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Updated: Feb 16, 2026
08:25
Measuring Nitrite and Nitrate, Metabolites in the Nitric Oxide Pathway, in Biological Materials using the Chemiluminescence Method
Published on: December 25, 2016
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Differential mitochondrial dinitrosyliron complex formation by nitrite and nitric oxide
Douglas D Thomas1, Catherine Corey2, Jason Hickok1
1Department of Medicinal Chemistry & Pharmacognosy, University of Illinois at Chicago, 833 South Wood St., Chicago IL 60612, USA.
Redox Biology
|January 6, 2018
Summary
Dietary nitrite increases dinitrosyliron complexes (DNIC) in organs, but these complexes do not protect against ischemia/reperfusion injury. Mitochondrial DNIC formation differs between nitric oxide (NO) and nitrite, impacting cell function.
Area of Science:
- Biochemistry
- Physiology
- Endocrinology
Background:
- Nitrite serves as a reservoir for nitric oxide (NO), a key mediator of physiological processes like cytoprotection during ischemia/reperfusion (I/R).
- Dinitrosyliron complexes (DNIC) form from nitrite and non-heme iron, but their in vivo formation kinetics and role in nitrite's protective effects are not fully understood.
Purpose of the Study:
- To investigate the kinetics of nitrite-dependent DNIC formation in vivo compared to NO-dependent DNIC formation.
- To determine if DNIC accumulation contributes to the cytoprotective effects of nitrite after hepatic I/R.
- To elucidate the role of mitochondrial DNIC formation in the differential effects of NO and nitrite.
Main Methods:
- Assessed DNIC concentrations in mouse liver and kidney following chronic or acute nitrite supplementation.
- Utilized an isolated mitochondrial model of anoxia/reoxygenation to compare NO and nitrite-induced S-nitrosothiol and DNIC formation.
- Evaluated mitochondrial dysfunction and aconitase activity in response to NO and nitrite.
Main Results:
- Chronic, but not acute, nitrite supplementation increased hepatic and renal DNIC concentrations.
- DNIC accumulation was not associated with nitrite-mediated cytoprotection after hepatic I/R.
- In mitochondria, NO led to greater DNIC formation than nitrite, correlating with mitochondrial dysfunction and inhibited aconitase activity.
Conclusions:
- Nitrite-dependent DNIC formation is a physiological outcome of dietary nitrite intake.
- Mitochondrial DNIC formation mechanisms differ between NO and nitrite, potentially explaining their distinct effects post-I/R.
- Mitochondrial DNIC accumulation may contribute to cytotoxic effects observed at high NO concentrations.
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