Narrow Results

The metalloporphyrin catalytic oxidation of hydrocarbons using dilute hydrogen peroxide as oxygen donor with a two-phase system in the presence of an excess of benzoic acid is studied. Porphyrins derived from meso-tetrakis(2,6-dichlorophenyl)porphyrin and bearing sulfonamide substituents at β or meso positions and halogens at β positions were used. The system allowed for very efficient catalytic epoxidations and hydroxylations of hydrocarbons. It is proved that the excess of benzoic acid is critical to the catalyst efficiency and stability. The role of the lipophilic acid in this system is discussed.

Oxidative stress has been implicated in the pathogenesis of different neurodegenerative disorders. To investigate the protective effects of Wuyaoshunqisan against H₂O₂-induced apoptosis in the central nervous system, the 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) method, flow cytometric analysis, and the DNA fragmentation assay were performed on cells of the hippocampal cell line HiB5. Through the morphological and biochemical analyses, it was shown that HiB5 cells treated with H₂O₂ exhibit classical apoptotic features, while the occurrence of such changes is reduced in cells pre-treated with Wuyaoshunqisan prior to H₂O₂ exposure.

The present study investigated whether Shenqi-wan possesses a protective effect against hydrogen peroxide (H₂O₂)-induced apoptosis of the hippocampal cell line HiB5. Through morphological and biochemical analyses, it was demonstrated that HiB5 cells treated with H₂O₂ exhibited several apoptotic features, while cells pre-treated with Shenqi-wan prior to H₂O₂ exposure showed a decrease in the occurrence of apoptosis. In addition, a patch clamp study revealed that Shenqi-wan inhibited profoundly N-methyl-D-aspartic acid (NMDA) receptor-activated ion current in acutely dissociated hippocampal CA1 neurons. These results suggest that Shenqi-wan may exert its protective effect against H₂O₂-induced apoptosis via inhibition of NMDA receptors in hippocampal neuronal cells.

The standard extracts of Hypericum perforatum L. (SEHP), a well-known medicinal plant, are used for the treatment of depression, exhibited upgrading and significant protective effects on the trauma of PC12 cells induced by 200 μM H₂O₂ in a dose-dependent manner within 24-hour treatment. Cell viability was assessed by the MTT method, and in situ cellular hydrogen peroxide (H₂O₂)-induced oxidative stress was examined by measurement of reactive oxygen species (ROS) formation using CDCFH procedures. Intra- and extra-cellular ROS levels decreased significantly to 71.9% and 50.0% of the control at a moderate concentration of 20 μg/ml, respectively, suggesting that SEHP could easily enter the cells and play important roles in reducing ROS levels. Our results were proved by detection of DNA fragmentation and inspection of cell morphology of PC12 cells. SEHP can obviously block DNA fragmentation and prevent the cells from shrinking and turning round of H₂O₂-induced apoptosis in PC12 cells at concentrations of 10~100 μg/ml. This data suggests SEHP may be a candidate for application in neurodegenerative diseases such as Alzheimer's disease or Parkinson's disease.

Hyperglycemia in diabetic conditions may cause oxidative stress in pancreatic ß-cells, leading to their dysfunction and insulin resistance within peripheral tissues. Previous studies suggest that American ginseng berry extract may have hypoglycemic effects, as well as offer antioxidant protection. We examined effects of American ginseng berry extract and ginsenoside Re in a pancreatic ß-cell line, MIN-6, to determine if these two properties are related. Cells were exposed to oxidative stress via hydrogen peroxide incubation and oxidative stress was measured by oxidation of 2′,7′-dichlorofluorescin diacetate. These cells showed a concentration-related response to hydrogen peroxide at 100–500 μM. In acute conditions where cells were treated with the extract for 10 min, we observed reduced oxidant injury suggesting direct scavenging effects. Chronic incubation of cells with the extract for 48 hours also demonstrated attenuation of oxidative stress. At high concentrations, Re showed a mild antioxidant effect in MIN-6 cells. Our insulin release observations also showed that the extract may help to increase insulin secretions from the cells. Our data suggest that the observed ability of ginseng to reduce blood glucose levels may be linked to its antioxidant effects on pancreatic ß-cells.

