Origin Of Reactive Oxygen Species Research Articles

A composite catalyst of sugarcane-derived N-doped biochar and Fe(NO3)3 for improved electron transfer in stepwise oxidation of 5-hydroxymethylfurfuran under air

Flexible catalysts for the efficient oxidation of 5-hydroxymethylfurfuran (HMF) into valuable chemicals are in urgent demand. In this contribution, the sugarcane-derived N-doped biochar (Su-NCs) was prepared by MgCl2 activation in the presence of urea via a one-step pyrolysis method, which constructed a composite catalyst with Fe(NO3)3 for HMF oxidation. The perfect combination of Su-NCs/Fe(NO3)3 revealed remarkably enhanced catalytic performance and HMF conversion of ca. 100.0% with a 92.0% total yield in air. The effects of specific N-doping sites on the catalytic activity and role of Fe3+ were explored. The results disclosed the electron-rich pyridine-N and Fe3+ synergistically implemented the stepwise oxidation of alcohol to aldehyde and then carboxylic acid. Importantly, the Fe2+ came from electron transfer between the electron-rich N-doped sites and Fe3+ was the origin of reactive oxygen species (∙O−2), which further determined the reactivity and product distributions. The ∙O−2was favorable for the oxidation of hydroxyl while the ∙OH evolved from ∙O−2 preferred to attack aldehyde on the furan ring. This work emphasizes the importance of surface electron transfer of Su-NCs on oxidation efficiency of HMF and creates an alternative chance to produce value-added chemicals from raw biomass.

Photocatalysis coupling hydrogen peroxide synthesis and in-situ radical transform for tetracycline degradation

Although much effort has been put into hydrogen peroxide (H2O2) synthesis, multifunctional catalytic systems suitable for in-situ H2O2 utilization in the field have rarely been investigated. In this study, carbon nitride nanorod (GCN-Rod) is designed to couple H2O2 generating and activation for efficient environment remediation. The limitation of the sluggish hole oxidation kinetics during the photocatalytic H2O2 production is overcome by oxidation of electrostatically adsorbed contaminant molecules. Acid-activated carbon nitride nanorod binds a large number of protons onto the surface, forming an acidic micro-environment prone to protonating organic molecules into positively charged molecules and adsorbed on the negative zeta-potential catalyst surface for oxidation reactions. The in situ synthesized H2O2 is confirmed to be the origin of reactive oxygen species by EPR and band position analysis. The photocatalytic tetracycline (10 ppm) degradation ability approaches approximately 100 % within 10 min under visible-light irradiation. Cycle tests also demonstrated sufficient stability. This work achieves a delicate coupling of H2O2 production and in-situ utilization, which is sufficient for continuous pollutant degradation, expanding the catalyst design methods.

Macrophages: shapes and functions

Macrophages are cells of the innate immune system and represent an important component of the first-line defense against pathogens and tumor cells. Here, their diverse functions in inflammation and tumor defense are described, and the mechanisms, tools, and activation pathways and states applied are presented. The main focus is on the role and origin of reactive oxygen species (ROS), the important signal pathways TLR/NF-κB, and the M1/​​M2 polarization of macrophages.Graphical abstract

Oxidative Stress Is a Key Modulator in the Development of Nonalcoholic Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide, and scientific studies consistently report that NAFLD development can be accelerated by oxidative stress. Oxidative stress can induce the progression of NAFLD to NASH by stimulating Kupffer cells, hepatic stellate cells, and hepatocytes. Therefore, studies are underway to identify the role of antioxidants in the treatment of NAFLD. In this review, we have summarized the origins of reactive oxygen species (ROS) in cells, the relationship between ROS and NAFLD, and have discussed the use of antioxidants as therapeutic agents for NAFLD.

