Supplementary MaterialsSupplements Fig. metabolic activity and cell cycle distribution were studied. The influence on radiosensitivity was determined via colony forming assays using different solvents of sodium selenite and treatment schedules. It was shown that sodium selenite inhibits growth and influences cell cycle distribution of both normal and tumour cells. Metabolic activity of normal cells decreased more rapidly compared to that of cancer cells. The influence of sodium selenite on radiation response depended on the different treatment schedules and was strongly affected by the Entacapone sodium salt solvent of the agent. It could be shown that the effect of sodium selenite on radiation response is strongly dependent on the respective experimental in vitro conditions and ranges from lead to an primarily suspected but eventually no genuine radioprotection to radiosensitizing as Entacapone sodium salt much as no impact in one as well as the same cell range. This might be considered a reason behind controversially referred to cell reactions to rays consuming sodium selenite in research up to now. Electronic supplementary materials The online edition of this content (10.1007/s12032-020-01437-y) contains supplementary materials, which is open to certified users. strong course=”kwd-title” Keywords: Sodium selenite, Ionizing irradiation, A549, BEAS-2B, Cell routine, Metabolic activity Intro Selenium as an important trace element can be used because the inorganic type sodium selenite to moderate the medial side effects of tumor therapy [1] and improve the mobile defence of healthful cells [2, 3]. The setting of actions of sodium selenite isn’t yet known at length. The effect is apparently predicated on different systems. On the main one hand, selenite offers Entacapone sodium salt immunomodulatory features and was referred to as influencing the disease fighting capability positively. Tumour cells possess free sulfhydryl organizations on the cell membranes, which shield them from episodes of proteolytic enzymes of phagocytic cells and mediate their uncontrolled development. Selenite can oxidize these protein-bound and free of charge sulfhydryl organizations to related disulfides, which inhibits the protecting (parafibrin-) hurdle of tumor cell membranes and make sure they are susceptible to the harmful activity of phagocytes [4, 5]. Furthermore, selenite causes a rise of immunocompetent cells Rabbit polyclonal to DUSP22 like macrophages and may direct activate organic killer (NK) cells [4, 6]. Selenitewith its unique redox chemistryshows prooxidant and antioxidant properties. Its focus, the intracellular redox position along with the activity of redox-sensitive protein and enzymes participate whether antioxidant or prooxidant actions prevail. The metabolic pathway of selenite, its redox-active properties in mammalian cells and cells and its outcomes were described in an exceedingly detailed way by Weekley and Harris [7]. Through the immunomodulatory impact Aside, it had been assumed for a long period how the positive aftereffect of selenite is due to its antioxidant properties, which support regular cells to lessen their oxidative tension level. It had been, therefore, regarded as that sodium selenite ought to be used like a rays safety agent in regular cells for the prophylaxis of rays results [8, 9]. In research, it was referred to that sodium selenite includes a radioprotective influence on parotid gland cells in rats [10]. By decreasing the quantity of lipid peroxide and raising glutathione and glutathione peroxidase activity, sodium selenite considerably improved the oxidative stress response of the uterus and ovaries induced by radiation [11]. During whole-body irradiation treatment with sodium selenite, mice were protected against radiation-induced genotoxicity and DNA damage in peripheral leukocytes, but it did not keep the animals from mortality or gastrointestinal and hematopoietic lesions [12]. However, overall, in the further literature, the effects of sodium selenite described on the cellular radiation sensitivity are contradictory. There are reports for sodium selenite from radiosensitizing [13, 14] to radioprotection [15]. Furthermore, in several studies no influence of sodium selenite on radiation response was observed [16, 17]. Meanwhile, toxicity of selenite on tumour cells is described as also being mediated because of its prooxidative character [18]. Selenite is involved in the production of reactive oxygen species (ROS), which leads the tumour cells, among others, to DNA damage, mainly DNA double-stranded breaks, induction of apoptosis, and.