The composite coatings prepared by mixing the 5 wt.% of polyaniline with commercial alkyd-based paint are applied on carbon steel. The polyaniline emeraldine chloride salt is prepared by procedure recommended by IUPAC, deprotonated by ammonia hydroxide, and reprotonated with the sulfamic, succinic, citric, and acetic acids with different doping degrees or oxidation states. The steel samples with base and composite coatings are immersed in 3% NaCl and the corrosion current density is determined after 96 h in-site using ASTM 1,10-phenanthroline method. The samples are also inspected by the optical microscope. It is shown that composite coatings reduce the possibility of blister formations and delamination. The corrosion current density and the appearance of the corrosion products, which area is determined by ImageJ softer, closely follow the initial oxidation state of the polyaniline. The role of the initial state of the polyaniline is discussed. It is suggested that such behavior could be connected with the oxygen reduction reaction mechanism that proceeds mainly via two electron paths on the polyaniline particles, releasing a much smaller amount of hydroxyl ions, responsible for the delamination and blister formations of the commercial coatings.

The inhibition impacts of 1,10-Phenanthroline-5,6-diamine (PTDA) on mild steel in 1 M HCl solution were investigated through weight loss method. The inhibition efficiencies of PTDA increase with increase in PTDA concentration at the temperature 303. Weight loss method indicate that PTDA is an excellent inhibitor the inhibition efficiency of 81.5% at the maximum PTDA concentration of 0.5 g/L at the temperature 303K.

Four 1,10-phenanthroline derivatives (1-4) have been synthesized as potential telomeric DNA binders, three substituted in their chains with thiosemicarbazones (TSCs), the neutral compound (1) and two ionic derivatives (PF6¯ and BF4¯ salts, 2 and 3, respectively), and a fourth corresponding to a 4-phenylthiazole derivative (4). Quadruplex and dsDNA interactions have been preliminarily studied, especially for the neutral derivative 1, by FRET-based DNA melting assays, equilibrium dialysis (both competitive and non-competitive), circular dichroism and viscosity titrations. The TSC derivatives bind and stabilize the telomeric Tel22 quadruplex more efficiently than dsDNA, with an estimated 24-fold selectivity determined by equilibrium dialysis for compound 1. In addition, cytotoxic activity against different tumor cells (PC-3, DU145, HeLa, MCF-7 and HT29), and two non-tumor cell lines (HFF-1 and RWPE-1) has been evaluated. Except for the 4-phenylthiazole derivative, which was inactive, the compounds show moderate cytotoxic properties, with the salts displaying lower IC50 values, compared to the neutral TSC. However, the neutral derivative was the only compound that exhibited a modest selectivity in the case of prostate cells (tumor PC-3 versus healthy RWPE-1). Cell cycle analysis and Annexin V/PI assays revealed that the compounds can produce cell death by apoptosis, an effect that has proven similar to that demonstrated by other known 1,10-phenanthroline G4 ligands endowed with antitumor properties, such as PhenDC3 or PhenQE8.

Metalloproteinases are zinc-dependent endopeptidases that function as primary effectors of tissue remodelling, cell-signalling, and many other roles. Their regulation is ferociously complex, and is exquisitely sensitive to their molecular milieu, making in vivo studies challenging. Phenanthroline (PhN) is an inexpensive, broad-spectrum inhibitor of metalloproteinases that functions by chelating the catalytic zinc ion, however its use in vivo has been limited due to suspected off-target effects. PhN is very similar in structure to phenanthrene (Phe), a well-studied poly aromatic hydrocarbon (PAH) known to cause toxicity in aquatic animals by activating the aryl hydrocarbon receptor (AhR). We show that zebrafish are more sensitive to PhN than Phe, and that PhN causes a superset of the effects caused by Phe. Morpholino knock-down of the AhR rescues the effects of PhN that are shared with Phe, suggesting these are due to PAH toxicity. The effects of PhN that are not shared with Phe (specifically disruption of neural crest development and angiogenesis) involve processes known to depend on metalloproteinase activity. Furthermore these PhN-specific effects are not rescued by AhR knock-down, suggesting that these are bona fide effects of metalloproteinase inhibition, and that PhN can be used as a broad spectrum metalloproteinase inhibitor for studies with zebrafish in vivo.