Effect of Quercetin on the Expression of NOXs and P-Smad3C in TGF-Β-Activated Hepatic Stellate Cell Line LX-2

Background: Hepatic stellate cells (HSCs) play a primary role in liver fibrogenesis. NOXs are the main origin of reactive oxygen species (ROS) in the liver. Among them, NOX1, NOX2, and NOX4 are expressed more in HSCs and are involved in the development of liver fibrosis. Quercetin, an abundant citrus flavonoid, is known to have beneficial effects on liver injury and hepatic fibrosis. Objectives: In this study, the effect of quercetin on NOX1, NOX2, and NOX4 expression and Smad3 phosphorylation induced by TGF-β in the human hepatic LX2 cell line was investigated. Methods: The cytotoxic effects of quercetin on the cells were determined by MTT assay. The cells were activated with 2 ng/mL of TGF-β for 24 h and then treated with different concentrations of Quercetin. The mRNA expression rates of NOX1, NOX2, NOX4, and phosphorylated Smad 3C (p-Smad3C) were analyzed using real-time polymerase chain reaction (PCR) and western blot assays. Results: TGF-β increased the mRNA expression of NOX1, NOX2, and NOX4 and the protein level of p-Smad3C in the LX2 cell line. Quercetin significantly decreased the mRNA expression of NOX1, NOX2, and NOX4 in the LX-2 cells. Moreover, quercetin significantly diminished the p-Smad3C level in the LX-2 cell line activated with TGF-β. Conclusions: Quercetin may be effective in improving hepatic fibrosis via the reduction of NOX1, NOX2, and NOX4 expression in activated HSCs. The main mechanism through which quercetin reduces the expression of these target genes may be related to the reduction of the p-Smad3C level.

On the Origin of Reactive Oxygen Species in Lithium-Excess Layered Oxide Cathode Materials

Lithium-excess layered oxide cathode materials (Li(1+x)TM(1-x)O2) for lithium-ion batteries achieve high specific capacities (~250 mAh/g) via redox participation of oxygen anions as well as the transition metals in the oxide cathode. While oxygen is initially present as O2- in the cathode, oxidized oxygen species such as peroxo-like oxygen (O2 2-) and oxygen gas (O2) are detected on charge. Possible sources of these oxygen species include both the lattice and cathode surface contaminants such as Li2CO3 and LiOH. In this work, differential electrochemical mass spectrometry (DEMS) is used to study the mechanisms by which these oxygen species form and react within the battery. DEMS results show that organic fragments containing diatomic oxygen are present on the cathode surface during the first charge starting around 4.2 V vs. Li/Li+. Since no O2 moieties exist in the carbonate electrolyte, these fragments must be a result of reactive oxygen attack on the electrolyte. In order to further understand the origin of these fragments, controlled amounts of 18O-enriched Li2CO3 are deposited on the cathode surface via reaction with CO2 gas before cycling. These results offer insight into the influence of surface contaminants and oxygen activity on interfacial reactivity in lithium-excess cathode materials.

椪柑原生质体分离与培养过程中活性氧动态变化及来源分析

分析原生质体分离与培养过程中活性氧(ROS)的动态变化与来源，对揭示原生质体再生能力差异的机制具有重要意义。本研究采用荧光标记法分析了ROS在椪柑原生质体分离与培养中的动态变化，同时通过ROS抑制剂处理探究了其ROS的来源。结果表明，ROS分布在原生质体的细胞质和细胞膜上；分离阶段愈伤组织原生质体的ROS水平显著低于叶肉原生质体，但在培养阶段显著高于叶肉原生质体；DPI与NaN3处理均显著降低了原生质体分离与培养过程中的ROS水平。因此，ROS在椪柑原生质体再生中具有重要调控作用。 In order to uncover the mechanisms underlying different regeneration capacity of protoplasts, we analyzed the dynamic changes and origin of reactive oxygen species (ROS) during isolation and culture of Citrus reticulata Blanco protoplasts. The dynamic changes of ROS were analyzed by flu-orescent markers, and ROS origin was investigated by ROS indicators. The results showed that ROS signals were visible in the cytoplasm and cell membrane of protoplasts; compared with mesophyll protoplasts, callus protoplasts contained significantly lower level of ROS during isolation, but significantly higher level of ROS during culture; a significant decrease in the level of ROS during isolation and culture of callus protoplasts was observed after DPI or NaN3 treatment. Our findings indicate ROS plays a crucial mediating role in protoplast regeneration of Citrus reticulata.

