SCN is thought to originate primarily from the diet. Daily intake of SCN varies between ethnic and cultural groups based on differences in diet, including those of glucosidic cyanogen-rich plants such as cassava, yam, maize, sugar cane, sorghum, and linseed [5] and [7]. SCN is also a known product of glucosinolate metabolism in addition to N-conjugated thiocyanates and the structurally related isothiocyanates (e.g., sulforaphane) [5]. The effects of cyanogens cannot be inferred as the direct effects of SCN because most cyanogens readily break down into a milieu of biomolecules, including cyanide, isothiocyanates, and nitriles [5]. The ubiquity of cyanogens in plant matter make it the most obvious dietary source of SCN and provide a rationale for the distribution of rhodanese activity across species, particularly ruminants where some segments of the alimentary tract may exceed the liver in sulfurtransferase activity [8]. Currently it is unknown whether SCN may also be synthesized from an endogenous source of cyanide, but the ubiquity of SCN in biologic systems and its ability to be rapidly concentrated in extracellular fluids [9] suggest this possibility. Interestingly, lung epithelial cells have measurable levels of apical and intracellular SCN when grown in media that is devoid of any detectable SCN source [9]. Some bacteria, including Pseudomonas aeruginosa (Pa), have been shown to generate cyanide from glycine [10], but it is unclear if similar pathways exist in eukaryotes.