A triphenylphosphine coordinated cinnamaldehyde-derived copper(i) Fenton-like agent with mitochondrial aggregation damage for chemodynamic therapy

Abstract

A new CDT agent, Cin-OD-Cu, which could continuously enrich in the mitochondria of A2780 cancer cells for generated ˙OH by Fenton-like reaction and induced mitochondrial damage, cell death.

Layered double hydroxide-based nanozyme for NO-boost multi-enzyme dynamic therapy with tumor specificity

“…Recently, chemodynamic therapy (CDT) has attracted a lot of attention, due to CDT being mainly aimed at special conditions, using Fenton reaction reagents and tumor microenvironment (TME) stimulation to generate ROS to induce cell apoptosis. [1][2][3][4][5] As another anti-tumor strategy, gas therapy is also a new type of cancer treatment method, which mainly introduces toxic gases such as NO, 6 H 2 S, 7 and CO. 8 In particular, high concentrations of NO can react with ROS to generate highly toxic peroxynitrite (ONOO À ) and other reactive nitrogen species (RNS), exhibiting more lethal oxidative properties, and inducing free radical peroxidation, thereby synergistically enhancing the therapeutic effect of ROS-based CDT. [9][10][11][12][13] However, CDT is often affected by insufficient H 2 O 2 in the TME and limited catalytic ability, resulting in low Fenton efficiency.…”

A mixed-valence biotinylated Cu(i/ii) complex for tumor-targeted chemodynamic therapy accompanied by GSH depletion

“…have been explored as CDT agents and have shown considerable therapeutic efficiency. [7][8][9] Despite many examples of excellent performance of CDT in cancer treatment, its therapeutic efficacy is commonly limited by the low and heterogeneous distribution of H 2 O 2 concentration (50-100 μM) inside the tumor region, although H 2 O 2 overproduction is one of the hallmarks of tumors compared with normal tissues. 10,11 Moreover, the upregulated antioxidant defense in a tumor (like overproduced glutathione, GSH, of up to 10 × 10 −3 M, about four-fold that of normal cells, which could scavenge • OH) also compromises the treatment efficiency of CDT.…”

A Cu(i)-based Fenton-like agent inducing mitochondrial damage for photo-assisted enhanced chemodynamic therapy

“…34 Thus, external light, serving as an adjunctive energy field, was introduced to realize potential PDT. Additionally, a triphenylphosphine molecule was introduced [35][36][37][38] to coordinate with the Fenton-like agent Cu(I), resulting in the formation of the 4-(dimethylamino)cinnamaldehyde oxalyl dihydrazone Cu(I) complex (DC-OD-Cu) which could increase cellular uptake and ensure the enrichment of the CDT agent in the mitochondria. The cellular uptake results showed that DC-OD-Cu was gradually taken up by the HeLa cells and subsequently localized in the mitochondria, where it could catalyse the conversion of endogenous H 2 O 2 into • OH via the Fenton-like reaction.…”