Bromides
Stanley R. Resor, Henn Kutt in The Medical Treatment of Epilepsy, 2020
At present it is not known how bromides act to prevent seizures, although there are several theories. As a halide, the bromide ion is handled similarly to chloride. Because its hydrated diameter is less than that of chloride it may pass through the membrane channels more readily and cause a hyperpolarization of the transmembrane potential, making neurons less likely to initiate a seizure discharge or to participate in the spread of the seizure (11). Other studies have shown that benzodiazepine binding is increased in the presence of bromides, suggesting that this ion may affect the function of the benzodiazepine/GABA ionophore (12). Other biochemical measures of GABA neurotransmission are not altered in the presence of bromide (13). It may also inhibit the action of carbonic anhydrase similarly to acetazolamide, which also has some antiepileptic activity (11).
Tin, Tumors, and the Thymus Gland*
Nate F. Cardarelli in Tin as a Vital Nutrient:, 2019
The select toxicology of trialkyl tin compounds seems to fit a pattern in both mammalian and nonmammalian systems. All toxicology appears to be dose related whether it concerns snails,28 mosquito larva,27 or with the involution of the thymus gland.16,17 Certain trialkyl tin compounds are known to carry chloride across the cell membrane and into the cell where the chloride ion is usually not found, except among certain marine animals.3 The trialkyl tin compounds exchange the chloride for hydroxide and then diffuse back into the intercellular media where they pick up another chloride and repeat the process.8 Accumulation of sufficient chloride within the cell disrupts vital processes and leads to cell death. This may explain why certain organotins are highly toxic to fresh water snails, but poor for salt water species. A membrane sensitivity to halide ion would explain the limited toxicity of the compounds. The fresh water mulluscs cannot tolerate the halide ion, whereas the salt water ones can.
Scintillation Detectors
Michael Ljungberg in Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
The first phase was the early use of ZnS, CaWO4 and barium platinocyanide screens as scintillators by Röntgen, Crookes, Rutherford, and many others. The second phase was triggered by the introduction of the photomultiplier tube in the mid 1940s and the discovery of the NaI(Tl) [10, 21] and CsI(Tl) [22] scintillators in the beginning of the 1950s. In the third phase, crystal growth from high-melting point materials could be handled, and the use of rare earth materials (REE) as luminescence centres was initiated. The use of REE elements (mainly Ce and Eu) as dopants in various types of materials expanded heavily during the fourth phase, and a number of lanthanide-activated halides were discovered. The technique of co-doping (see below) and dedicated bandgap engineering improved various properties in already-existing scintillation materials and improved manufacturing technologies brought forward garnet compounds and ceramic scintillators. The fundamental understanding of the scintillation phenomena through both experimental and theoretical work enabled adjusting fundamental properties of already-existing scintillators through so called bandgap engineering. Current research (the fifth phase) focuses, from a medical point of view, on further improving energy resolution and developing very fast scintillators for TOF-PET.
Genotoxic potential of different nano-silver halides in cultured human lymphocyte cells
Published in Drug and Chemical Toxicology, 2023
Devrim Güzel, Merve Güneş, Burçin Yalçın, Esin Akarsu, Eyyüp Rencüzoğulları, Bülent Kaya
One of the remarkable breakthroughs in the domain of nanotechnology is the use of silver halides (AgBr, AgCl, and AgI) in many medical applications as antimicrobial agents (Bahri-Kazempourab et al.2013). In line with this, is the present research aims to investigate the possible genotoxic, clastogenic, and cytotoxic effects of silver ion (Ag+), AgNP and nano-sized silver halides/salts (AgBr, AgCl, and AgI) on healthy human peripheral blood lymphocyte cells in vitro. The chromosomal and DNA damages that these test substances may cause with clastogenic or aneugenic effects are evaluated on healthy human cells through the CA test and cytokinesis-blocked micronucleus (CBMN) test. The genotoxic effects resulting from the DNA strand breaks are evaluated through the Comet test on healthy human lymphocyte cells.
Discovery of novel drugs for Chagas disease: is carbonic anhydrase a target for antiprotozoal drugs?
Published in Expert Opinion on Drug Discovery, 2022
Alane Beatriz Vermelho, Giseli Capaci Rodrigues, Alessio Nocentini, Felipe R. P. Mansoldo, Claudiu T. Supuran
Pan et al. [87] investigated the Inhibition of TcCA with inorganic simple and complex anions and other molecules interacting with zinc proteins, among which halides, cyanate, thiocyanate hydrogen sulfide, trithiocarbonate, diethyldithiocarbamate, and sulfamide. They were all medium-weak TcCA inhibitors, showing KI in the milli- to micromolar range. This study demonstrated exciting correlations between the nature of the anion and its inhibitory activity against TcCA. In halides cases, the TcCA inhibitory action increased with the halogen’s atomic weight, making iodide a rather potent TcCA inhibitor. Anions inhibitors probably bind to the metal ion in the TcCA active site in either tetrahedral or trigonal-bipyramidal geometries of the Zn(II) [87]. This study evidenced that diethyldithiocarbamate 31, which contains the CS2− zinc-binding group, represents a new class of CAIs, with a KI of 5 μM [29]. It is important to note that, like the sulfonamides, the CAIs from other classes discussed so far have various zinc-binding groups. However, there are other yet unexplored α-CA inhibition mechanisms, anchoring the inhibitor to the zinc coordinated water or occluding the active site entrance [51,54]. However, such inhibitors were not yet designed or investigated for the Inhibition of TcCA. Table 2 summarizes the zinc-binding TcCA inhibitors studied far apart from the sulfonamides. Table 2 summarizes some non-sulfonamide, TcCA inhibitors.
A patent review of anticancer CDK2 inhibitors (2017–present)
Published in Expert Opinion on Therapeutic Patents, 2022
Mohamed A. Said, Mohamed A. Abdelrahman, Mohammed A.S. Abourehab, Mohamed Fares, Wagdy M. Eldehna
Moreover, Ye et al. illustrated the applied synthetic procedures that could be used to prepare the target compounds. Appropriately substituted compound 42 can react with 1-tertbutoxy-N,N,N’,N’-tetramethyl methane diamine (a) to produce compounds 43. Compounds formed using scaffold 43 can then be converted into compounds of the scaffold 46 via reaction with appropriately substituted sulphaguanidine compounds (b) in the presence of a suitable base such as sodium ethoxide. Alternatively, compounds of formula 46 can be obtained by reacting with guanidine hydrochloride (c) instead of compounds of substituted sulphaguanidine derivatives (b), followed by a suitable C–N cross-coupling with appropriately substituted halides (d) including Buchwald – Hartwig amination in a suitable solvent such as 1,4-dioxane. Synthesis of compounds of formula 46 can also be achieved by a suitable C–N cross-coupling certain amines intermediates of pathway (e) with bromide derivatives of compounds 45, which can be obtained from compounds of intermediates 44 via Sandmeyer reaction (Scheme 8) [50].