Cytosolic and mitochondrial ROS: which one is associated with poor chromatin remodeling?

The aim of this study was to determine if there are any associations between impaired chromatin packaging and the origin of reactive oxygen species (ROS) production. Cytosolic ROS, mitochondrial ROS, DNA protamination, and apoptosis were evaluated with dichlorofluoresceindiacetate (DCFH-DA), dihydrorhodamine 123 (DHR123), chromomycin A3 (CMA3), and YO-Pro-1 (Y1)/propidium iodide (PI), respectively, by flow cytometry (FCM) in 40 infertile individuals. Percentages DCF+ and R123+ sperm were positively associated with percentage CMA3+ sperm and negatively associated with percentage apoptotic sperm. No correlation was observed between CMA3+ sperm and the percentage of apoptotic sperm. Under protamination of sperm is not associated with the origin of ROS production, but their relationship may suggest an association with general physiological dysfunction of sperm. Furthermore, under protamination does make sperm prone to apoptosis. Rather, it is likely that apoptosis is induced by ROS production. Considering that these conclusions are derived from correlative analyses, additional studies including an interventive approach are required.

New insights in the contribution and origin of reactive oxygen species in inflammation-induced mitochondrial damage, cell death, cardiovascular failure and shock

New insights in the contribution and origin of reactive oxygen species in inflammation-induced mitochondrial damage, cell death, cardiovascular failure and shock

Vascular C-Reactive Protein in the Pathogenesis of Coronary Artery Disease:Role of Vascular Inflammation and Oxidative Stress

Atherosclerosis is considered to be a chronic inflammatory disease. Vascular inflammation occurs in response to injury induced by various stimuli, such as oxidative stress, shear stress, infection, and so on. This concept is supported by the recent clinical findings that C-reactive protein (CRP) is an independent risk factor for coronary heart disease. CRP, which was originally identified as a protein that could precipitate the C-polysaccharide of pneumococcal cell walls, has been widely used as a clinical marker of the state of inflammation, since its production by hepatocytes increases during the acute phase of the inflammatory response. Recent investigations have provided two new concepts for the research field of CRP, namely, its extra-hepatic production and its potent biological activities such as the induction of adhesion molecules and chemokines. Recently, we demonstrated that smooth muscle cells and macrophages in coronary arteries expressed CRP protein and mRNA, as evaluated using coronary specimens of coronary artery disease (CAD) patients obtained by atherectomy. The expression of vascular CRP was closely associated with NAD(P)H oxidase, an important enzymatic origin of reactive oxygen species (ROS) in vessel walls. Furthermore, CRP directly up-regulated NAD(P)H oxidase p22(phox) and enhanced ROS generation in cultured coronary artery smooth muscle cells. Thus, vascular CRP is likely to be a direct participant in vascular inflammation and lesion formation via its potent biological effects. Since lysophosphatidylcholine, a major atherogenic lipid of oxidized LDL, was reported to activate vascular NAD(P)H oxidase, we speculate that there is a vicious circle consisting of vascular NAD(P)H oxidase, ROS and oxidized LDL. Since phagocytic NAD(P)H oxidase is at the first line of the host defense system, it is important to selectively suppress vascular NAD(P)H oxidase in the localized inflammatory lesions in therapeutic strategies for CAD. In this review, we will discuss the roles of vascular CRP and NAD(P)H oxidase in the pathogenesis of CAD from the viewpoint of oxidative stress.

The origin of reactive oxygen species in adrenocorticotropic hormone-induced hypertension in the rat

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TNF-alpha activates at least two apoptotic signaling cascades.

