SELENIUM PREVENTS CANCER:
STILL MORE DATA AS THE AVERAGE
GOVERNMENT "HEALTH" EXPERT &
TRADITIONAL DOCTORS IGNORE
According to the following studies selenium can be effective in destroying cancer cells. Swedish researchers have found out that selenium reduces the risks of cancer. Other previous studies found 200 micrograms daily reduced dramatically prostate, lung, colon, and liver cancer. Selenium was also able to destroy even such cancer cells, which were resistant towards normal cancer medications:
Kerstin Jönsson Videsätter. 2004. Expression of multidrug resistance genes and proteins and effects of slenite in anthracycline - resistant human tumor cell lines. Department of Medicine and Department of Laboratory Medicine, Division of pathology, Karolinska Institute, Stockholm, Sweden.
Linda Björkhem Bergman 2004. Thioredoxin reductase and selenium in carcinogenesis and multidrug resistance. Department of Laboratory Medicine, Karolinska Institute, Karolinska University Hospital, Huddinge, Sweden.
Doktorsavhandling vid Karolinska Institutet
Bjšrkhem Bergman, Linda
Thioredoxin reductase and selenium in carcinogenesis and multidrug resistance
Fredagen den 11 juni 2004, kl. 9.15.
Birkeaulan 1, F-huset, plan 5, Karolinska Universitetssjukhuset, Huddinge.
ISBN: 91-7349-954-4 Diss: 04:224
The thioredoxin system, comprising thioredoxin, thioredoxin reductase (TrxR) and NADPH, is a redox system of great importance in the defence against oxidative stress and is involved in the regulation of several cellular processes, such as apoptosis and cell proliferation. In addition, TrxR is a selenoenzyme and is a key enzyme in selenium metabolism.
The aim of this study was to elucidate the role of TrxR in carcinogenesis and in resistant cancer cells and to investigate the tumor preventive effects and the cytotoxicity of selenium compounds.
In this study we have defined the subcellular localisation and recorded activity alterations of TrxR in a rat model for chemically induced hepatocarcinogenesis. Enzymatic activity as well as mRNA expression of TrxR was found to be four times higher in premalignant neoplastic liver lesions than in normal liver. The cytosolic TrxR activity increased in the premalignant liver tissue during the carcinogenetic process compared to control tissue whereas the mitochondrial activity decreased. During the promotion phase selenite administration significantly decreased the volume fraction of preneoplastic liver nodules in parallel with a decrease in cell proliferation in the lesions. Selenite administration during the progression phase resulted in a lower volume fraction of liver tumors and a decreased proliferation within the tumors. If the selenite treatment was limited to the phase of diethylnitrosamine initiation only, no effect was seen on the number or volume fraction of preneoplastic liver lesions.
In an attempt to find new therapeutic strategies to cancers resistant to common chemotherapy we have examined the cytotoxic effect of selenite in multidrug resistant cancer cells. Drugresistant cells appeared to be considerably more sensitive to selenite cytotoxicity than drugsensitive cells. Further studies showed presence of caspase-independent selenite-induced apoptosis in the drug-resistant cells. The selenite sensitivity observed in the drug-resistant cells was not associated with the up-regulation of TrxR seen in the drug-sensitive cells during selenite exposure.
To further investigate the role of TrxR in selenite cytotoxicity, we used cells over-expressing this enzyme. The TrxR over-expressing cells showed an increased resistance towards selenite cytotoxicity compared to control cells. After preincubation with selenite, in a low, enzymesaturating dose, an even higher resistance against selenite toxicity was obtained.
In conclusion, our data suggest that TrxR is important in neoplastic liver lesions and demonstrate that selenium supplementation prevent the carcinogenetic process both during the promotion and progression phases. Moreover, we report selenite-induced apoptosis occurring in the drug-resistant cells and an increase in TrxR activity appears to be crucial for cell resistance against selenium cytotoxicity.
List of papers
- Increased levels of cytosolic thioredoxin reductase activity and mRNA in rat liver nodules.
Bjorkhem L, Teclebrhan H, Kesen E, Olsson JM, Eriksson LC, Bjornstedt M
J Hepatol, 2001; 35(2): 259-64
- Selenite prevents tumor development in a rat model for chemical carcinogenesis.
Bjorkhem-Bergman L, Torndal UB, Eken S, Nystrom C, Olsson JM, Capitanio A, Larsen EH, Bjornstedt M, Eriksson LC
- Drug-resistant human lung cancer cells are more sensitive to selenium cytotoxicity. Effects on thioredoxin reductase and glutathione reductase.
Bjorkhem-Bergman L, Jonsson K, Eriksson LC, Olsson JM, Lehmann S, Paul C, Bjornstedt M
Biochem Pharmacol, 2002; 63(10): 1875-84
- Selenite-induced apoptosis in doxorubicin-resistant cells and effects on the thioredoxin system.
Jonsson-Videsater K, Bjorkhem-Bergman L, Hossain A, Soderberg A, Eriksson LC, Paul C, Rosen A, Bjornstedt M
Biochem Pharmacol, 2004; 67(3): 513-22
- The role of thioredoxin reductase activity in selenium induced cytotoxicity.
Madeja Z, Sroka J, Nystrom C, Bjorkhem-Bergman L, Nordman T, Damdimopoulos A, Nalvarte I, Eriksson LC, Spyrou G, Olsson JM, Bjornstedt M
We suggest all pateints consider 200 micrograms of selenium methionine per day (Selenium methionine 200mcg). If they are folks with big bellies that make cancerous estrogen metabolites we strongly suggest this treatment. They are priming themselves for prostate cancer, uterus cancer and breast cancer, in addition to massive diabetes risks.
Regarding the comments above, the FDA, the DEA, no state medical board nor any medical agency from the USA endorses none of what I have said above. I am merely offering these ideas to ponder with your current physician(s).