Ultrasmall Copper–Gallic Acid Nanodots for Chemodynamic Therapy. Issue 24 (12th November 2021)

• Record Type: Journal Article
• Authors: Hao, Ya‐Nan; Gao, Yi‐Ru; Li, You; Fei, Teng; Shu, Yang; Wan, Jian‐Hua
• Is Part Of: Advanced materials interfaces. Volume 8:Issue 24(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-11-12
• Subjects: chemodynamic therapy -- copper–gallic acid polymers -- Fenton reaction -- glutathione -- hydrogen peroxide -- reactive oxygen species -- tumor; Materials science -- Periodicals; 620.11
• DOI: 10.1002/admi.202101173
• Languages: English
• ISSNs: 2196-7350

Abstract

Abstract: An ultrasmall chemodynamic therapeutic (CDT) agent with favorable specificity to tumor microenvironment, i.e., high level of glutathione (GSH) and hydrogen peroxide (H2 O2 ), is reported. The coordination polymer nanodot between divalent copper (Cu 2+ ) and gallic acid (GA) is shortly named as Cu–GA. The ultrasmall size of Cu–GA (2.16 ± 0.3 nm) results in a large specific surface area, which is beneficial for improving its catalytic performance. After endocytosis into tumor cell interior, Cu–GA promotes GSH‐activated and H2 O2 ‐reinforced CDT in situ, wherein divalent Cu(II) is reduced to monovalent Cu(I) by GSH and induced GSH depletion. Subsequently, the generated Cu(I) catalyzes local H2 O2 to generate toxic hydroxyl radical (OH) via Fenton‐like reaction, and OH leads to tumor cell apoptosis. The higher levels of GSH and H2 O2 in the tumor cell interior significantly improve the efficiency of CDT, and meanwhile protect the normal cells. In addition, the ultrasmall size of Cu–GA facilitates its fast clearance and eliminates long‐term body retention, with minimized systemic toxicity during the treatment in vivo. Therefore, as a novel copper‐based nanoformulation specifically responsive to the tumor microenvironment, Cu–GA provides promising potentials in CDT. Abstract : An ultrasmall polymer nanodot (Cu–GA, 2.16 ± 0.3 nm) is prepared through coordination between divalent copper (Cu 2+ ) and gallic acid (GA). After endocytosis into tumor cell interior, divalent Cu(II) in Cu–GA is reduced to monovalent Cu(I) by glutathione and induced glutathione depletion. Cu(I)–GA subsequently catalyzes intracellular H2 O2 to produce OH to kill tumor cells.