Reactive oxygen species (ROS) are small reactive molecules produced by cellular metabolism and regulate various physiological and pathological functions. Many studies have shown that ROS plays an essential role in the proliferation and inhibition of tumor cells. Different concentrations of ROS can have a "double-edged sword" effect on the occurrence and development of tumors. A certain concentration of ROS can activate growth-promoting signals, enhance the proliferation and invasion of tumor cells, and cause damage to biomacromolecules such as proteins and nucleic acids. However, ROS can enhance the body's antitumor signal at higher levels by initiating oxidative stress-induced apoptosis and autophagy in tumor cells. This review analyzes ROS's unique bidirectional regulation mechanism on tumor cells, focusing on the key signaling pathways and regulatory factors that ROS affect the occurrence and development of tumors and providing ideas for an in-depth understanding of the mechanism of ROS action and its clinical application.

• MeSH
• Antioxidants metabolism   MeSH
• Carcinogenesis * MeSH
• Humans MeSH
• Neoplasms * metabolism   MeSH
• Oxidative Stress physiology   MeSH
• Reactive Oxygen Species metabolism   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Review MeSH
• Names of Substances
• Antioxidants MeSH
• Reactive Oxygen Species MeSH

A new drug-delivery system of polymer nanoparticles (NPs) bearing pinacol-type boronic ester and alkyne moieties displaying triggered self-immolative polymer degradation in the presence of reactive oxygen species (ROS) with the capability of cellular imaging is presented. The NPs specifically release their drug cargo under concentrations of ROS that are commonly found in the intracellular environment of certain tumors and of inflamed tissues and exhibit significant cytotoxicity to cancer cells compared to their non-ROS-responsive counterparts.

• MeSH
• Fluorescent Dyes chemistry   pharmacokinetics   MeSH
• Microscopy, Fluorescence methods   MeSH
• Cells, Cultured MeSH
• Boronic Acids chemistry   MeSH
• Drug Delivery Systems methods   MeSH
• Humans MeSH
• Nanoparticles chemistry   MeSH
• Drug Carriers chemistry   pharmacokinetics   MeSH
• Oxazines chemistry   pharmacokinetics   MeSH
• Polymers chemistry   MeSH
• Reactive Oxygen Species pharmacology   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Fluorescent Dyes MeSH
• Boronic Acids MeSH
• nile red MeSH Browser
• Drug Carriers MeSH
• Oxazines MeSH
• Polymers MeSH
• Reactive Oxygen Species MeSH

It is well known that biological systems, such as microorganisms, plants, and animals, including human beings, form spontaneous electronically excited species through oxidative metabolic processes. Though the mechanism responsible for the formation of electronically excited species is still not clearly understood, several lines of evidence suggest that reactive oxygen species (ROS) are involved in the formation of electronically excited species. This review attempts to describe the role of ROS in the formation of electronically excited species during oxidative metabolic processes. Briefly, the oxidation of biomolecules, such as lipids, proteins, and nucleic acids by ROS initiates a cascade of reactions that leads to the formation of triplet excited carbonyls formed by the decomposition of cyclic (1,2-dioxetane) and linear (tetroxide) high-energy intermediates. When chromophores are in proximity to triplet excited carbonyls, the triplet-singlet and triplet-triplet energy transfers from triplet excited carbonyls to chromophores result in the formation of singlet and triplet excited chromophores, respectively. Alternatively, when molecular oxygen is present, the triplet-singlet energy transfer from triplet excited carbonyls to molecular oxygen initiates the formation of singlet oxygen. Understanding the mechanism of the formation of electronically excited species allows us to use electronically excited species as a marker for oxidative metabolic processes in cells.

