Nitric oxide (NO) and reactive oxygen species originated from [Ru(pc)(pz)₂{Ru(bpy)₂(NO)}₂](PF₆)₆(I) have been postulated to act synergistically against cancer cells. NO is released from (I) by the reduction process and singlet oxygen formation by light irradiation at 660 nm.

Nitric oxide (NO) donors are substances that can release NO. Vascular relaxation induction is among the several functions of NO, and the administration of NO donors is a pharmacological alternative to treat hypertension. This review will focus on the physicochemical description of ruthenium-derived NO donor complexes that release NO via reduction and light stimulation. In particular, we will discuss the complexes synthesized by our research group over the last ten years, and we will focus on the vasodilation and arterial pressure control elicited by these complexes. Soluble guanylyl cyclase (sGC) and potassium channels are the main targets of the NO species released from the inorganic compounds. We will consider the importance of the chemical structure of the ruthenium complexes and their vascular effects.

Phthalocyanine (Pc) dyes are photoactive molecules that can absorb and emit light in the visible spectrum, especially in the red region of the spectrum, with great potential for biological scopes. For this target, it is important to guarantee a high Pc solubility, and the use of suitable pyridinium units on their structure can be a good strategy to use effective photosensitizers (PSs) for photodynamic therapy (PDT) against cancer cells. Zn(II) phthalocyanines (ZnPcs) conjugated with thiopyridinium units (1–3) were evaluated as PS drugs against B16F10 melanoma cells, and their photophysical, photochemical, and in vitro photobiological properties were determined. The photodynamic efficiency of the tetra- and octa-cationic ZnPcs 1–3 was studied and compared at 1, 2, 5, 10, and 20 µM. The different number of charge units, and the presence/absence of a-F atoms on the Pc structure, contributes for their PDT efficacy. The 3-(4′,5′-dimethylthiazol-2′-yl)-2,5-diphenyl tetrazolium bromide (MTT) assays on B16F10 melanoma cells show a moderate to high capacity to be photoinactivated by ZnPcs 1–3 (ZnPc 1 > ZnPc 2 > ZnPc 3). The best PDT conditions were found at a Pc concentration of 20 μM, under red light (λ = 660 ± 20 nm) at an irradiance of 4.5 mW/cm² for 667 s (light dose of 3 J/cm²). In these conditions, it is noteworthy that the cationic ZnPc 1 shows a promising photoinactivation ratio, reaching the detection limit of the MTT method. Moreover, these results are comparable to the better ones in the literature.

The synthesis of [Ru(NO₂)L(bpy)₂]⁺ (bpy = 2,2′-bipyridine and L = pyridine (py) and pyrazine (pz)) can be accomplished by addition of [Ru(NO)L(bpy)₂](PF₆)₃ to aqueous solutions of physiological pH. The electrochemical processes of [Ru(NO₂)L(bpy)₂]⁺ in aqueous solution were studied by cyclic voltammetry and differential pulse voltammetry. The anodic scan shows a peak around 1.00 V vs. Ag/AgCl attributed to the oxidation process centered on the metal ion. However, in the cathodic scan a second peak around −0.60 V vs. Ag/AgCl was observed and attributed to the reduction process centered on the nitrite ligand. The controlled reduction potential electrolysis at −0.80 V vs. Ag/AgCl shows NO release characteristics as judged by NO measurement with a NO-sensor. This assumption was confirmed by ESI/MS⁺ and spectroelectrochemical experiment where cis-[Ru(bpy)₂L(H₂O)]²⁺ was obtained as a product of the reduction of cis-[Ru^II(NO₂)L(bpy)₂]⁺. The vasorelaxation observed in denuded aortic rings pre-contracted with 0.1 μmol L⁻¹ phenylephrine responded with relaxation in the presence of cis-[Ru^II(NO₂)L(bpy)₂]⁺. The potential of rat aorta cells to metabolize cis-[Ru^II(NO₂)L(bpy)₂]⁺ was also followed by confocal analysis. The obtained results suggest that NO release happens by reduction of cis-[Ru^II(NO₂)L(bpy)₂]⁺ inside the cell. The maximum vasorelaxation was achieved with 1 × 10⁻⁵ mol L⁻¹ of cis-[Ru^II(NO₂)L(bpy)₂]⁺ complex.