Inhibition of chemical carcinogenesis and tumorigenesis by selenium.
Selenium is effective in inhibiting the incidence and total number of tumors resulting from treatment with various chemical carcinogens. This inhibition occurs both at the initiation and promotion phases of chemical carcinogenesis. At least part of the inhibition of the initiation stage is associated with changes in the metabolism of the parent carcinogen. Studies with 7,12-dimethylbenz(a)anthracene suggest that selenium specifically blocks the enzyme(s) responsible for the formation of anti-dihydrodiol epoxide adducts to DNA. Selenium is also effective in reducing the in vitro and in vivo growth of numerous neoplastic cells. However, differences in the sensitivity to selenium are evident in the various tumor cell lines that have been examined. Continuous selenium intake appears to be necessary to maximal inhibition in both models of carcinogenesis. Evidence suggests that selenodiglutathione or some other intermediate in selenium metabolism is responsible for the anticarcinogenic and antitumorigenic properties of this trace element. The mechanism by which selenium produces these effects is unknown, but it may relate to alterations in either RNA transcription or translation. These and other data strongly suggest that selenium is a naturally occurring anticarcinogenic and antitumorigenic agent.
D015127:9,10-Dimethyl-1,2-benzanthracene; D000818:Animals; D002273:Carcinogens / Q000378:metabolism; D004247:DNA / Q000378:metabolism; D005260:Female; D006801:Humans; D009369:Neoplasms / Q000097:blood; D009374:Neoplasms, Experimental / Q000517:prevention & control*; D012643:Selenium / Q000097:blood / Q000627:therapeutic use*
D002273:Carcinogens; D015127:9,10-Dimethyl-1,2-benzanthracene; D004247:DNA; D012643:Selenium