Self-assembled monolayers for electrostatic electrocatalysis and enhanced electrode stability in thermogalvanic cells.

Waste heat is ubiquitous; as such, sustainable and long-lasting devices are required to convert it into more useful forms of energy that can make use of this abundant potential resource. Thermogalvanic cells (or thermocells) can use the thermoelectrochemical properties of redox couples to achieve this; entropy-driven redox reactions allow them to act as liquid thermoelectrics. However, excellent electrocatalysis at the electrode surface is required for optimum conversion efficiency. Serendipitous observation of Nafion-based electrocatalysis prompted the exploration of electrostatically charged self-assembled monolayers (SAMs) inside a thermocell. Both electrostatic electrocatalysis and improved electrode stability were observed; in an aqueous K3[Fe(CN)6]/K4[Fe(CN)6]-based cell, modification with (3-trimethylammonium bromide)thiopropane resulted in higher electrical power, and protection against [Fe(CN)6]3-/4--induced gold passivation, relative to bare gold. Molecular-based electrostatic electrocatalysis could be an alternative to precious metal-based nanomaterial electrocatalysis, and could be integrated with (nano)carbon-based electrodes to further enhance the ability of thermogalvanic and other electrochemical energy conversion devices, e.g. redox flow batteries.

High Seebeck coefficient thermogalvanic cells via the solvent-sensitive charge additivity of cobalt 1,8-diaminosarcophagine.

Thermogalvanic devices can chemically convert low grade (<200 °C) waste thermal energy into electrical energy. A temperature gradient across the device drives an entropically favourable electrochemical redox reaction, resulting in continuous current production. The voltage correlates with the entropy change during the redox reaction, which favours high valence metal complexes with high charge densities. Here we investigate cobalt (II/III) sarcophagine ([Co(SAR)]2+/3+) for application in thermogalvanic cells, as a function of solvent; the two uncoordinated amine groups 1,8-diaminosarcophagine are typically protonated to form tetracationic/pentacationic [Co(SARH2)]4+/5+. In water, [Co(SARH2)]4+/5+ gave a thermogalvanic Seebeck coefficient (Se) of +0.43 mV K-1, which is entropically consistent with just the Co2+/3+ core valence, whereas DMSO and ionic liquid solvents gave Se values of +1.84 and +2.04 mV K-1, respectively, in line with the 'Co4+/5+' overall complex. This work proves how the ionic charge on pendant moieties can undergo charge-additivity with the metal core to significantly boost entropically-driven processes, but only in suitably low dielectric and bulky solvents.

Investigating the Effect of Steric Hindrance within CdS Single-Source Precursors on the Material Properties of AACVD and Spin-Coat-Deposited CdS Thin Films.

Cadmium sulfide (CdS) is an important semiconductor for electronic and photovoltaic applications, particularly when utilized as a thin film for window layers in CdTe solar cells. Deposition of thin-film CdS through the decomposition of single-source precursors is an attractive approach due to the facile, low-temperature, and rapid nature of this approach. Tailoring the precursor to affect the decomposition properties is commonly employed to tune desirable temperatures of decomposition. However, altering the precursor structure and the effect this has on the nature of the deposited material is an area far less commonly investigated. Here, we seek to investigate this by altering the ligands around the Cd metal center to increase the steric hindrance of the precursor and investigate the effect this has on the decomposition properties and the properties of deposited thin-film CdS from these precursors. For this, we report the synthesis of four CdS precursors with xanthate and pyridyl ligands ([Cd(n-ethyl xanthate)2(3-methyl pyridine)2] [1], [Cd(n-ethyl xanthate)2(3,5-lutidine)2] [2], [(Cd2(isopropyl xanthate)4(3-methyl pyridine)2)n] [3], and [Cd(isopropyl xanthate)2(3,5-lutidine)2] [4]). These single-source precursors for CdS were fully characterized by elemental analysis, NMR spectroscopy, single-crystal X-ray diffraction (XRD), and thermogravimetric analysis. It was found that even with subtle alterations in the xanthate (n-ethyl to isopropyl) and pyridine (3-methyl and 3,5-dimethyl) ligands, a range of hexa-coordinate precursors were formed (two with cis configuration, one with trans configuration, and one as a one-dimensional (1D) polymer). These four precursors were then used in aerosol-assisted chemical vapor deposition (AACVD) and spin-coating experiments to deposit eight thin films of CdS, which were characterized by Raman spectroscopy, powder X-ray diffraction, and scanning electron microscopy. Comparative quantitative information concerning film thickness and surface roughness was also determined by atomic force microscopy. Finally, the optical properties of all thin films were characterized by ultraviolet-visible (UV-Vis) absorption spectroscopy, from which the band gap of each deposited film was determined to be commensurate with that of bulk CdS (ca. 2.4 eV).

