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Dietary supplementation with methylseleninic acid, but not selenomethionine, reduces spontaneous metastasis of Lewis lung carcinoma in mice
Author(s) -
Yan Lin,
Demars Lana C
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.376.2
Subject(s) - lewis lung carcinoma , metastasis , plasminogen activator , medicine , angiogenesis , ratón , endocrinology , carcinoma , cancer
The present study investigated the effects of dietary supplementation with methylseleninic acid (MSeA), in comparison with selenomethionine (SeMet), on spontaneous metastasis of Lewis lung carcinoma (LLC) in male C57BL/6 mice using intramuscular and subcutaneous injection models. Mice were fed AIN93G control diet or that diet supplemented with MSeA or SeMet at 2.5 mg selenium/kg for 4 weeks at which time they were injected intramuscularly or subcutaneously with 2.5 × 105 viable LLC cells. Experiments were terminated 2 weeks later for mice injected intramuscularly or 2 weeks after surgical removal of primary tumors from mice subcutaneously injected with cancer cells. Dietary supplementation with MSeA significantly reduced pulmonary metastatic yield compared with the controls (P < 0.05) in both models; however, SeMet did not have such an effect. Supplementation with MSeA significantly lowered plasma concentrations of uPA (P < 0.05) and PAI‐1 (P < 0.05). Furthermore, MSeA significantly reduced plasma concentrations of VEGF (P < 0.05), FGF‐basic (P < 0.05) and PDGF‐BB (P < 0.05) compared with the controls. Selenomethionine did not affect any of the aforementioned measurements. These results demonstrate that MSeA reduces spontaneous metastasis of LLC in mice, perhaps through inhibition of the urokinase plasminogen activator system and reducing angiogenesis.