Objective To investigate the effects of bis(acetylacetonato)oxovanadium(IV)[VO(acac)?]on human adrenocortical carcinoma cell lines SW-13 and NCI-H295R in vitro,aiming to determine whether VO(acac)?promotes or inhibits the proliferation,migration,and invasion of these cells.Methods SW-13 and NCI-H295R cells in logarithmic growth phase were exposed to VO(acac)? at concentrations of 6.25,12.5,25,50,75,100,and 200 μmol/L for 24 and 48 hours,respectively.Mitotane served as the positive control.Cell viability was assessed using the CCK-8 assay to evaluate the effects of VO(acac)? on SW-13 and NCI-H295R cells.Subsequently,cells were treated with VO(acac)? at concentrations of 0,6.25,12.5,and 25 μmol/L for 48 hours,and flow cytometry was employed to investigate the impact of VO(acac)? on apoptosis.The migratory ability of the cells was evaluated using a wound healing assay,while their invasive capacity was assessed via a Transwell assay.Additionally,the clonogenic assay was used to determine the proliferative potential of SW-13 and NCI-H295R cells following VO(acac)?treatment.Results The CCK-8 results demonstrated that VO(acac)2 inhibited the viability of SW-13 and NCI-H295R cells in a time-and concentration-dependent manner.Specifically,the half-maximal inhibitory concentra-tions(IC50)for VO(acac)2 against SW-13 cells were 62.98±6.67 μmol/L after 24 hours and(14.61±1.66)μmol/L after 48 hours of treatment,while the corresponding IC50 values for NCI-H295R cells were 46.78±7.89 μmol/L and 12.61±2.98 μmol/L,respectively.Flow cytometry analysis revealed that VO(acac)2 induced apoptosis in both SW-13 and NCI-H295R cells in a concentration-dependent manner(P<0.05).The wound healing assay indicated a significant reduction in the migratory rate of SW-13 and NCI-H295R cells with increasing concentrations of VO(acac)2(P<0.05).Transwell assay results showed that VO(acac)2 significantly inhibited the invasive ability of SW-13 and NCI-H295R cells in a concentration-dependent fashion.Finally,the clonogenic assay confirmed that VO(acac)2 suppressed the proliferative capacity of SW-13 and NCI-H295R cells in a concentration-dependent manner.Conclusion VO(acac)2 inhibits the proliferation,migration,and invasion of human adrenocortical carcinoma cells(SW-13 and NCI-H295R),while inducing apoptosis in these cell lines.

Objective To investigate the effects of bis(acetylacetonato)oxovanadium(IV)[VO(acac)?]on human adrenocortical carcinoma cell lines SW-13 and NCI-H295R in vitro,aiming to determine whether VO(acac)?promotes or inhibits the proliferation,migration,and invasion of these cells.Methods SW-13 and NCI-H295R cells in logarithmic growth phase were exposed to VO(acac)? at concentrations of 6.25,12.5,25,50,75,100,and 200 μmol/L for 24 and 48 hours,respectively.Mitotane served as the positive control.Cell viability was assessed using the CCK-8 assay to evaluate the effects of VO(acac)? on SW-13 and NCI-H295R cells.Subsequently,cells were treated with VO(acac)? at concentrations of 0,6.25,12.5,and 25 μmol/L for 48 hours,and flow cytometry was employed to investigate the impact of VO(acac)? on apoptosis.The migratory ability of the cells was evaluated using a wound healing assay,while their invasive capacity was assessed via a Transwell assay.Additionally,the clonogenic assay was used to determine the proliferative potential of SW-13 and NCI-H295R cells following VO(acac)?treatment.Results The CCK-8 results demonstrated that VO(acac)2 inhibited the viability of SW-13 and NCI-H295R cells in a time-and concentration-dependent manner.Specifically,the half-maximal inhibitory concentra-tions(IC50)for VO(acac)2 against SW-13 cells were 62.98±6.67 μmol/L after 24 hours and(14.61±1.66)μmol/L after 48 hours of treatment,while the corresponding IC50 values for NCI-H295R cells were 46.78±7.89 μmol/L and 12.61±2.98 μmol/L,respectively.Flow cytometry analysis revealed that VO(acac)2 induced apoptosis in both SW-13 and NCI-H295R cells in a concentration-dependent manner(P<0.05).The wound healing assay indicated a significant reduction in the migratory rate of SW-13 and NCI-H295R cells with increasing concentrations of VO(acac)2(P<0.05).Transwell assay results showed that VO(acac)2 significantly inhibited the invasive ability of SW-13 and NCI-H295R cells in a concentration-dependent fashion.Finally,the clonogenic assay confirmed that VO(acac)2 suppressed the proliferative capacity of SW-13 and NCI-H295R cells in a concentration-dependent manner.Conclusion VO(acac)2 inhibits the proliferation,migration,and invasion of human adrenocortical carcinoma cells(SW-13 and NCI-H295R),while inducing apoptosis in these cell lines.

Objective:To explore the disturbance of metal element balance in mice after exposure to radon.Methods:Mice were randomly divided into control group, radon exposure of 30 WLM group, 60 WLM group and 120 WLM groups, with 10 mice in each group. After radon exposure with the cumulative dose, the lung function of mice was detected by a non-invasive pulmonary function testing instrument. Mice blood was taken from eyeballs. The lungs, heart, liver, kidney and spleen were also collected. HE staining was used to observe the pathological changes of lung tissue. Inductively coupled plasma mass spectrometry (ICP-MS) was used to detect the content of metal elements, including essential trace elements in the body: chromium (Cr), molybdenum (Mo), cobalt (Co), selenium (Se), copper (Cu), zinc (Zn), manganese (Mn), nickel (Ni), and potentially toxic elements: arsenic (As), tin (Sn), lead (Pb), aluminum (Al), mercury (Hg), cadmium (Cd), and silver (Ag).Results:Compared with the control group, lung ventilation function of the radon-exposed mice was decreased, alveolar structure was destroyed, and the contents of pulmonary metal elements Cr, Al, Pb, Sn( F=0.34, 0.66, 3.14, 1.16, P<0.05) and essential trace elements Mn, Cr, Zn, and Mo in the blood were decreased( F=0.65, 1.44, 0.97, 2.08, P<0.05), while the elements of Cu, Mo, Se and As in the lungs were increased( F=1.31, 1.26, 0.81, 2.04, P<0.05), and the element contents in other tissues also fluctuated. Conclusions:Inhalation of a certain cumulative dose of radon can reduce the lung ventilation function of mice and induce lung inflammation, as well reduce the content of essential trace elements in the lung and blood so that the content of metal elements in the body fluctuates.