Biophysical analysis of cancer stem cell-potent copper(ii) coordination complexes.

Copper(ii) coordination complexes, 1 and 2, containing nonsteroidal anti-inflammatory drugs (NSAIDs) potently kill breast cancer stem cells (CSCs) and bulk breast cancer cells. Although detailed biological studies have been conducted to shed light on their mechanism of cytotoxicity, little is known about their molecular level mechanism of action. This biophysical study, aided by the preparation of a fluorophore-containing analogue, 3, reveals that the complexes operate by undergoing reduction to a copper(i) form and releasing the associated NSAIDs.

The Next Generation of Anticancer Metallopharmaceuticals: Cancer Stem Cell-Active Inorganics.

Cancer stem cells (CSCs) are heavily linked to fatal incidences of cancer relapse and metastasis. Conventional cancer therapies such as surgery, chemotherapy and radiation are largely futile against CSCs. Therefore, highly original approaches are needed to overcome CSCs and to provide durable, long-term clinical outcomes. Many academia- and pharmaceutical-led studies aimed at developing chemical or biological anti-CSC agents are ongoing; however, the application of inorganic compounds is rare. In this minireview, we discuss how the chemical diversity and versatility offered by metals has been harnessed to develop an unprecedented, emerging class of metallopharmaceuticals: CSC-active inorganics. A detailed account of their mechanism(s) of action is provided, and possible future directions for exploration are also put forward.

Highly Charged, Cytotoxic, Cyclometalated Iridium(III) Complexes as Cancer Stem Cell Mitochondriotropics.

The cancer stem cell (CSC) toxicity and mechanism of action of a series of iridium(III) complexes bearing polypridyl and charged 1-methyl-2-(2-pyridyl)pyridinium ligands, 1-4 is reported. The most effective complex (containing 1,10-phenanthroline), 3, kills CSCs and bulk cancer cells with equal potency (in the micromolar range), indicating that it could potentially remove heterogenous tumour populations with a single dose. Encouragingly, 3 also inhibits mammopshere formation to a similar extent as salinomycin, a well-established anti-CSC agent. This complex induces CSC apoptosis by mitochondrial membrane depolarization, inhibition of mitochondrial metabolism, and intracellular reactive oxygen species (ROS) generation. To the best of our knowledge, this is the first study to investigate the anti-CSC properties of iridium complexes.

A Copper(II) Phenanthroline Metallopeptide That Targets and Disrupts Mitochondrial Function in Breast Cancer Stem Cells.

The breast cancer stem cell (CSC) and bulk breast cancer cell potency of a series of metallopeptides containing dichloro(1,10-phenanthroline)copper(II) and various organelle-targeting peptide sequences is reported. The mitochondria-targeting metallopeptide 1 exploits the higher mitochondrial load in breast CSCs over the corresponding non-CSCs and the vulnerability of breast CSCs to mitochondrial damage to potently and selectively kill breast CSCs. Strikingly, 1 reduces the formation and size of mammospheres to a greater extent than salinomycin, an established CSC-potent agent. Mechanistic studies show that 1 enters CSC mitochondria, induces mitochondrial dysfunction, generates reactive oxygen species (ROS), activates JNK and p38 pathways, and prompts apoptosis. To the best of our knowledge, 1 is the first metallopeptide to selectivity kill breast CSCs in vitro.