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Objective: To explore the effects of methylseleninic acid (MeSeA), selenomethionine (SeMet) and methylselenocysteine (MeSeCys) on proliferation, migration and adhesion of HeLa cells., Methods: HeLa cells were cultured and treated with MeSeA, SeMet and MeSeCys for 12 - 72 h respectively. MTT assay, healing assay and in vitro cell Matrigel adhesion assay were used to detect the proliferation, migration and adhesion of HeLa cells., Results: Compared to the control group, the proliferation of HeLa cells was remarkably inhibited by MeSeA (P <0. 01). The migration of HeLa cells in MeSeA group was inhibited by 34% (P < 0. 05) and 26% (P < 0. 05) in 4 h and 8 h, respectively. However, the migration of HeLa cells with inhibitions of 18% and 13% was in SeMet group in 4 h and 8 h. The inhibitions of HeLa cell migration in MeSeCys group was 28% (P < 0.05) and 5% in 4 h and 8 h, respectively. In addition, the adhesive function of HeLa cells in the MeSeA group, the SeMet group as well as the MeSeCys group were inhibited by 36% (P < 0. 01), 25% and 49% (P < 0. 01)., Conclusion: The proliferation and migration of HeLa cell were effectively inhibited by MeSeA, while the adhesive function of HeLa cell was remarkably inhibited by MeSeCys.

The action potentials of ventricular myocardial cells were recorded with glass microelectrodes inside the cells from neonatal Wistar rats treated with selenomethionine and sodium selenite in concentrations of 1.0, 2.0, and 4.0 mg/L selenium. Both of selenomethionine and sodium selenite decreased the action potential parameters, such as action potential amplitude(APA), overshoot(OS), threshold potential(TP), maximum diastolic potential (MDP) and maximum rate of depolarization (Vmax). Selenomethionine decreased the action potential duration at 10%, 50% and 90% repolarization (APD10, APD50 and APD90), while sodium selenite prolonged APD10, APD50 and APD90 at dose of 4.0 mg/L selenium and decreased APD50 and APD90 at dose of 1.0 and 2.0 mg/L selenium. The results indicated that both sodium selenite and selenomethionine inhibit the transmembrane movement of Ca2- and sodium selenite also inhibits transmembrane movement of K+.

Inhibition bioassay of sister chromatid exchanges (SCE) and DNA synthesis was carried out to study the mechanism that selenium, as a chemical agent for intervention, could antagonize the effects of arsenic on body damage and lower incidence of tumor. Results demonstrated that SCE frequency in peripheral lymphocytes induced by As2O3 could be significantly reduced by preincubation with 5 x 10(-7), 1 x 10(-6) mol/L Na2SeO3 and co-exposure of 1 x 10(-6) mol/L selenomethionine. Inhibition of DNA synthesis could be antagonized by preincubation in with 5 x 10(-6) mol/L Na2SeO3 and co-exposure of 1 x 10(-6), 5 x 10(-6) mol/L selenomethionine. But, the mechanism that protective effects of selenium on the damage to cell genetic material induced by arsenic should be studied further.