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Bromides
Published in Stanley R. Resor, Henn Kutt, 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).
Interaction of the benzodiazepines with the GABAA receptor
Published in Adam Doble, Ian L Martin, David Nutt, Calming the Brain: Benzodiazepines and related drugs from laboratory to clinic, 2020
Adam Doble, Ian L Martin, David Nutt
The binding of benzodiazepines to the GABAA receptor can be stimulated by certain inorganic anions, notably chloride (Martin and Candy, 1978). It was suggested that the potency of these ions appeared to correlate with their ability to permeate the GABAA receptor chloride channel, as measured by reversal of inhibitory postsynaptic potentials in motoneu-rons (Costa et al, 1979). The later observation that the effect of halides on benzodiazepine binding could be blocked by chloride channel blockers, such as DIDS and SITS (Costa et al, 1981), argued for a specific effect of halides on the receptor. However, no direct correlation could be found between the ability of these anions to enhance benzodiazepine binding and to mediate inhibitory postsynaptic potentials in the neocortex (Martin and Candy, 1980).
Chemistry and Isotopes of Iodine
Published in Erwin Regoeczi, Iodine-Labeled Plasma Proteins, 2019
Halides are compounds of two elements, one of which is a halogen. Iodine form salts with many metals (e.g., Ag, Al, Cu, Hg, Pb) to yield iodides. Here we only consider two compounds of iodine with alkali metals, namely NaI and KI.
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.
Anion inhibition studies of the α-carbonic anhydrases from Neisseria gonorrhoeae
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Alessio Nocentini, Chad S. Hewitt, Margaret D. Mastrolorenzo, Daniel P. Flaherty, Claudiu T. Supuran
Inhibition constants in the range of 1.3–9.6 mM were measured for the following anions: all the halides, azide, bicarbonate, carbonate, stannate, perosmate, diphosphate, divanadate, perruthenate, and trifluoromethanesulfonate. The last anion is an interesting case, as it does not considerably inhibits hCA I and II (KIs > 100 mM) being thus an NgCA-selective (although weak) inhibitor. Among the halides, fluoride and iodide were weaker inhibitors than chloride and bromide (which was the most effective one among the halides). Bicarbonate, with a KI of 1.3 mM is a rather effective inhibitor (and this substrate of the enzyme is a much weaker hCA I and especially hCA II inhibitor, see Table 1), which presumably may constitute a way to inhibit the activity of this highly effective enzyme by one of the reaction products, which might be physiologically significant. This hypothesis needs to be checked, but it is known for example that in the case of V. cholerae, bicarbonate, generated by the activity of the various CAs present in this pathogen, induces virulence gene expression1;