Study On Mechanism Of Cytotoxicity Induced By Indium Sulfate And Tea Polyphenols Rival Effect

Objective:Indium is a rare metal element which belonging to the first Ⅲ A family. The indium which have low melting point,high boiling point and good conductivity. Its main purposes are:production of indium tin oxide (ITO) target (the total amount of indium,60%～70%). The indium which is absorbed into the bloodstream quickly and combined with The plasma protein (transferrin, alpha globulin and albumin) and transported to the soft tissue and bones. the colloid indium is sent to the reticuloendothelial system of liver and spleen. The indium primarily accumulation in the bones of the body; when subcutaneous injection, the primarily indium accumulation in the skin and muscles; when intraperitoneal injection, the primarily indium accumulation in the mesentery and liver, and then transferred to the spleen, kidneys and bones. The metal indium is non-toxic, but the soluble indium compound is poisonous. The soluble indium salt is most toxic one among these. The indium sulfate which used in this study (indium sulfate) is a representative soluble indium compounds.The aim of the research is to examine the effect of sulfate on cell viability and oxidative stress injury, to explore the toxic mechanism and rivalry of tea polyphenols on the L929cell. And to provide the laboratory data for the prevention of the environmental exposure in the future.Methods:The research is divided into three parts. Part I:the L929cells as an experimental system to detect different concentrations of sulfuric acid indium effect on L929cells after changes in cell survival by tetrazolium salt method (MTT assay). And does-effect relation could be decided.According to the result, we can make the dosage of the indium sulfate for the rest of the experiment; the cell cycle distribution of L929cell treated with indium sulfate by propidium iodide (PI), to find the status of the impact to the growth of L929cells and to make sure the cytotoxicity of L929cell. Part II:In the concentration of indium exposure dose range form first part, the cell apoptosis detected by Annexin V-FITC/PI apoptosis kit, and to explore possible mechanisms that Indium leading to cell damage. And observe the influence of indium sulfate to the content of total protein, vigor of the superoxide dismutase (T-SOD) activity, and malondialdehyde (MDA). Part III:We discuss the possible mechanism by Indium sulfate leading to cell damage, and the antagonistic effect by tea polyphenols. And observe cell survival of L929, apoptosis, T-SOD activity and MDA content when we mix the tea polyphenols to the cell culture food.Results:There are significant cell survival in a concentration-time-dependent manner on. L929cell by Indium sulfate(treated24h, from, the concentration of3.0mmol/L or treated2h.from the concentration of6.0mmol/L). Under the function of indium sulfate, there are significant changes in cell cycle which G1phase cells were decreased,G2/M phase and. S phase cells were increased significantly. And apoptosis rate of L929cells were increased. The T-SOD activities were decreased, but the levels of MDA were increased of the indium sulfate concentration.The statistic difference was significant(P<0.05).There are a protective effect in the cell injury of L929by presence of0.2mg/ml tea polyphenols in the indium sulfate. And cell apoptosis rate were significantly reduced by1.0mg/ml tea polyphenols,1.0mg/ml tea polyphenols cells T-SOD increased activity,0.2mg/ml tea polyphenols let MDA content decreased, the difference was statistically significant (P<0.05).Conclusion:The results showed:The L929cell proliferation can be significantly inhibited by low concentrations of indium sulfate in a short time, and cell cycle can be changed too. Indium Sulfate may cause the increase in rate of apoptosis, while the T-SOD activity were decreased and the MDA content were increased. And we can finding that the oxidative stress injury by indium sulfate on L929cells. And the tea Polyphenols rival the oxidative stress injury to some extent the damage. From the above, it indicate that the L929cell is in an active state of oxidative stress. Subsequently the lipid peroxidation changes the distribution of cell cycle and increases the cell apoptosis rate.