Abstract
Oxidative stress and mitochondrial dysfunction have been associated with metabolic and agerelated diseases. Thus, the prevention of mitochondrial oxidative damage is nowadays a recognized pharmacological strategy to delay disease progression. Epidemiological studies suggested an association between the consumption of polyphenol-rich diet and the prevention of different pathologies, including diseases with a mitochondrial etiology. The development of mitochondrialtargeted antioxidants based on dietary antioxidants may decrease mitochondrial oxidative damage. Herein, we report the design and synthesis of two new mitochondriotropic antioxidants based on hydroxybenzoic acids (AntiOxBENs). The results obtained showed that the novel antioxidants are accumulated inside rat liver mitochondria driven by the organelle transmembrane electric potential and prevented lipid peroxidation, exhibiting low toxicity. Some of the observed effects on mitochondrial bioenergetics resulted from an increase of proton leakage through the mitochondrial inner membrane. The new derivatives present a higher lipophilicity than the parent compounds (protocatechuic and gallic acids) and similar antioxidant and iron chelating properties. AntiOxBENs are valid mitochondriotropic antioxidant prototypes, which can be optimized and used in a next future as drug candidates to prevent or slow mitochondrial oxidative stress associated to several pathologies.

Abstract
Targeting mitochondrial oxidative stress is an effective therapeutic strategy. In this context, a rational design of mitochondriotropic antioxidants (compounds 22-27) based on a dietary antioxidant (caffeic acid) was performed. Jointly named as AntiOxCINs, these molecules take advantage of the known ability of the triphenylphosphonium cation to target active molecules to mitochondria. The study was guided by structure-activity-toxicity-property relationships, and we demonstrate in this work that the novel AntiOxCINs act as mitochondriotropic antioxidants. In general, AntiOxCINs derivatives prevented lipid peroxidation and acted as inhibitors of the mitochondrial permeability transition pore. AntiOxCINs toxicity profile was found to be dependent on the structural modifications performed on the dietary antioxidant. On the basis of mitochondrial and cytotoxicity/antioxidant cellular data, compound 25 emerged as a potential candidate for the development of a drug candidate with therapeutic application in mitochondrial oxidative stress-related diseases. Compound 25 increased GSH intracellular levels and showed no toxicity on mitochondrial morphology and function.

Abstract
An electrochemical biosensor was developed by merging the features of Molecular Imprinting technique and Screen-Printed Electrode (SPE) for the simple and fast screening of cardiac biomarker myoglobin (Myo) in point-of-care (POC). The MIP artificial receptor for Myo was prepared by electrooxidative polymerization of phenol (Ph) on a AuSPE in the presence of Myo as template molecule. The choice of the most effective protein extraction procedure from the various extraction methods tested (mildly acidic/basic solutions, pure/mixed organic solvents, solutions containing surfactants and enzymatic digestion methods), and the optimization of the thickness of the polymer film was carefully undertaken in order to improve binding characteristics of Myo to the imprinted polymer receptor and increase the sensitivity of the MIP biosensor. The film thickness was optimized by adjusting scan rate and the number of cycles during cyclic voltammetric electropolymerization of Ph. The thickness of the polyphenol nanocoating of only few nanometres (similar to 4.4 nm), and similar to the protein diameter, brought in significant improvements in terms of sensor sensitivity. The binding affinity of MIP receptor film was estimated by fitting the experimental data to Freundlich isotherm and a similar to 8 fold increase in the binding affinity of Myo to the imprinted polymer (K-F = 0.119 +/- 0.002 ng(-1) mL) when compared to the non- imprinted polymer (K-F = 0.015 +/- 0.002 ng(-1) mL) which demonstrated excellent (re) binding affinity for the imprinted protein. The incubation of the Myo MIP receptor modified electrode with increasing concentration of protein (from 0.001 ng mL(-1) to 100 mu g mL(-1)) resulted in a decrease of the ferro/ferricyanide redox current. LODs of 2.1 and 14 pg mL(-1) were obtained from calibration curves built in neutral buffer and diluted artificial serum, respectively, using SWV technique, enabling the detection of the protein biomarker at clinically relevant levels. The prepared MIP biosensor was applied to the determination of Myo spiked serum samples with satisfactory results.

Abstract
In this work, the analytical use of facilitated ion transfer of catecholamines by dibenzo-18-crown-6 was investigated at the water/1,6-dichlorohexane interface using electrochemical methods (cyclic and square wave voltammetry). The experimental conditions for the analytical determination of noradrenaline and dopamine were established and detection limits of 1.7 and 0.35µM were obtained, respectively. The effect of excess ascorbic acid on the transfer and detection of the two catecholamines was investigated. The selectivity coefficients obtained for dopamine and noradrenaline in the presence of ascorbic acid were 3.5×10-4 and 2.5×10-3, respectively. © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Abstract
In this work, the ion transfer mechanism of the anticancer drug daunorubicin (DNR) at a liquid/liquid interface has been studied for the first time. This study was carried out using electrochemical techniques, namely cyclic voltammetry (CV) and differential pulse voltammetry (DPV). The lipophilicity of DNR was investigated at the water/1,6-dichlorohexane (DCH) interface, and the results obtained were presented in the form of an ionic partition diagram. The partition coefficients of both neutral and ionic forms of the drug were determined. The analytical parameter for the detection of DNR was also investigated in this work. An electrochemical DNR sensor is proposed by means of simple ion transfer at the water/DCH interface, using DPV as the quantification technique. Experimental conditions for the analytical determination of DNR were established, and a detection limit of 0.80 mu M was obtained.

Abstract
We describe here a voltammetric method based on the ion transfer at a water/oil interface for the electrochemical study of the interaction between high molecular weight dsDNA and two molecules of biological interest: the anthracycline drug daunorubicin (DNR) and the neurotransmitter dopamine (DA). The binding constants of the complexes were determined by performing an amperometric titration, following the decrease of ion transfer currents upon addition of dsDNA, using differential pulse voltammetry (DPV) technique. Binding constants were interpreted in terms of the main interaction mode of the molecules with DNA. A binding constant of 1.7 x 10(4) M-1 was obtained for the intercalation complex of DNR into DNA base pairs (bp), while a binding constant of 1.8 x 10(3) M-1 was obtained for the electrostatic interaction between positively charged DA and negatively charged dsDNA, using a non-linear binding model. The binding site size, in terms of base pairs, for the interaction between the two molecules and DNA was also estimated using non-linear regression analysis. Two binding site models were tested and compared in this work.