Apoptosis, the process whereby cells activate an intrinsic death program, can be induced in HeLa cells by TNF-alpha treatment. The aims of the present study were (i) to examine the precise role and the origin of Reactive Oxygen Species (ROS) in the TNF-alpha-induced programmed cell death, (ii) to characterize and order the morphological and mitochondrial changes associated with this process and (iii) to link these events with the activation of caspases. Analyses were performed on TNF-alpha-treated cells in the presence of an anti-oxidant, or of a general caspase inhibitor. To assess the role of mitochondria in the cell death signal transduction, these studies were also realized on HeLa-variant cell lines lacking functional mitochondrial respiratory chain. We show that at least two separate signaling cascades, both mediated by Z-VAD-sensitive caspase(s), contribute to the TNF-alpha-induced apoptosis of HeLa cells. One signaling pathway involves an early mitochondria-dependent ROS production, the other being ROS-independent.

Molecular biology of human male infertility: links with aging, mitochondrial genetics, and oxidative stress?

Molecular biology of human male infertility: links with aging, mitochondrial genetics, and oxidative stress?

Origin of reactive oxygen species in erythrocytes infected with Plasmodium falciparum

Oxidative radicals are demonstrably produced in malaria-infected erythrocytes. In order to verify the biochemical origin of these radicals, erythrocyte lysate was brought to acid pH to mimic the environment of the parasite food vacuole into which host cell cytosol is transferred during parasite feeding. Oxyhemoglobin, but not deoxyhemoglobin, is rapidly converted to methemoglobin at rates which decline with increasing pH. The rate of conversion is further increased in the presence of the catalase inhibitor 3-amino-1,2,4-triazole (3-AT) and the extent of inhibition of the lysate catalase increases upon acidification, implying that H 2O 2 is thus produced by the spontaneous dismutation of superoxide radicals generated during methemoglobin formation. Intact Plasmodium falciparum trophozoite-infected human red blood cells (TRBC) were shown to produce H 2O 2 and OH radicals about twice as much as normal erythrocytes, as evidenced by the inhibition of endogenous catalase activity in the presence of 3-AT and the degradation of deoxyribose, respectively. Increased H 2O 2 levels and catalase activity were found in both host cell and parasite compartments. No increase in H 2O 2 production over that observed in uninfected erythrocytes could be detected at the ring stage when host cell digestion is absent. H 20 2 and OH radicals production in TRBC was considerably reduced when digestion of host cell cytosol was inhibited either by antiproteases (which reduce the proteolysis of imported catalase) or by its alkalinization with NH 4C1 (which reduce methemoglobin formation). These results suggest that reactive oxygen species are produced in the parasite's food vacuole during the digestion of host cell cytosol, and are able to egress from the parasite to the host cell compartment.

Origin of reactive oxygen species in human semen: spermatozoa or leucocytes?

Peroxidative damage induced by reactive oxygen species (ROS) has been proposed as one of the major causes of defective sperm function. In previous studies of the production of ROS in semen, the contribution of contaminating leucocytes was not assessed. We determined the levels of ROS in 60 semen samples from men attending our infertility clinic and demonstrated by performing extraction experiments with antibody-coated magnetic beads that, within this unselected population of patients, leucocytes were the major source of ROS in the low-density Percoll fraction. Of the sperm motion parameters examined using computerized semen analysis, beat-cross frequency was the only one significantly affected by the ROS in semen.

The origin of reactive oxygen species in mouse embryos cultured in vitro.

The increase in production of reactive oxygen species such as H2O2 at the G2/M phase of the second cell cycle may be related to the in vitro block to development of mouse 2-cell embryos. The occurrence of the H2O2 rise is independent of the activation of the embryonic genome and of passage through the S, G2 and M phases of the first cell cycle and G1 and M phases of the second cell cycle, but does require the activation of the unfertilized oocyte. The H2O2 is produced via dismutation of superoxide by the enzyme superoxide dismutase. Production of superoxide via mitochondrial, NADPH-oxidase and xanthine/xanthine oxidase systems has been investigated. The evidence suggests that superoxide, and thereby H2O2, is produced by the xanthine/xanthine oxidase system, but an involvement of the other superoxide generating systems has not been excluded. The relation between H2O2 and development in vitro is discussed.