The nitric oxide–iron interplay in mammalian cells: Transport and storage of dinitrosyl iron complexes

Richardson, Des R.; Lok, Hiu Chuen

doi:10.1016/j.bbagen.2007.12.009

Cited by 63 publications

(57 citation statements)

References 154 publications

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“…Clearly, a weak DNIC EPR signal was still observed in GSTP1 knock-out cells as other molecules apart from GST P1-1 (e.g. iron-sulfur cluster-containing proteins) are also known to form DNICs (1,28,29). Of relevance, WT-MEFs and GST P1-1 KO-MEFs incubated with control medium alone did not display a DNIC signal (supplemental Fig.…”

Section: Epr At 77 K Shows That Gst P1-1 Expression Increases Intensimentioning

confidence: 99%

“…Indeed, the efficient efflux of the DNICs by MRP1 out of VP cells may limit NO binding to other iron-containing molecules (e.g. iron-sulfur clusters that are known to form DNICs (1,28,29)), preventing their generation and removing this "background DNIC signal." In contrast, in WT cells, MRP1 is not present at significant levels ( Fig.…”

Section: Epr At 77 K Shows That Gst P1-1 Expression Increases Intensimentioning

confidence: 99%

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Nitric Oxide Storage and Transport in Cells Are Mediated by Glutathione S-Transferase P1-1 and Multidrug Resistance Protein 1 via Dinitrosyl Iron Complexes

Lok

Rahmanto

Hawkins

et al. 2012

Journal of Biological Chemistry

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105

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Background: Nitrogen monoxide (NO) can target intracellular iron pools, leading to dinitrosyl iron complexes (DNICs). Results: NO storage and transport are mediated by glutathione S-transferase P1-1 (GST P1-1) and multidrug resistance protein 1 (MRP1), respectively. Conclusion: GST P1-1 and MRP1 form an integrated detoxification unit regulating storage and transport of DNICs. Significance: These results have broad implications for understanding the transport, storage, and signaling roles of NO.

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Section: Epr At 77 K Shows That Gst P1-1 Expression Increases Intensimentioning

confidence: 99%

Section: Epr At 77 K Shows That Gst P1-1 Expression Increases Intensimentioning

confidence: 99%

Nitric Oxide Storage and Transport in Cells Are Mediated by Glutathione S-Transferase P1-1 and Multidrug Resistance Protein 1 via Dinitrosyl Iron Complexes

Lok

Rahmanto

Hawkins

et al. 2012

Journal of Biological Chemistry

Self Cite

105

View full text Add to dashboard Cite

show abstract

“…Iron-proteins constitute a predominant scavenger mechanism of NO (Angelo et al 2008, Richardson & Lok 2008. As iron is mainly provided by the heme group, it constitutes an additional link between the functions of NO and the respiratory cycle (Chung et al 2008).…”

mentioning

confidence: 99%

The effects of nitric oxide on the immune system during Trypanosoma cruzi infection

Gutierrez

Mineo

Pavanelli

et al. 2009

Mem. Inst. Oswaldo Cruz

109

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“…In the nuclear debris, NO rose rapidly at 12 h similar to labile iron. This parallel response suggests that nitric oxide synthase (NOS) on/near the plasma membrane generates NO for imported/ released iron (Watts et al 2003;Richardson et al 2008). A similar change in NO and labile iron was observed for mitochondria at 48 h, suggesting that mitochondrial NOS may act as a protective blockade against the devastating effect of iron.…”

Section: Changes In Iron No Ros and Atp In The Cellular Fractionsmentioning

confidence: 74%

Temporal changes in mitochondrial activities of rat heart after a single injection of iron, including increased complex II activity

Kim

Song

2010

Animal Cells and Systems

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Male rats were given a single injection of iron, and temporal changes in iron content and iron-induced effects were examined in heart cellular fractions. Over a period of 72 h, the contents of total and labile iron, reactive oxygen species, and NO in tissue homogenate, nuclear debris, and postmitochondrial fractions were mostly constant, but in mitochondria they continuously increased. An abrupt decrease in membrane potential and NAD(P)H at 12 h was also found in mitochondria. The respiratory control ratio was reduced slowly with a slight recovery at 72 h, suggesting uncoupling by iron. While the ATP content of tissue homogenate decreased steadily until 72 h, it showed a prominent increase in mitochondria at 12 h. Total iron and calcium concentration also progressively increased in mitochondria over 72 h. Enzyme activity of the oxidative phosphorylation system was significantly altered by iron injection: activities of complexes I, III, and IV were reduced considerably, but complex II activity and the ATPase activity of complex V were enhanced. A reversal of activity in complexes I and II at 12 h suggested reverse electron transfer due to iron overload. These results support the argument that mitochondrial activities including oxidative phosphorylation are modulated by excessive iron.

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The nitric oxide–iron interplay in mammalian cells: Transport and storage of dinitrosyl iron complexes

Cited by 63 publications

References 154 publications

Nitric Oxide Storage and Transport in Cells Are Mediated by Glutathione S-Transferase P1-1 and Multidrug Resistance Protein 1 via Dinitrosyl Iron Complexes

Nitric Oxide Storage and Transport in Cells Are Mediated by Glutathione S-Transferase P1-1 and Multidrug Resistance Protein 1 via Dinitrosyl Iron Complexes

The effects of nitric oxide on the immune system during Trypanosoma cruzi infection

Temporal changes in mitochondrial activities of rat heart after a single injection of iron, including increased complex II activity

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