Official websites use. Share sensitive information only on official, secure websites. HOSCN is a potent microbicidal agent that kills or nullifies invading pathogens but is better tolerated by host tissue. Some controversy exists as to whether physiologic levels of HOSCN are non-toxic to host tissue, but the disagreement appears to be based on results of enzymatic generation yielding moderate steady-state exposure versus direct high level acute exposure in mammalian cell lines.
This apparent duality is also true of other endogenous oxidants such as hydrogen peroxide and relates to the difference between physiologically relevant oxidant production versus supra-physiologic bolus dosing approaches. SCN has antioxidant properties that include the ability to protect cells against oxidizing agents such as hypochlorous acid HOCl and repair protein chloramines.
SCN is an important endogenous molecule that has the potential to interact in complex and elegant ways with its host environment and foreign organisms. SCN is a small, strongly acidic [ 1 ] pseudohalide thiolate Fig. SCN enters the body from the diet such as cruciferous vegetables [ 5 ] or is synthesized from cyanide by sulfurtransferase enzymes including mitochondrial rhodanese and cytosolic mercaptopyruvate sulfurtransferase [ 6 ].
SCN has been studied both in host defense and as a detoxification product of cyanide. 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 , 7 ]. SCN is also a known product of glucosinolate metabolism in addition to N-conjugated thiocyanates and the structurally related isothiocyanates e.
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 ].
