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An in situ reaction of two optoelectronically active organic ligands (anionic thenoyltrifluoroacetylacetone, tta−, and neutral triphenylphosphine oxide, tppo) with erbium(III) ion in the presence of a base yielded a new erbium complex, [Er(tta)3(tppo)]. The solid and solution structure of the complex was established by X-ray crystallography, NMR, ESI-MS, FTIR, TGA and Raman spectroscopy. They indicate that the Er(III) ion is coordinated to seven oxygen atoms of three tta ligands and one tppo ligand in a monocapped octahedral geometry. The Judd–Ofelt parameters of the complex were determined by a least squares fitting and dealt with its chemical structure. On UV excitation through ligand mediation, the complex shows the characteristic near-infrared emission of the corresponding Er(III) ion at 1534 nm. Furthermore, a near infra-red organic light emitting diode (NIR-OLED) was fabricated with structure: ITO/[N,N′-bis(naphthalen-2-yl)-N,N′-bis(phenyl)benzidine]/[Er(tta)3(tppo)]/[2,2′,2′′-(1,3,5-benzinetriyl)-tris(1-phenyl-1-H-benzimidazole)]/LiF/Al. This device, with maximum applied voltage of 23 V, shows a total quenching of visible emission and electroluminescence in the C-band region (1534 nm) which is suitable for third communication window applications in fiber optics. Finally, an organic diode was fabricated to determine charge carrier mobility of the complex using a steady-state method.

The interaction of dibenz[a,h]anthracene and its ultimate carcinogenic 3,4-diol-1,2-epoxide with lung surfactant phospholipid bilayers was successfully performed using molecular dynamics. The DPPC/DPPG/cholesterol bilayer (64 : 64 : 2) was used as the lung surfactant phospholipid bilayer model and compared with the DPPC bilayer as a reference. Dibenz[a,h]anthracene and its 3,4-diol-1,2-epoxide were inserted in water and lipid phases in order to investigate their interactions with the lung surfactant phospholipid bilayers. The radial distribution function between two P atoms in polar heads shows that the 3,4-diol-1,2-epoxide affects the order between the P atoms in the DPPC/DPPG/cholesterol model more than dibenz[a,h]anthracene, which is a consequence of its preference for the polar heads and dibenz[a,h]anthracene prefers to be located in the hydrocarbon chain of the phospholipid bilayers. Dibenz[a,h]anthracene and its 3,4-diol-1,2-epoxide may form aggregates in water and lipid phases, and in the water–lipid interface. The implications for the possible effect of dibenz[a,h]anthracene and its 3,4-diol-1,2-epoxide in the lung surfactant phospholipid bilayers are discussed.

Primaquine is a traditional antimalarial drug with low parasitic resistance and generally good acceptance at higher doses, which has been used for over 60 years in malaria treatment. However, several limitations related to its hematotoxicity have been reported. It is believed that this toxicity comes from the hydroxylation of the C-5 and C-6 positions of its 8-aminoquinoline ring before binding to the molecular target: the quinone reductase II (NQO2) human protein. In this study we propose primaquine derivatives, with substitution at position C-6 of the 8-aminoquinoline ring, planned to have better binding to NQO2, compared to primaquine, but with a reduced toxicity related to the C-5 position being possible to be oxidized. On this sense the proposed analogues were suggested in order to reduce or inhibit hydroxylation and further oxidation to hemotoxic metabolites. Five C-6 substituted primaquine analogues were selected by de novo design and further submitted to docking and molecular dynamics simulations. Our results suggest that all analogues bind better to NQO2 than primaquine and may become better antimalarials. However, the analogues 3 and 4 are predicted to have a better activity/toxicity balance.