We observe for the first time a structural phase transition in the oxyborate ${\mathrm{Fe}}_3{\mathrm{O}}_2{\mathrm{BO}}_3$ which occurs along three leg ladders present in this material. X-ray diffraction shows that this transition at 283 K is associated with a new phase where atomic displacements occur in alternate directions perpendicular to the axis and within the plane of the ladders. Magnetic data show that these displacements lead to the formation of singlet pairs which dissociate close to the structural transition. Anomalies in the transport properties also occur close to 283 K showing that the structural transition is related to a charge ordering phenomenon in a low dimensional structure.

Background and purpose:  The discovery of the pharmacological functions of nitric oxide has led to the development of NO donor compounds as therapeutic agents. A new generation of ruthenium NO donors, cis‐[Ru(NO)(bpy)₂L]X_n, has been developed, and our aim was to show that these complexes are able to lyse Trypanosoma cruzi in vitro and in vivo.Experimental approach:  NO donors were incubated with T. cruzi and their anti‐T. cruzi activities evaluated as the percentage of lysed parasites compared to the negative control. In vivo, trypanocidal activity was evaluated by observing the levels of parasitaemia, survival rate and elimination of amastigotes in mouse myocardial tissue. The inhibition of GAPDH was monitored by the biochemical reduction of NAD⁺ to NADH.Key results:  The NO donors cis‐[Ru(NO)(bpy)₂L]X_n presented inhibitory effects on T. cruzi GAPDH (IC₅₀ ranging from 89 to 153 µM). The crystal structure of the enzyme shows that the inhibitory mechanism is compatible with S‐nitrosylation of the active cysteine (cys166) site. Compounds cis‐[Ru(NO)(bpy)₂imN](PF₆)₃ and cis‐[Ru(NO)(bpy)₂SO₃]PF₆, at a dose of 385 nmol·kg⁻¹, yielded survival rates of 80 and 60%, respectively, in infected mice, and eradicated any amastigotes from their myocardial tissue.Conclusions and implications:  The ruthenium compounds exhibited potent in vitro and in vivo trypanocidal activities at doses up to 1000‐fold lower than the clinical dose for benznidazole. Furthermore, one mechanism of action of these compounds is via the S‐nitrosylation of Cys166 of T. cruzi GAPDH. Thus, these compounds show huge potential as candidates for the development of new drugs for the treatment of Chagas's disease.This article is commented on by Machado et al., pp. 258–259 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00662.x and to view a related paper in this issue by Guedes et al. visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00576.x