Table 1. Selenium compounds for cancer prevention and therapy.

Forms of Se	Active metabolites	Remarks
Sodium selenite	Hydrogen selenide	50% absorbed and retained. High toxicity – genotoxic, induces single strand DNA breaks in vitro. Conversion to methylselenol is a rate-limiting step and occurs when selenite is present in excess, selenite do not regulate the expression of NKG2D ligand that trigger immune activation [22]
Sodium selenate	Hydrogen selenide	Low toxicity - almost completely absorbed but most gets excreted in urine before being incorporated into protein. Activator of PP2A phosphatase
Methyl selininic acid	Methyl selenol	High toxicity with low dose tolerance and of little nutritional value. Regulates expression of NKG2D ligand that trigger immune activation [22]
Selenocysteine	Hydrogen selenide, Methyl selenol	Toxic in higher concentration similar to selenite [57]. Chemically unstable and difficult to handle.
Selenomethionine	Methyl selenol Hydrogen selenite,	Well tolerated, low toxicity but binds to plasma components. Multiple step conversion to methylselenol. Hydrogen selenite conversion into methylselenol is a rate-limiting step and occurs only when selenite is present in excess [22]
Methylselenocysteine	Methyl selenol	90% absorbed, accumulates in a free pool post ingestion. Lowest toxicity amongst Se compounds and more bioactive making it the most ideal candidate for supplementation and therapeutic usage. Bind relatively less to plasma components. A single step conversion β-lyase leads to methylselenol. It regulate the expression of NKG2D ligand that trigger immune activation [22]