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Activatable Fluorescent Quantum Dots
Published in Vladimir Torchilin, Handbook of Materials for Nanomedicine, 2020
Tyler Maxwell, Ziyang Huang, Stephen Smith, Morgan Schaff, Swadeshmukul Santra
Chemiluminescent Qdots have been successfully developed for in vivo ROS sensing and imaging. Chemiluminescence (CL) is the emission of luminescence through chemical reaction not photoexcitation. This property can effectivity avoid autofluorescence interference by photoexcitation, thus is a promising strategy for ROS sensing and imaging [96, 97]. Zhou et al. (2016) developed thioglycolic acid capped CdTe QDs that can selectively detect peroxynitrite in living cells [98]. The authors mentioned that peroxynitrite can decompose into oxidizing (•OH) and reducing (O2•−) radical pairs. The oxidizing •OH radical can generate a hole in the HOMO of the QDs, forming oxidized CdTe QDs. The reducing O2•− radical can goes into the LUMO of the QDs to produce reduced CdTe QDs. The electron-transfer annihilation between oxidized and reduced CdTe QDs can generate a strong CL (Fig. 6.10). Both •OH and O2•− radical are necessary to produce CL in the Qdots. The sensor was selective for peroxynitrite as it constantly produces both radicals. Incubating with a single type of ROS such as 1O2, H2O2, •OH, O2•−, or ClO− produced negligible CL as there was not a sustained release of radicals. The CL intensity showed a linear relationship to the concentration of peroxynitrite from 0.46 to 46 µM, and the detection limit for peroxynitrite was 0.1 µM.
Green Synthesis of Silver (Ag), Gold (Au), and Silver–Gold (Ag–Au) Alloy Nanoparticles: A Review on Recent Advances, Trends, and Biomedical Applications
Published in Deepak Kumar Verma, Megh R. Goyal, Hafiz Ansar Rasul Suleria, Nanotechnology and Nanomaterial Applications in Food, Health, and Biomedical Sciences, 2019
Joseph Adetunji Elegbede, Agbaje Lateef
Nitric oxide (NO) is involved in many biological functions, such as neurotransmission, smooth muscle relaxation, blood pressure regulation, antitumor, and antimicrobial activities. However, it contributes to oxidative damage, because of the ability to react with superoxide that leads to the formation of peroxynitrite anion, which may result to DNA fragmentation and instigate lipid peroxidation.126,152 Therefore, NO generation must be tightly regulated to curtail the harmful effects. Moreover, oxidation of ABTS by potassium persulfate can lead to generation of ABTS radicals which is an exceptional means to estimate antioxidant activity of chain breaking and hydrogen-donating antioxidants that scavenge lipid peroxyl radicals.97 Also, ferric ion reducing antioxidant power (FRAP) is another important method that can be used to evaluate the antioxidant competence of foods, nutritional supplements and beverages containing polyphenols. The FRAP assay is a simple and fast technique to estimate antioxidant activities.121
Marine Algae in Diabetes and Its Complications
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Non-enzymatic glycation of proteins by glucose may form oxidants (Baynes and Thorpe, 1999). The activation of the polyol pathway brings about oxidative stress by reduction of NADPH that leads to depletion of reduced glutathione reductase and an increase in its oxidized counterpart, as NADPH is a common co-factor to both GSH and AR (De Mattia et al., 1994). Hyperglyaemia-induced increased PKC activation enhances oxidative stress due to activation of mitochondrial NADPH oxidase (Inoguchi et al., 2000). This leads to the formation of hydrogen peroxide (H2O2) and hydroxyl radical (OH.-) from the conversion of the superoxide anion (O2.-) (Nishikawa et al., 2000). Polyol pathway activation also leads to decreased NADPH/NADP+ ratios, increasing oxidative stress. This happens as regeneration of the cellular antioxidant GSH is reduced and also reducing the activity of catalase breaking down H2O2 to H2O as NADPH gets depleted. Additionally, inflamed vascular tissue stimulates inducible nitric oxide synthase (NOS) expression in smooth muscle cells and macrophages, consequently forming the free radical NO that reacts with superoxide ions to form highly reactive peroxynitrite. Lipid peroxidation, oxidation of low-density lipoprotein (LDL), and protein nitration are the lethal effects of peroxynitrite (Griendling and FitzGerald, 2003). Oxidative-reductive changes of transcription factors and enzymes and acutely, as well as fluctuating NADPH/NADP+ ratios, mediate cellular signaling under normal physiological conditions. Hydrogen peroxide originating from metabolism in mitochondrial activates the c-Jun N-terminal kinase (JNK) and inhibits the synthesis from glycogen synthase (Nemoto et al., 2000; Sundaresan et al., 1995). Oxidant production persistently may adversely affect cellular function and physiology. Enhanced PKC or inducible NO (iNO) activities may alter the normal functioning of affected tissues. Production of H2O2 in normal physiological levels encourages cell cycle progression responding to growth factors, while its exorbitant production may halt DNA synthesis through the induction of Cdc25c (Savitsky and Finkel, 2002). Excessive oxidative stress can decrease the neural conductivity of nerves affected by diabetes (Hounsom et al., 2001). Breaks in DNA strands may also be induced by oxidative stress in individual cells, thereby inducing death (Du et al., 2003). The mechanism of diabetic neuropathy contributed by various pathways is summarized in Figure 2.2.
