Modulation of hypochlorous acid (HOCl) induced damage to vascular smooth muscle cells by thiocyanate and selenium analogues

• DOI: 10.1016/j.redox.2021.101873
• Publication Date: 2021-01-22T03:43:59Z
• Authors: Konstantina Flouda; Bente Gammelgaard; Michael J. Davies; Clare L. Hawkins
• Keywords: Hypochlorous acid; Thiocyanate

The production of hypochlorous acid (HOCl) by myeloperoxidase (MPO) plays a key role in immune defense, but also induces host tissue damage, particularly chronic inflammatory pathologies, including atherosclerosis. This has sparked interest the development therapeutic approaches that decrease HOCl formation during inflammation, use alternative MPO substrates. Thiocyanate (SCN−) supplementation decreases favouring hypothiocyanous (HOSCN), which is more selectively toxic to bacterial cells. Selenium-containing compounds are attractive agents as they react rapidly with and can be catalytically recycled. In this study, we examined ability SCN−, selenocyanate (SeCN−) selenomethionine (SeMet) modulate HOCl-induced damage human coronary artery smooth muscle cells (HCASMC), critical both normal vessel function lesion Addition SCN− prevented cell death, altered pattern extent intracellular thiol oxidation, decreased perturbations calcium homeostasis pro-inflammatory signaling. Protection was observed SeCN− SeMet, though SeMet less effective than SCN−. Amelioration detected sub-stoichiometric ratios added compound HOCl. effects consistent conversion HOSCN. Whilst similar resulting product hyposelenocyanous (HOSeCN), HCASMC These results provide support for and/or selenium analogues scavengers, cellular at sites atherosclerosis other pathologies.