Biodegradable copper-iodide clusters modulate mitochondrial function and suppress tumor growth under ultralow-dose X-ray irradiation

Xiaoqian Ma, Nuo Lin, Qing Yang, Peifei Liu, Haizhen Ding, Mengjiao Xu, Fangfang Ren, Zhiyang Shen, Ke Hu, Shanshan Meng and Hongmin Chen ()
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Xiaoqian Ma: Xiamen University
Nuo Lin: Xiamen University
Qing Yang: Xiamen University
Peifei Liu: Xiamen University
Haizhen Ding: Xiamen University
Mengjiao Xu: Xiamen University
Fangfang Ren: Xiamen University
Zhiyang Shen: Xiamen University
Ke Hu: Xiamen University
Shanshan Meng: Xiamen University
Hongmin Chen: Xiamen University

Nature Communications, 2024, vol. 15, issue 1, 1-13

Abstract: Abstract Both copper (Cu2+/+) and iodine (I−) are essential elements in all living organisms. Increasing the intracellular concentrations of Cu or I ions may efficiently inhibit tumor growth. However, efficient delivery of Cu and I ions into tumor cells is still a challenge, as Cu chelation and iodide salts are highly water-soluble and can release in untargeted tissue. Here we report mitochondria-targeted Cu-I cluster nanoparticles using the reaction of Cu+ and I− to form stable bovine serum albumin (BSA) radiation-induced phosphors (Cu-I@BSA). These solve the stability issues of Cu+ and I− ions. Cu-I@BSA exhibit bright radioluminescence, and easily conjugate with the emission-matched photosensitizer and targeting molecule using functional groups on the surface of BSA. Investigations in vitro and in vivo demonstrate that radioluminescence under low-dose X-ray irradiation excites the conjugated photosensitizer to generate singlet oxygen, and combines with the radiosensitization mechanism of the heavy atom of iodine, resulting in efficient tumor inhibition in female mice. Furthermore, our study reveals that BSA protection causes the biodegradable Cu-I clusters to release free Cu and I ions and induce cell death by modulating mitochondrial function, damaging DNA, disrupting the tricarboxylic acid cycle, decreasing ATP generation, amplifying oxidative stress, and boosting the Bcl-2 pathway.

Date: 2024
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DOI: 10.1038/s41467-024-52278-6

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