“…These data are supported by studies comparing the ability of HOSCN and HOSeCN to kill bacterial cells. Thus, supplementation with SeCN − has been shown to be more effective in killing bacteria and fungi when compared to SCN − [ 37 , 57 , 58 ]. Similarly, SeCN − -containing compounds have therapeutic applications for cancer treatment and prevention [ 59 ].…”
Section: Discussionmentioning
confidence: 99%
“…Whether SeCN − supplementation is of value in vivo in mitigating chronic inflammation has yet to be established, though promotion of HOSeCN formation may be beneficial in inflammatory situations where there is pathogen involvement (e.g. sepsis), in light of its superior bactericidal properties compared to HOSCN [ 37 , 57 , 58 , 67 ].…”
The production of hypochlorous acid (HOCl) by myeloperoxidase (MPO) plays a key role in immune defense, but also induces host tissue damage, particularly in chronic inflammatory pathologies, including atherosclerosis. This has sparked interest in the development of therapeutic approaches that decrease HOCl formation during chronic inflammation, including the use of alternative MPO substrates. Thiocyanate (SCN
−
) supplementation decreases HOCl production by favouring formation of hypothiocyanous acid (HOSCN), which is more selectively toxic to bacterial cells. Selenium-containing compounds are also attractive therapeutic agents as they react rapidly with HOCl and can be catalytically recycled. In this study, we examined the ability of SCN
−
, selenocyanate (SeCN
−
) and selenomethionine (SeMet) to modulate HOCl-induced damage to human coronary artery smooth muscle cells (HCASMC), which are critical to both normal vessel function and lesion formation in atherosclerosis. Addition of SCN
−
prevented HOCl-induced cell death, altered the pattern and extent of intracellular thiol oxidation, and decreased perturbations to calcium homeostasis and pro-inflammatory signaling. Protection was also observed with SeCN
−
and SeMet, though SeMet was less effective than SeCN
−
and SCN
−
. Amelioration of damage was detected with sub-stoichiometric ratios of the added compound to HOCl. The effects of SCN
−
are consistent with conversion of HOCl to HOSCN. Whilst SeCN
−
prevented HOCl-induced damage to a similar extent to SCN
−
, the resulting product hyposelenocyanous acid (HOSeCN), was more toxic to HCASMC than HOSCN. These results provide support for the use of SCN
−
and/or selenium analogues as scavengers, to decrease HOCl-induced cellular damage and HOCl production at inflammatory sites in atherosclerosis and other pathologies.
“…These data are supported by studies comparing the ability of HOSCN and HOSeCN to kill bacterial cells. Thus, supplementation with SeCN − has been shown to be more effective in killing bacteria and fungi when compared to SCN − [ 37 , 57 , 58 ]. Similarly, SeCN − -containing compounds have therapeutic applications for cancer treatment and prevention [ 59 ].…”
Section: Discussionmentioning
confidence: 99%
“…Whether SeCN − supplementation is of value in vivo in mitigating chronic inflammation has yet to be established, though promotion of HOSeCN formation may be beneficial in inflammatory situations where there is pathogen involvement (e.g. sepsis), in light of its superior bactericidal properties compared to HOSCN [ 37 , 57 , 58 , 67 ].…”
The production of hypochlorous acid (HOCl) by myeloperoxidase (MPO) plays a key role in immune defense, but also induces host tissue damage, particularly in chronic inflammatory pathologies, including atherosclerosis. This has sparked interest in the development of therapeutic approaches that decrease HOCl formation during chronic inflammation, including the use of alternative MPO substrates. Thiocyanate (SCN
−
) supplementation decreases HOCl production by favouring formation of hypothiocyanous acid (HOSCN), which is more selectively toxic to bacterial cells. Selenium-containing compounds are also attractive therapeutic agents as they react rapidly with HOCl and can be catalytically recycled. In this study, we examined the ability of SCN
−
, selenocyanate (SeCN
−
) and selenomethionine (SeMet) to modulate HOCl-induced damage to human coronary artery smooth muscle cells (HCASMC), which are critical to both normal vessel function and lesion formation in atherosclerosis. Addition of SCN
−
prevented HOCl-induced cell death, altered the pattern and extent of intracellular thiol oxidation, and decreased perturbations to calcium homeostasis and pro-inflammatory signaling. Protection was also observed with SeCN
−
and SeMet, though SeMet was less effective than SeCN
−
and SCN
−
. Amelioration of damage was detected with sub-stoichiometric ratios of the added compound to HOCl. The effects of SCN
−
are consistent with conversion of HOCl to HOSCN. Whilst SeCN
−
prevented HOCl-induced damage to a similar extent to SCN
−
, the resulting product hyposelenocyanous acid (HOSeCN), was more toxic to HCASMC than HOSCN. These results provide support for the use of SCN
−
and/or selenium analogues as scavengers, to decrease HOCl-induced cellular damage and HOCl production at inflammatory sites in atherosclerosis and other pathologies.
“…These structures present several pharmacological properties and biological activity . In the particular case of organoselenocyanates, pronounced antileishmanial, antitrypanosomal, antibacterial, antifungal, and antitumor activities were observed.…”
Candida is a genus that causes the highest number of fungal infections on people around the world, responsible for high mortality rates in critical and immunocompromised patients. Even though several antifungals are commercially available, most of these have side effects or are only available for intravenous administration. In view of this aspect, the susceptibility of twelve allylic selenocyanate (AS) compounds, five of them novel, were tested against 36 Candida strains. The AS were active for all Candida strains reaching minimal inhibitory concentrations (MIC) in the order of ng mL−1 (0.39–50 μg mL−1). The sorbitol and ergosterol assay show that these compounds do not act on the cell wall and fungal membrane, suggesting a different mechanism of action. Cytotoxicity and irritability tests showed that only three molecules already studied (2 b, 2 j and 2 i) for this series manifested damage to the leukocyte cell and chorioallantoic membrane, but at higher concentrations than the MICs. Considering the susceptibility results and parameters of Lipinski, molecules 2 c (0.39–12.5 μg mL−1) and 2 d (0.78–6.2 μg mL−1) look promising for the development of a new antifungal agent against Candida infections.
“…[60] Similarly, selenium plays an important role in normal biological function [61] through its incorporation into processes that protect against oxidative stress, and its bioactivity mechanism has been studied using DFT calculations. [62] Selenocyanatecontaining derivatives have been found to possess anticancer and chemopreventive, [63][64][65] antifungal, [66] and antileishmanial [67,68] activity. Therefore, their synthesis, characterization, and uses in chemistry and molecular recognition have recently gained a lot of interest.…”
In this manuscript the different noncovalent interactions established between (HYCN)2 dimers (Y=S, Se and Te) have been studied at the MP2 and CCSD(T) level of theory. Several homodimers have been taken into account, highlighting the capacity of these compounds to act both as electron donor and acceptor. The main properties studied were geometries, binding energy (Eb), and molecular electrostatic potential (MEP). Given the wide application of chalcogen bonds, and more specifically of cyano‐chalcogen moieties in molecular recognition, natural bond orbital (NBO), “atoms‐in‐molecules” (AIM), and electron density shift (EDS) analysis were also used to analyse the different noncovalent interactions upon complexation. The presence of hydrogen, chalcogen and dipole‐dipole interactions was confirmed and their implications on molecular recognition were analysed.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.