Enhanced Cisplatin Chemotherapy by Iron Oxide Nanocarrier-Mediated Generation of Highly Toxic Reactive Oxygen Species.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 28139118.
- Also identified by DOI 10.1021/acs.nanolett.6b04269.
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Abstract
Reactive oxygen species (ROS) plays a key role in therapeutic effects as well as side effects of platinum drugs. Cisplatin mediates activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX), which triggers oxygen (O<sub>2</sub>) to superoxide radical (O<sub>2</sub><sup>•</sup><sup>-</sup>) and its downstream H<sub>2</sub>O<sub>2</sub>. Through the Fenton's reaction, H<sub>2</sub>O<sub>2</sub> could be catalyzed by Fe<sup>2+</sup>/Fe<sup>3+</sup> to the toxic hydroxyl radicals (<sup>•</sup>OH), which cause oxidative damages to lipids, proteins, and DNA. By taking the full advantage of Fenton's chemistry, we herein demonstrated tumor site-specific conversion of ROS generation induced by released cisplatin and Fe<sup>2+</sup>/Fe<sup>3+</sup> from iron-oxide nanocarriers with cisplatin(IV) prodrugs for enhanced anticancer activity but minimized systemic toxicity.
Medical subject headings
- Antineoplastic Agents
- Cisplatin
- Ferric Compounds
- Metal Nanoparticles
- Reactive Oxygen Species