Viburnum opulus fruit extract-capped gold nanoparticles attenuated oxidative stress and acute inflammation in carrageenan-induced paw edema model
Published in Green Chemistry Letters and Reviews, 2022
Cristina Bidian, Gabriela Adriana Filip, Luminița David, Bianca Moldovan, Ioana Baldea, Diana Olteanu, Mara Filip, Pompei Bolfa, Monica Potara, Alina Mihaela Toader, Simona Clichici
Proinflammatory cytokines are immunoregulatory mediators secreted by immune cells (macrophages and monocytes) and non-immune cells (fibroblasts and endothelial cells) in response to various stimuli (10). TNF-α and IL-1β stimulate PGE2 formation after COX-2 activation. In addition, TNF-α triggers iNOS expression, increases neutrophil migration (11) and initiates nitric oxide (NO) synthesis. The constitutive isoforms, neuronal NOS (nNOS) and endothelial NOS (eNOS), produce small amounts of NO, which acts as a neurotransmitter and vasodilator. Inducible isoform (iNOS) generates large amounts of NO, especially during inflammatory reactions (12–14). At high concentrations, NO reacts with superoxide anions to form peroxynitrite, which is responsible for oxidative stress and inflammatory cellular changes (15). To counteract the inflammation, the anti-inflammatory cytokines such as IL-10, IL-11, IL-13, IL-4 and IL-5 are secreted (16, 17).
Co(II)-porphyrin complexes with nitrogen monoxide and imidazole: synthesis, optimized structures, electrochemical behavior and photochemical stability
Published in Journal of Coordination Chemistry, 2021
Elena Yu. Kaigorodova, Galina M. Mamardashvili, Olga R. Simonova, Nataliya V. Chizhova, Nugzar Zh. Mamardashvili
Not only nitrogen monoxide but also its conversion products are physiologically active. Especially important among them are peroxynitrite, nitrites, and nitrates, as well as nitrosothiol, heme- and non-heme nitrosyl complexes. All of them, except peroxynitrite, are capable of releasing nitrogen monoxide in its free state in certain conditions and, thus, act as an NO repository. It is well-known that the only compensatory-adaptive form of depositing and utilization of NO is complex formation with haemoglobin that proceeds in the form of axial coordination on the protoheme. NO excess in the body, in turn, can lead to intoxication, including DNA damage, protein nitration causing cell death, peroxynitrite (ONOO–) formation with subsequent formation of highly reactive free radicals.
Essential oil composition and biological activities of Aleppo pine (Pinus halepensis Miller) needles collected from different Tunisian regions
Published in International Journal of Environmental Health Research, 2023
Sarra Dakhlaoui, Soumaya Bourgou, Sarra Bachkouel, Rim Ben Mansour, Mariem Ben Jemaa, Slim Jallouli, Wided Megdiche-Ksouri, Kamel Hessini, Kamel Msaada
In this part, we set out to investigate the effect of the needles P. halepensis EOs on nitric oxide (NO) production by LPS-stimulated RAW264.7 cells. First, cell viability assay (resazurin test) was performed to ensure the non-cytotoxicity of the EO concentrations. All studied EOs does not affect macrophage cell viability until 100 µg/mL. Hence, a range of non-toxic concentrations were preferentially used for the subsequent experiment. Treatment with LPS increases the production of NO in macrophage cells. In fact, the high NO production can lead to an oxidative damage, as NO acts with free radicals to produce the highly reactive peroxynitrite, leading to cell damage. Interestingly, P. halepensis EOs drastically decreased LPS-induced NO production by RAW 264.7 in a dose-dependent manner and IC50 were then calculated per a negative control (Table 3). The obtained results highlighted a very potent anti-inflammatory property of P. halepensis needles EOs. This activity is highly influenced by the provenance factor (P < 0.001). EOs from Bej, Bou, Tab and Hou demonstrated the most potent activity (IC50 = 19.48, 19.5, 20.37 and 23.29 µg/mL, respectively) with no significant difference between them. This could be attributed to the presence of a high amount of caryophyllene. In fact, previous studies have shown that this sesquiterpene was able to inhibit the production of the inducible nitric oxide synthase (iNOS) and the tumor necrosis factor-α (TNFα) that are known to stimulate the NO release (Fernandes et al. 2007). In addition, in vivo potentials of caryophyllene as an anti-inflammatory agent were also reported namely in induced edema models (Dahham and Tabana 2016), in induced gastric mucosal injuries (Tambe et al. 1996) and in neuroblastoma and lymphoma cells (Sain et al. 2014).