A potent antibacterial and antitumor Zn–4Ag–2Se alloy for biodegradable orthopedic applications

材料科学 合金 冶金
作者
Miao Zhang,Fei Li,Yilong Dai,Jianguo Lin,Xiaokai Zhang,Dechuang Zhang,Yuncang Li,Cuié Wen
出处
期刊:Rare Metals [Springer Science+Business Media]
卷期号:44 (10): 7615-7633 被引量:13
标识
DOI:10.1007/s12598-025-03417-5
摘要

Abstract Zinc (Zn) alloys exhibit substantial potential for application in the domain of metal materials that are both biodegradable and implantable because of their appropriate degradation rate and biocompatibility. Selenium (Se) has been widely employed in tumor treatment, positioning Zn‐Se alloys as promising candidates for the development of the next generation of antitumor degradable materials. However, the considerable disparity in melting points and the volatility of elemental Zn and Se pose significant challenges for alloying using conventional melting methods. Here, we report a Zn–4Ag–2Se alloy using silver selenide (Ag 2 Se) as the Se source for biodegradable implant materials. The alloy’s antibacterial and antitumor capabilities, along with its mechanical, corrosion, and biocompatibility properties, were assessed and then compared to the properties of a Zn‐4Ag alloy. Both alloys consisted primarily of η‐Zn and ε‐AgZn 3 phases, with the Zn–4Ag–2Se alloy additionally containing a minor amount of a ZnSe phase. The hot‐rolled (HR) Zn–4Ag–2Se alloy exhibited an ultimate tensile strength of 211.5 ± 2.3 MPa and elongation of 24.9% ± 0.6%. Additionally, the HR Zn–4Ag–2Se alloy demonstrated an electrochemical corrosion rate of 105.51 ± 1.21 μm year −1 and degradation rate of 59.8 ± 0.2 μm year −1 in Hanks’ solution, meeting the performance criteria for degradable implant materials. The HR Zn–4Ag–2Se alloy also exhibited excellent antibacterial activity, evidenced by an inhibition zone diameter (IZD) of 2.22 ± 0.01 mm and colony‐forming unit count of 58 ± 2. The HR Zn–4Ag–2Se alloy did not inhibit the proliferation of MC3T3‐E1 cells but promoted reactive oxygen species production and finally cell death toward MG63 osteosarcoma cells.
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