oxidant, NPBI has the ability to convert hydrogen peroxide into the highly toxic hydroxyl radical.…”

Section: Introductionmentioning

confidence: 99%

Iron metabolism and lipid peroxidation products in infants with hypoxic ischemic encephalopathy

2008

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Background: Iron delocalization or misregulation of iron metabolism may play a critical role in the pathology of hypoxic ischemic encephalopathy (HIE).Objective: To study iron metabolism and lipid peroxidation in newborn infants and to correlate non-protein-bound iron (NPBI) concentration with the severity of the post-asphyxial injury and subsequent short-term outcomes.Study Design: Concentrations of NPBI and malondialdehyde (MDA) in the serum and in the cerebrospinal fluid (CSF) were measured in eight healthy newborn infants and nine newborn infants suffering from moderately severe HIE. Short-term outcomes (death, survival with or without neurological abnormality) were noted at hospital discharge.Result: Serum and CSF concentrations of both NPBI and MDA were significantly increased in HIE infants when compared to controls. Serum iron was significantly increased and total iron binding capacity was significantly decreased in HIE infants compared to controls. Out of the nine HIE infants, four infants died and two infants survived with abnormal neurological findings at hospital discharge. These six infants with clinical sequels had significantly increased concentrations of NPBI in the serum and in the CSF; and increased concentrations of MDA in the CSF when compared to the other three who survived without short-term abnormalities. Conclusion:We conclude that hypoxia ischemia alters iron metabolism and lipid peroxidation in newborn infants; and that NPBI and MDA in the CSF are increased in infants with HIE. This study supports a role for iron in oxidative injury to the central nervous system after hypoxic ischemic insults.

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“…The importance of this interaction cannot be overstated because several Fe-S cluster proteins located within mitochondria comprise the most abundant non-heme proteins within the cell. Candidate proteins include: aconitase, NADH ubiquinone oxidoreductase (complex I), succinate ubiquinone oxidoreductase (complex II), and ubiquinol cytochrome C oxidoreductase (complex III) (16,17). Excess NO is known to inhibit cell respiration presumably by targeting mitochondrial Fe-S cluster proteins.…”

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confidence: 99%

Non-heme iron protein: A potential target of nitric oxide in acute cardiac allograft rejection

Pieper

Halligan

Hilton

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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EPR characterization of molecular targets for NO in mammalian cells and organelles

Cited by 366 publications

References 59 publications

Schedule and concentration-dependent induction of apoptosis in leukemia cells by nitric oxide

Schedule and concentration-dependent induction of apoptosis in leukemia cells by nitric oxide

Iron metabolism and lipid peroxidation products in infants with hypoxic ischemic encephalopathy

Non-heme iron protein: A potential target of nitric oxide in acute cardiac allograft rejection

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