In vitro assays have demonstrated that vanadium compounds interact with biological molecules similar to protein kinases and phosphatases and have also shown that vanadium oxides decrease the proliferation of cells, including human lymphocytes; however, the mechanism, the phase in which the cell cycle is delayed and the proteins involved in this process are unknown. Therefore, we evaluated the effects of vanadium oxides (V₂O₃, V₂O₄ and V₂O₅) in human lymphocyte cultures (concentrations of 2, 4, 8, or 16 μg/ml) on cellular proliferation and the levels of the p53, p21 and Cdc25C proteins. After 24 h of treatment with the different concentrations of vanadium oxides, the cell cycle phases were determined by evaluating the DNA content using flow cytometry, and the levels of the p21, p53 and Cdc25C proteins were assessed by Western blot analysis. The results revealed that the DNA content remained unchanged in every phase of the cell cycle; however, only at high concentrations did protein levels increase. Although, according to previous reports, vanadium oxides induce a delay in proliferation, DNA analysis did not show this occurring in a specific cell cycle phase. Nevertheless, the increases in p53 protein levels may cause this delay.

中文翻译：

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氧化钒改变体外处理的人淋巴细胞中 p21、p53 和 Cdc25C 蛋白的表达水平

体外试验表明，钒化合物与类似于蛋白激酶和磷酸酶的生物分子相互作用，并且还表明钒氧化物会降低细胞（包括人类淋巴细胞）的增殖；然而，细胞周期延迟的机制、阶段以及参与该过程的蛋白质尚不清楚。因此，我们评估了钒氧化物（V ₂ O ₃、V ₂ O ₄和 V ₂ O ₅) 在人淋巴细胞培养物中（浓度为 2、4、8 或 16 μg/ml）对细胞增殖和 p53、p21 和 Cdc25C 蛋白水平的影响。用不同浓度的钒氧化物处理 24 小时后，通过使用流式细胞术评估 DNA 含量来确定细胞周期阶段，并通过蛋白质印迹分析评估 p21、p53 和 Cdc25C 蛋白的水平。结果表明，DNA含量在细胞周期的每个阶段都保持不变；然而，只有在高浓度下，蛋白质水平才会增加。尽管根据之前的报道，钒氧化物会导致增殖延迟，但 DNA 分析并未显示这发生在特定的细胞周期阶段。然而，p53 蛋白水平的增加可能会导致这种延迟。