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Review
. 2015;10(17):2709-23.
doi: 10.2217/nnm.15.108. Epub 2015 Sep 2.

Reactive oxygen species-activated nanomaterials as theranostic agents

Kye S Kim  1 , Dongwon Lee  2 , Chul Gyu Song  3 , Peter M Kang  1
Affiliations
Review

Reactive oxygen species-activated nanomaterials as theranostic agents

Kye S Kim et al. Nanomedicine (Lond). 2015.

Abstract

Reactive oxygen species (ROS) are generated from the endogenous oxidative metabolism or from exogenous pro-oxidant exposure. Oxidative stress occurs when there is excessive production of ROS, outweighing the antioxidant defense mechanisms which may lead to disease states. Hydrogen peroxide (H2O2) is one of the most abundant and stable forms of ROS, implicated in inflammation, cellular dysfunction and apoptosis, which ultimately lead to tissue and organ damage. This review is an overview of the role of ROS in different diseases. We will also examine ROS-activated nanomaterials with emphasis on hydrogen peroxide, and their potential medical implications. Further development of the biocompatible, stimuli-activated agent responding to disease causing oxidative stress, may lead to a promising clinical use.

Keywords: hydrogen peroxide; nanomaterials; nanoparticles; oxidative stress; reactive oxygen species; theranostics.

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Conflict of interest statement

Financial & competing interests disclosure This study was supported in part by the grants from NIH R44DK103389–01 (PM Kang), Brain Korea 21 Plus program from Ministry of Education, Science and Technology, South Korea (D Lee, PM Kang), Basic Science Research Program 2013R1A1A2A10061828 through National Research Foundation of Korea and Korean Health Technology R&D Project HI13C13700000 (both to D Lee). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.

Figures

<b>Figure 1.</b>
Figure 1.. General paradigm of physiologic and pathologic reactive oxygen species/oxidative stress.
The net ROS concentration is tightly balanced by the endogenous and the exogenous production of ROS, and the cellular antioxidant defense mechanisms. If there is an acute or chronic defect due to excessive antioxidant defense mechanism or excessive production of ROS that overwhelms normal cellular defense mechanisms, cellular dysfunction and diseases could ensue. ROS: Reactive oxygen species.
<b>Figure 2.</b>
Figure 2.. A general schematic diagram of reactive oxygen species including reactive nitrogen species production and conversion.
(1) Conversion of superoxide anion formed at mitochondrial matrix to H2O2 by SOD2. (2) Conversion of superoxide anion to H2O2 by SOD1 in the cytosol. (3) Conversion of superoxide anion to H2O2 by SOD3 in the extracellular compartment. (4) NADPH oxidase (NOX) enzymatic redox reaction of NADPH to NADP and O2 to superoxide anion which is rapidly converted to H2O2. (5) Degradation of lipid and alcohol in peroxisome to H2O2. (6) Generation of ROS (superoxide, H2O2) along with ferrous ion generation in lysosome. Ferrous ions can be released from ferritin when ion concentration is depleted. (7) H2O2 can diffuse across the membranes and can react with metal ions such as ferrous ions to produce hydroxyl radicals by Fenton reaction. (8) Nitric oxide is generated by nitric oxide synthase (NOS) and can react with superoxide anion to form damaging oxidant, peroxynitrite (ONOO-). (9) H2O2 is converted to water and oxygen by catalase (CAT). (10) H2O2 can convert to hypochlorous acid (HClO) by myeloperoxidase (MPO). (11) Intracellular antioxidant defense is under tight control by coupled reactions of glutathione peroxidase (Gpx; conversion H2O2 to water and glutathione [GSH] to glutathione disulfide [GSSH]). Other reaction by glutathione reductase (GR; reducing GSSH to GSH and NADPH to NADP+). CAT couples peroxiredoxin (from Prx-HOS to Prx-HS) and formation of water from H2O2.
See this image and copyright information in PMC

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