Insight into the relevance of dinitrosyl iron complex (DNIC) formation in the absence of thiols in aqueous media.

DNIC can be formed in aqueous media in the absence of thiols via mechanisms that depend exclusively on Fe(II) and NO. However, these reactions do not take place at intracellular concentrations of Fe(II) and NO, reinforcing the relevance of thiols to assist Fe(II) to Fe(I) reduction during DNIC formation in biological media.

Carbon dioxide redox metabolites in oxidative eustress and oxidative distress.

High carbon dioxide tensions (hypercapnia) are toxic to mammals by both pH-dependent and pH-independent mechanisms that remain partially understood. Relevantly, carbon dioxide reacts with biologically ubiquitous oxygen metabolites such as peroxynitrite and hydrogen peroxide to produce carbonate radical and peroxymonocarbonate, respectively. These metabolites are redox active making it timely to discuss the potential role of carbon dioxide redox metabolites in oxidative eustress and oxidative distress conditions.

The labile iron pool attenuates peroxynitrite-dependent damage and can no longer be considered solely a pro-oxidative cellular iron source.

The ubiquitous cellular labile iron pool (LIP) is often associated with the production of the highly reactive hydroxyl radical, which forms through a redox reaction with hydrogen peroxide. Peroxynitrite is a biologically relevant peroxide produced by the recombination of nitric oxide and superoxide. It is a strong oxidant that may be involved in multiple pathological conditions, but whether and how it interacts with the LIP are unclear. Here, using fluorescence spectroscopy, we investigated the interaction between the LIP and peroxynitrite by monitoring peroxynitrite-dependent accumulation of nitrosated and oxidized fluorescent intracellular indicators. We found that, in murine macrophages, removal of the LIP with membrane-permeable iron chelators sustainably accelerates the peroxynitrite-dependent oxidation and nitrosation of these indicators. These observations could not be reproduced in cell-free assays, indicating that the chelator-enhancing effect on peroxynitrite-dependent modifications of the indicators depended on cell constituents, presumably including LIP, that react with these chelators. Moreover, neither free nor ferrous-complexed chelators stimulated intracellular or extracellular oxidative and nitrosative chemistries. On the basis of these results, LIP appears to be a relevant and competitive cellular target of peroxynitrite or its derived oxidants, and thereby it reduces oxidative processes, an observation that may change the conventional notion that the LIP is simply a cellular source of pro-oxidant iron.

Biological activity of ruthenium nitrosyl complexes.

Nitric oxide plays an important role in various biological processes, such as neurotransmission, blood pressure control, immunological responses, and antioxidant action. The control of its local concentration, which is crucial for obtaining the desired effect, can be achieved with exogenous NO-carriers. Coordination compounds, in particular ruthenium(III) and (II) amines, are good NO-captors and -deliverers. The chemical and photochemical properties of several ruthenium amine complexes as NO-carriers in vitro and in vivo have been reviewed. These nitrosyl complexes can stimulate mice hippocampus slices, promote the lowering of blood pressure in several in vitro and in vivo models, and control Trypanosoma cruzi and Leishmania major infections, and they are also effective against tumor cells in different models of cancer. These complexes can be activated chemically or photochemically, and the observed biological effects can be attributed to the presence of NO in the compound. Their efficiencies are explained on the basis of the [Ru(II)NO(+)](3+)/[Ru(II)NO(0)](2+) reduction potential, the specific rate constant for NO liberation from the [RuNO](2+) moiety, and the quantum yield of NO release.

Nitrosyl induces phosphorous-acid dissociation in ruthenium(II).

The trans-[Ru(NO)(NH(3))(4)(P(OH)(3))]Cl(3) complex was synthesized by reacting [Ru(H(2)O)(NH(3))(5)](2+) with H(3)PO(3) and characterized by spectroscopic ((31)P-NMR, δ = 68 ppm) and spectrophotometric techniques (λ = 525 nm, ε = 20 L mol(-1) cm(-1); λ = 319 nm, ε = 773 L mol(-1) cm(-1); λ = 241 nm, ε = 1385 L mol(-1) cm(-1); ν(NO(+)) = 1879 cm(-1)). A pK(a) of 0.74 was determined from infrared measurements as a function of pH for the reaction: trans-[Ru(NO)(NH(3))(4)(P(OH)(3))](3+) + H(2)O ⇌ trans-[Ru(NO)(NH(3))(4)(P(O(-))(OH)(2))](2+) + H(3)O(+). According to (31)P-NMR, IR, UV-vis, cyclic voltammetry and ab initio calculation data, upon deprotonation, trans-[Ru(NO)(NH(3))(4)(P(OH)(3))](3+) yields the O-bonded linkage isomer trans- [Ru(NO)(NH(3))(4)(OP(OH)(2))](2+), then the trans-[Ru(NO)(NH(3))(4)(OP(H)(OH)(2))](3+) decays to give the final products H(3)PO(3) and trans-[Ru(NO)(NH(3))(4)(H(2)O)](3+). The dissociation of phosphorous acid from the [Ru(NO)(NH(3))(4)](3+) moiety is pH dependent (k(obs) = 2.1 × 10(-4) s(-1) at pH 3.0, 25 °C).