• Keywords
• chromophores, electronically excited species, hydrogen peroxide, hydroxyl radical, oxidative radical reactions, reactive oxygen species, singlet oxygen, superoxide anion radical,
• MeSH
• Oxygen metabolism   MeSH
• Humans MeSH
• Oxidation-Reduction MeSH
• Energy Transfer MeSH
• Reactive Oxygen Species metabolism   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Oxygen MeSH
• Reactive Oxygen Species MeSH

Abstract Reactive oxygen species (ROS) and reactive nitrogen species have generally been considered as being highly reactive and cytotoxic molecules. Besides their noxious effects, ROS participate in physiological processes in a carefully regulated manner. By way of example, microbicidal ROS are produced in professional phagocytes, ROS function as short-lived messengers having a role in signal transduction and, among other processes, participate in the synthesis of the iodothyronine hormones, reproduction, apoptosis and necrosis. Because of their ability to mediate a crosstalk between key molecules, their role might be dual (at least in some cases). The levels of ROS increase from a certain age, being associated with various diseases typical of senescence. The aim of this review is to summarize the recent findings on the physiological role of ROS. Other issues addressed are an increase in ROS levels during ageing, and the possibility of the physiological nature of this process.

• MeSH
• Humans MeSH
• Reactive Nitrogen Species physiology   MeSH
• Reactive Oxygen Species metabolism   MeSH
• Signal Transduction physiology   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Reactive Nitrogen Species MeSH
• Reactive Oxygen Species MeSH

Photosysthetic cleavage of water molecules to molecular oxygen is a crucial process for all aerobic life on the Earth. Light-driven oxidation of water occurs in photosystem II (PSII) - a pigment-protein complex embedded in the thylakoid membrane of plants, algae and cyanobacteria. Electron transport across the thylakoid membrane terminated by NADPH and ATP formation is inadvertently coupled with the formation of reactive oxygen species (ROS). Reactive oxygen species are mainly produced by photosystem I; however, under certain circumstances, PSII contributes to the overall formation of ROS in the thylakoid membrane. Under limitation of electron transport reaction between both photosystems, photoreduction of molecular oxygen by the reducing side of PSII generates a superoxide anion radical, its dismutation to hydrogen peroxide and the subsequent formation of a hydroxyl radical terminates the overall process of ROS formation on the PSII electron acceptor side. On the PSII electron donor side, partial or complete inhibition of enzymatic activity of the water-splitting manganese complex is coupled with incomplete oxidation of water to hydrogen peroxide. The review points out the mechanistic aspects in the production of ROS on both the electron acceptor and electron donor side of PSII.

• MeSH
• Electrons MeSH
• Photosystem II Protein Complex metabolism   MeSH
• Reactive Oxygen Species metabolism   MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Photosystem II Protein Complex MeSH
• Reactive Oxygen Species MeSH

Reactive oxygen species (ROS) are formed in photosystem II (PSII) under various types of abiotic and biotic stresses. It is considered that ROS play a role in chloroplast-to-nucleus retrograde signaling, which changes the nuclear gene expression. However, as ROS lifetime and diffusion are restricted due to the high reactivity towards biomolecules (lipids, pigments, and proteins) and the spatial specificity of signal transduction is low, it is not entirely clear how ROS might transduce signal from the chloroplasts to the nucleus. Biomolecule oxidation was formerly connected solely with damage; nevertheless, the evidence appears that oxidatively modified lipids and pigments are be involved in chloroplast-to-nucleus retrograde signaling due to their long diffusion distance. Moreover, oxidatively modified proteins show high spatial specificity; however, their role in signal transduction from chloroplasts to the nucleus has not been proven yet. The review attempts to summarize and evaluate the evidence for the involvement of ROS in oxidative signaling in PSII.

• Keywords
• Chloroplast-to-nucleus retrograde signaling, Lipid peroxidation, Protein oxidation, Reactive oxygen species,
• MeSH
• Chloroplasts * metabolism   MeSH
• Photosystem II Protein Complex * metabolism   MeSH
• Lipids MeSH
• Oxidative Stress MeSH
• Reactive Oxygen Species metabolism   MeSH
• Signal Transduction physiology   MeSH
• Publication type
• Journal Article MeSH
• Review MeSH
• Names of Substances
• Photosystem II Protein Complex * MeSH
• Lipids MeSH
• Reactive Oxygen Species MeSH

