AI Article Synopsis
- Amplifying oxidative stress can effectively trigger cancer cell death by manipulating their redox balance, particularly through the use of disulfide compound BAPS.
- BAPS depletes glutathione (GSH) and generates superoxide anions, making it particularly effective in cancer cells that have high GSH levels.
- When combined with the new fluoropolymer delivery system PFSNM, BAPS can be transported to hypoxic tumor cells, leading to significant tumor growth inhibition in a new kind of chemodynamic therapy.
Article Abstract
Amplification of intracellular oxidative stress has been found to be an effective strategy to induce cancer cell death. Herein, the effect of a disulfide, 2,2'-dithiobis(5-aminopyridine) (BAPS), is revealed on depleting glutathione (GSH) circularly and generating superoxide anion (O) spontaneously to manipulate intracellular redox homeostasis. Thus, BAPS is able to work as an oxidative stress amplifier in cancer cells with high GSH concentrations and kill them efficiently. Moreover, leveraging a new class of water-soluble fluoropolymers poly(N-(2-((2,2,2-trifluoroethyl)sulfonyl)ethyl)acrylamide) (PFSNM), BAPS, together with oxygen, can be effectively delivered into hypoxic tumor cells through circulation and significantly inhibit the tumor growth. Therefore, BAPS-loaded PFSNM is an oxidative regulation nanosystem with remarkable therapeutic efficacy for chemodynamic therapy.
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| http://dx.doi.org/10.1016/j.ejpb.2022.10.010 | DOI Listing |
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