Selenium carcinogenesis

Lanfear, J., Fleming, J., Wu, L., Webster, G., and Harrison, P. R. (1994). The selenium metabolite selenodiglutathione induces p53 and apoptosis Relevance to the chemopre-vention effects of selenium Carcinogenesis 15,1387-1392. 

Ip C, Lisk DJ. 1995. Efficacy of cancer prevention by high-selenium garlic is primarily dependent on the action of selenium. Carcinogenesis 16(ll) 2649-2652. 

Ip C, Lisk DJ. 1994. Enrichment of selenium in album vegetables for cancer prevention. Carcinogenesis 15 1881-1885. 

Results of the second experiment (Table 3) show that Se-enriched broccoli sprouts have properties similar to enriched broccoli florets that contain SeMSC as the predominant form of Se (13). Consumption of Se from high-Se broccoli sprouts, as compared to Se from selenite, resulted in a significant decrease in the number of aberrant crypts. Additional experimentation is needed to determine whether the decrease in carcinogenesis is a result primarily of the presence of SeMSC, and if there is a correlation between SeMSC content in enriched plants and the reduction of carcinogenesis. If such a correlation is established, then the SeMSC content of various enriched plants could be used to screen for the greatest efficacy in tumor reduction. Se-enriched broccoli appears to be similar to enriched broccoli florets, for which the predominant form of selenium was also shown to be SeMSC (13). 

Also, selenium-dependent glutathione peroxidase activity has been shown to be reduced in selenium-deficient rats (C. Reddy, ( li). Selenium appears to inhibit both the initiation and promotion phases of carcinogenesis (Milner,... 

These results suggest that selenium is critical for glutathione peroxidase activity, but apparently functions in other ways as well to inhibit carcinogenesis. 

Milner, J.A. (1985) The Effect of Selenium on Carcinogenesis. This Volume. 

In five of six nondietary tumor-promotion experiments, sodium selenide significantly reduced the number of mice with tumors induced by 7,12-dimethyl-benzanthracene (DMBA)-croton oil (1). In these experiments, sodium selenide was applied concomitantly along with croton oil to female Swiss albino mice initiated with DMBA. Riley has also observed a reduction in DMBA-phorbol ester carcinogenesis by sodium selenide (2). The effect of selenium-deficient and selenium-adequate diets on DMBA-croton oil and benzopyrene skin carcinogenesis has also been studied. Supplemental dietary selenium inhibited both types of carcinogenesis. 

Inhibition of the initiation phase of carcinogenesis does not appear to totally explain the anticarcinogenicity of selenium. 

Furthermore, while the effect of selenium on the action of direct acting carcinogens is less than observed with compounds requiring metabolic activation, a reduction in total tumor number is often observed. Therefore, selenium probably inhibits both the initiation and promotion phases of carcinogenesis. 

P. D. Whanger, Selenium in the treatment of heavy metal poisoning and chemical carcinogenesis, J. Trace Elem. Electrol. Health Dis., 6 (1992), 209-221. 

H. E. Ganther, Selenium metabolism, selenoproteins and mechanisms of cancer prevention complexities with thioredoxin reductase, Carcinogenesis, 20 (1999), 1657D1666. 

Anonymous, Possible enhancement of carcinogenesis by selenium in an animal tumor model, Nutr. Rev., 47 (1989), 173D175. 

CONSENSUS REPORTS NTP 10th Report on Carcinogens. NCI Carcinogenesis Bioassay (dermal) Inadequate Studies mouse NCITR NCI-CG-TR-197,80 (gavage) Clear Evidence mouse, rat NCITR NCI-CG-TR-194,80. Selenium and its compounds are on the Community Right-To-Know List. 

Kazantzis G. 1981. Role of cobalt, iron, lead, manganese, mercury, platinum, selenium, and titanium in carcinogenesis. Environ Health Perspect 40 143-161. 

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