Ultra-weak photon emission originates from the relaxation of electronically excited species formed in the biological systems such as microorganisms, plants and animals including humans. Electronically excited species are formed during the oxidative metabolic processes and the oxidative stress reactions that are associated with the production of reactive oxygen species (ROS). The review attempts to overview experimental evidence on the involvement of superoxide anion radical, hydrogen peroxide, hydroxyl radical and singlet oxygen in both the spontaneous and the stress-induced ultra-weak photon emission. The oxidation of biomolecules comprising either the hydrogen abstraction by superoxide anion and hydroxyl radicals or the cycloaddition of singlet oxygen initiate a cascade of oxidative reactions that lead to the formation of electronically excited species such as triplet excited carbonyl, excited pigments and singlet oxygen. The photon emission of these electronically excited species is in the following regions of the spectrum (1) triplet excited carbonyl in the near UVA and blue-green areas (350-550nm), (2) singlet and triplet excited pigments in the green-red (550-750nm) and red-near IR (750-1000nm) areas, respectively and (3) singlet oxygen in the red (634 and 703nm) and near IR (1270nm) areas. The understanding of the role of ROS in photon emission allows us to use the spontaneous and stress-induced ultra-weak photon emission as a non-invasive tool for monitoring of the oxidative metabolic processes and the oxidative stress reactions in biological systems in vivo, respectively.

• Keywords
• Chemiluminescence, Chlorophyll, Hydrogen peroxide, Hydroxyl radical, Lipid peroxidation, Metabolic oxidative processes, Reactive oxygen species, Singlet oxygen, Skin pigment, Superoxide anion radical,
• MeSH
• Electrons MeSH
• Photobiology methods   MeSH
• Photons * MeSH
• Humans MeSH
• Oxidation-Reduction MeSH
• Reactive Oxygen Species metabolism   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Reactive Oxygen Species MeSH

The catalytic role of iron in the Haber-Weiss chemistry, which results in propagation of damaging reactive oxygen species (ROS), is well established. In this review, we attempt to summarize the recent evidence showing the reverse: That reactive oxygen and nitrogen species can significantly affect iron metabolism. Their interaction with iron-regulatory proteins (IRPs) seems to be one of the essential mechanisms of influencing iron homeostasis. Iron depletion is known to provoke normal iron uptake via IRPs, superoxide and hydrogen peroxide are supposed to cause unnecessary iron uptake by similar mechanism. Furthermore, ROS are able to release iron from iron-containing molecules. On the contrary, nitric oxide (NO) appears to be involved in cellular defense against the iron-mediated ROS generation probably mainly by inducing iron removal from cells. In addition, NO may attenuate the effect of superoxide by mutual reaction, although the reaction product-peroxynitrite-is capable to produce highly reactive hydroxyl radicals.

• MeSH
• Humans MeSH
• Iron-Sulfur Proteins metabolism   MeSH
• Reactive Nitrogen Species metabolism   MeSH
• Reactive Oxygen Species metabolism   MeSH
• Iron metabolism   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Iron-Sulfur Proteins MeSH
• Reactive Nitrogen Species MeSH
• Reactive Oxygen Species MeSH
• Iron MeSH

Increasing evidence points to the respiratory Complex II (CII) as a source and modulator of reactive oxygen species (ROS). Both functional loss of CII as well as its pharmacological inhibition can lead to ROS generation in cells, with a relevant impact on the development of pathophysiological conditions, i.e. cancer and neurodegenerative diseases. While the basic framework of CII involvement in ROS production has been defined, the fine details still await clarification. It is important to resolve these aspects to fully understand the role of CII in pathology and to explore its therapeutic potential in cancer and other diseases.

• Keywords
• OXPHOS, Respiratory complex II, cancer, mitochondria, reactive oxygen species, succinate, succinate dehydrogenase, tricarboxylic acid cycle,
• MeSH
• Molecular Targeted Therapy * MeSH
• Humans MeSH
• Mitochondrial Diseases drug therapy   metabolism   pathology   MeSH
• Mitochondria metabolism   pathology   MeSH
• Reactive Oxygen Species metabolism   MeSH
• Electron Transport Complex II metabolism   MeSH
• Electron Transport MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Review MeSH
• Names of Substances
• Reactive Oxygen Species MeSH
• Electron Transport Complex II MeSH

• Keywords
• Adverse Outcome Pathway (AOP), harmonization, in silico, oxidative stress, reactive oxygen species (ROS),
• MeSH
• Animal Testing Alternatives * MeSH
• Oxidative Stress * MeSH
• Reactive Oxygen Species MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Editorial MeSH
• Names of Substances
• Reactive Oxygen Species MeSH