## 3 Results and Discussion
### Antitumor Property
The degradation of Mg metals led to metal ions release accompanied by high alkalinity, which might be key factors causing cell death. The pH value of the ZK60 and ZK60-La extracts after immersing for 5 days is shown in Figure 5A. The pH value of the ZK60 extract was 8.8. The pH values of ZK60-La extracts were lower than that of the ZK60 extract, and pH value of ZK60-1.0 La extract was 8.2, which was the lowest among them. It could be inferred that ZK60-1.0 La had the slowest degradation rate and the least OH\({}^{+}\) release, providing a more favorable environment for cell growth. Thus, HEK 293 cells exhibited the highest cell viability in ZK60-1.0 La extract. The ion concentrations of the extracts were illustrated in Figure 5B. The La ion concentrations in ZK60-La extracts were 0.5 \(\pm\) 0.1 \(\upmu\)g/mL for ZK60-0.5 La alloy, 1.2 \(\pm\) 0.2 \(\upmu\)g/mL for ZK60-1.0 La alloy, 1.9 \(\pm\) 0.1 \(\upmu\)g/mL for ZK60-1.5 La alloy, and 3.5 \(\pm\) 0.1 \(\upmu\)g/mL for ZK60-2.0 La alloy. The concentration of La ion increased with the La content increasing in ZK60-La. Although higher concentrations of La ions were more conducive to killing tumor cells, they also impaired the biocompatibility of ZK60-La [40]. The mechanism of ZK60-La inducing tumor cell death is illustrated in Figure 5C. The ZK60-La released a mass of La\({}^{3+}\) when they degraded. The La\({}^{3+}\) was transported into the tumor cell through the ion channels on the cell membrane. The radius of the La\({}^{3+}\) (1.061 A) were close to that of calcium ion (Ca\({}^{2+}\)) (0.99 A) [41]. However, the La\({}^{3+}\) possessed the greater ratio of the electric charge to radius (3/1.061 A = 2.83) than that of the Ca\({}^{2+}\) (2/0.99 A = 2.02), which made it possess a stronger bonding force with divalent binding sites than the Ca\({}^{2+}\)[42]. Thus, the La\({}^{3+}\) could replace the Ca\({}^{2+}\) binding to the binding sites on the mitochondrial permeability transition pore (mPTP) [43]. The opening of mPTP could result in ionic balance disorders between the mitochondrial matrix and cytoplasm. The redistribution of ions on both sides of the membrane led to the decrease of mitochondrial membrane potential. As a result, the electron transport chain was blocked, which resulted in the reactive oxygen species generation. In addition, the ability to scavenge free radicals for cells could also be weakened in a high alkaline environment by suppressed activity of related enzymes in cells, leading to the reactive oxygen species accumulation [44]. The ROS accumulated in the tumor cells could result in oxidative stress, regulating the expression of related proteins, finally causing tumor cell apoptosis. The apoptosis was a typically form of programmed cell death regulated by genes, which played a role in the cell death. A local burst of ROS also could induce oxidation of nucleotides in DNA [45]. Irreparable DNA damage prevented proper protein synthesis, which led to cell death [46]. Figure 4: (**a**) The mitochondrial membrane potential (MMP) and (**b**) reactive oxygen species (ROS) in U2 OS cells after incubating in the different extracts.