Nitrative and Oxidative Stress in Cell Death and Human Diseases

Topic Information

Dear Colleagues,

Reactive species include several molecules produced not only under pathological situations but also during physiological cellular metabolism, where they are involved in regulating the activity of many key enzymes. Excessive generation of these species can elicit an intracellular state known as oxidative stress, where cellular antioxidant systems are no longer able to maintain physiological redox homeostasis. The term “oxidative stress” is, however, often used in an inappropriate manner as the primary target of the initial oxidative radical, superoxide, is nitric oxide, which, being in large excess, acts as a “buffer”, yielding reactive nitrogen species. It is only once the superoxide fluxes exceed the nitric oxide fluxes that true “oxidative stress” occurs. Nitro-oxidative stress is therefore a more appropriate term that takes into account the evolving generation of reactive nitrogen and oxygen species and their effects on cell and organ pathophysiology. One of the potential deleterious consequences of nitro-oxidative stress is the occurrence of DNA mutations as well as the generation of toxic oxidized macromolecules such as (per)oxidized lipids and carbonylated proteins. These phenomena can lead to cell death or, worse, to uncontrolled proliferation and cancer. Nitro-oxidative stress has thus been shown to be involved in a great number of pathologies, particularly those associated with low- or high-grade inflammation as well as cancer. The understanding of the biochemical mechanisms of its generation and of its pathophysiological consequences is therefore crucial for the development of novel therapeutic strategies, some of which have recently emerged. Accordingly, the discovery of naturally occurring antioxidants, especially in food, may open new perspectives in preventive medicine. This Topic, entitled “Oxidative Stress in Cell Death and Human Diseases”, aims to cover the more recent advances and insights into the research in these different areas, ranging from biochemistry to pathophysiology and aimed at developing novel health and medical applications. We look forward to receiving your contributions.

Prof. Dr. Serge P. Bottari
Dr. Maria Elena Giordano
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Antioxidants antioxidants	7.675	8.8	2012	16.8 Days	2400 CHF
Cells cells	7.666	9.0	2012	16.4 Days	2400 CHF
International Journal of Molecular Sciences ijms	6.208	7.8	2000	15.9 Days	2500 CHF
Kidney and Dialysis kidneydial	-	-	2021	20.5 Days	1000 CHF
Oxygen oxygen	-	-	2021	13.3 Days	1000 CHF

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All Antioxidants Cells IJMS Kidney and Dialysis Oxygen

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Open AccessArticle

Antioxidant, Enzyme, and H₂O₂-Triggered Melanoma Targeted Mesoporous Organo-Silica Nanocomposites for Synergistic Cancer Therapy

by

Hyung Woo Choi

,

Jae Hyun Lim

,

Taewook Kang

and

Bong Geun Chung

Antioxidants 2022, 11(11), 2137; https://doi.org/10.3390/antiox11112137 - 28 Oct 2022

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Abstract

The multi-stimuli responsive drug delivery system has recently attracted attention in cancer treatments, since it can reduce several side effects and enhance cancer therapeutic efficacy. Herein, we present the intracellular antioxidant (glutathione, GSH), enzyme (hyaluronidase, HAase), and hydrogen peroxide (H₂O₂ [...] Read more.

The multi-stimuli responsive drug delivery system has recently attracted attention in cancer treatments, since it can reduce several side effects and enhance cancer therapeutic efficacy. Herein, we present the intracellular antioxidant (glutathione, GSH), enzyme (hyaluronidase, HAase), and hydrogen peroxide (H₂O₂) triggered mesoporous organo-silica (MOS) nanocomposites for multi-modal treatments via chemo-, photothermal, and photodynamic cancer therapies. A MOS nanoparticle was synthesized by two-types of precursors, tetraethyl orthosilicate (TEOS) and bis[3-(triethoxysilyl)propyl] tetrasulfide (BTES), providing large-sized mesopores and disulfide bonds cleavable by GSH. Additionally, we introduced a new β-cyclodextrin-hyaluronic acid (CDHA) gatekeeper system, enabling nanocomposites to form the specific interaction with the ferrocene (Fc) molecule, control the drug release by the HAase and H₂O₂ environment, as well as provide the targeting ability against the CD44-overexpressing melanoma (B16F10) cells. Indocyanine green (ICG) and doxorubicin (Dox) were loaded in the MOS-Fc-CDHA ([email protected]) nanocomposites, allowing for hyperthermia and cytotoxic reactive oxygen species (ROS) under an 808 nm NIR laser irradiation. Therefore, we demonstrated that the [email protected] nanocomposites were internalized to the B16F10 cells via the CD44 receptor-mediated endocytosis, showing the controlled drug release by GSH, HAase, and H₂O₂ to enhance the cancer therapeutic efficacy via the synergistic chemo-, photothermal, and photodynamic therapy effect. Full article

(This article belongs to the Topic Nitrative and Oxidative Stress in Cell Death and Human Diseases)

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Open AccessArticle

Visualization of DNA Damage and Protection by Atomic Force Microscopy in Liquid

by

Tinghui Dai

,

Yanwei Wang

and

Guangcan Yang

Int. J. Mol. Sci. 2022, 23(8), 4388; https://doi.org/10.3390/ijms23084388 - 15 Apr 2022

Viewed by 1178

Abstract

DNA damage is closely related to cancer and many aging-related diseases. Peroxynitrite is a strong oxidant, thus a typical DNA damage agent, and is a major mediator of the inflammation-associated pathogenesis. For the first time, we directly visualized the process of DNA damage [...] Read more.

DNA damage is closely related to cancer and many aging-related diseases. Peroxynitrite is a strong oxidant, thus a typical DNA damage agent, and is a major mediator of the inflammation-associated pathogenesis. For the first time, we directly visualized the process of DNA damage by peroxynitrite and DNA protection by ectoine via atomic force microscopy in liquid. We found that the persistence length of DNA decreases significantly by adding a small amount of peroxynitrite, but the observed DNA chains are still intact. Specifically, the persistence length of linear DNA in a low concentration of peroxynitrite (0 µM to 200 µM) solution decreases from about 47 nm to 4 nm. For circular plasmid DNA, we observed the enhanced superhelices of plasmid DNA due to the chain soften. When the concentration of peroxynitrite was above 300 µM, we observed the fragments of DNA. Interestingly, we also identified single-stranded DNAs during the damage process, which is also confirmed by ultraviolet spectroscopy. However, if we added 500 mM ectoine to the high concentration PN solution, almost no DNA fragments due to double strand breaks were observed because of the protection of ectoine. This protection is consistent with the similar effect for DNA damage caused by ionizing radiation and oxygenation. We ascribe DNA protection to the preferential hydration of ectoine. Full article

(This article belongs to the Topic Nitrative and Oxidative Stress in Cell Death and Human Diseases)

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