## 1 Introduction  
Selenium (Se) is a vital nutritional trace element involved in antioxidative metabolism with antitumor and chemo-preventive properties [1]. Se, being a chalcogen, exhibits a similar chemical behavior as sulfur, which is the central redox active element in biochemistry. Hence, Se, in some cases, can replace sulfur, as it is found in the amino acids, such as selenocysteine or selenomethionine. Chemical derivatives of selenium consist of organic compounds, like selenomethone and selenomethyl-selenocysteine, and inorganic compounds, such as selenite [2]. The modulation of the cellular redox-environment is an increasing target for compounds that are employed as antibiotic or selective targeting of cancer cells in chemotherapy. Sulfur containing compounds, including natural products, such as thiosulfinates or polysulfanes are well-established examples of agents affecting the cellular redox status, thus, exhibiting cytotoxic effects [3]. Also, selenium-containing compounds or Reactive Selenium Species (RSeS) can redox modulate the oxidative stress (OS) present in various cancer cells [4]. Se compounds are well-established redox modulatorswith increased selectivity for cancer cells [5]. These compounds can cause an increase in the oxidative stress in cancer cells, thus, acting as pro-oxidants, which seems to be responsible for the cytotoxic and antiproliferative activities of such RSeS [5]. Selenocyanates are selenium analogues of naturally occurring thiocyanates and constitute an important group of organoselenium compounds [6]. These compounds are versatile as they serve as precursor for the synthesis of numerous new organoselenium compounds, such as selenium acids and diselenides in synthetic chemistry and as potent cytotoxic agents in biology [7]. Various selenocyanates were synthesized and have shown pronounced antimicrobial activity against multidrug resistant ESKAPE bacteria [8]. The naturally occurring and synthetic selenocyanates have shown efficacy against various cancers [9]. These compounds are able to produce superoxide, nitric oxide and other ROS _via_ redox cycle [10]. Various mechanisms of action of selenium compounds have been proposed. In relation to anticarcinogenesis, these agents are transformed to various metabolites, such as methyl selenol (CH\({}_{3}\)Se') and hydrogen selenide (HSe'), acting as pro-oxidants. These metabolites increase ROS _via_ redox cycling with glutathione (GSH) or the Trx/Grx systems producing ROS [11]. Glutathione (a tripeptide) performs a variety of functions in living organisms [12]. Glutathione interacts with ROS, thus, acting as antioxidant [13]. RSeS are also able to alter the intracellular redox balance by the oxidation of intracellular thiols [14]. Redox modification of thiols results in iron and calcium homeostasis [15], and ultimately may lead to the loss of biological function of proteins [16]. Another cytotoxic mode of action of these compounds involves the interaction of selenium with cell cycle which leads to apoptosis. For instance, methylselenide causes caspase-mediated apoptosis in G1 phase, while selenite is involved in the cell cycle arrest in S phase and results in caspase-independent apoptosis. Similarly, DNA damage can be caused by selenite treatment [17]. Prolonged treatment of normal and malignant tissues with selenium results in DNA damage [18] and such modifications may lead to DNA repair. An enhancement in selenite-induced growth impairment in yeast was observed in strains devoid of pathways of DNA repair [19]. Chromatin and/histone modifications are more recent novel mechanisms of action of organo-selenium compounds [20]. Literature reveals a marvelous amount of data concerning the anticancer activity of selenocyanates. However, to understand in more detail how these compounds exhibit an anticancer activity, it is hard to work with cell cultures.