Cornu Bubali (water buffalo horn, WBH) is an animal-derived product which is widely used in Traditional Chinese Medicine (TCM) for dispelling heat, relieving convulsions and cooling blood. The purpose of this study was to investigate the antipyretic activity of WBH aqueous extract and its potential mechanism. Two hyperthermia models, yeast-induced (infectious) and skimmed milk-induced (noninfectious) hyperthermia were employed to evaluate the antipyretic effect and the results showed that rectal temperature of hyperthermia animals was decreased significantly after oral administration of WBH extract. The production of tumor necrosis factor-α (TNF-α)-induced prostaglandin E₂ (PGE₂) in rat cerebral microvascular endothelial cells (rCMECs) was inhibited by WBH extract in the concentrations of 10 μg/ml and 100 μg/ml. The WBH extract protected rCMECs survival from hydrogen peroxide (H₂O₂)-induced toxicity and inhibited the H₂O₂-induced leakage of lactate dehydrogenase (LDH) enzyme release at a dose ranging from 5 μg/ml to 100 μg/ml. It could also increase the superoxide dismutase (SOD) and catalase (CAT) enzyme activities. The results suggest that Cornu Bubali exhibits antipyretic activity on both infectious and noninfectious hyperthermia. The antipyretic activity of WBH may be due to the effects on enhancing antioxidation enzyme activities, decreasing PGE₂ production, and protecting the rCMECs against H₂O₂-induced injury.

The hepatoprotective activity of Pinus massoniana bark extract (PMBE) against hydrogen peroxide (H₂O₂)-induced damage in normal human liver L-02 cells and carbon tetrachloride (CCl₄)-induced acute hepatotoxicity in mice was investigated. The L-02 cells were pre-treated with PMBE for 24 hours prior to exposure to 0.5 mM H₂O₂ for 3 or 24 hours. The cell viability, level of malondialdehyde (MDA) and glutathione (GSH), and the catalase (CAT) activity were evaluated. For in vivo experiments, mice were divided into groups and PMBE administered orally, after which each group was assigned a further treatment. Histopathological examination, the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and GSH, the liver tissue levels of MDA and GSH, the activities of CAT and glutathione peroxidase (GSH-Px), were evaluated. PMBE treatment decreased the level of MDA and increased the cell viability, GSH content and CAT activity in H₂O₂ treated L-02 cells treated for 3 hours. PMBE obviously decreased serum ALT, AST, ALP, and liver tissue MDA, while increasing serum GSH, and liver tissue CAT and GSH-Px activities. In conclusion, PMBE treatment prevents H₂O₂ and CCl₄-induced liver damage, and therefore could have a potential clinical usage.

Hydrogen peroxide (H₂O₂) has been shown to promote neurodegeneration by inducing the activation of nuclear factor-κB (NF-κB). In this study, NF-κB activation was induced by H₂O₂ in human neuroblastoma SH-SY5Y cells. Whether paeonol, one of the phenolic phytochemicals isolated from the Chinese herb Paeonia suffruticosa Andrews (MC), would attenuate the H₂O₂-induced NF-κB activity was investigated. Western blot results showed that paeonol inhibited the phosphorylation of IκB and the translocation of NF-κB into the nucleus. The ability of paeonol to reduce DNA binding ability and suppress the H₂O₂-induced NF-κB activation was confirmed by an electrophoretic mobility shift assay and a luciferase reporter assay. Using a microarray combined with gene set analysis, we found that the suppression of NF-κB was associated with mature T cell up-regulated genes, the c-jun N-terminal kinase pathway, and two hypoxia-related gene sets, including the hypoxia up-regulated gene set and hypoxia inducible factor 1 targets. Moreover, using network analysis to investigate genes that were altered by H₂O₂ and reversely regulated by paeonol, we found that NF-κB was the primary center of the network and amyloid precursor protein (APP) was the secondary center. Western blotting showed that paeonol inhibited APP at the protein level. In conclusion, our work suggests that paeonol down-regulates H₂O₂-induced NF-κB activity, as well as NF-κB-associated APP expression. Furthermore, the gene expression profile accompanying the suppression of NF-κB by paeonol was identified. The new gene set that can be targeted by paeonol provided a potential use for this drug and a possible pharmacological mechanism for other phenolic compounds that protect against oxidative-related injury.

The injury of endothelial cell is the critical event of vascular disease. In endothelial cell, oxidative stress is regarded as critical to pathogenic factors in endothelial cell injury and apoptosis. Tanshinone IIA is the main effective component of Salvia miltiorrhiza known as "Danshen" in traditional Chinese medicine for treating cardiovascular disorders, but the mechanism by which it exerts the protective effect is not well established. The present study was designed to test the hypothesis that tanshinone IIA can inhibit hydrogen peroxide (H₂O₂)-induced injury and unravel its intracellular mechanism in human umbilical vein endothelial cells (HUVECs). In this study, HUVECs were treated with tanshinone IIA in the presence/absence of H₂O₂. The protective effects of tanshinone IIA against H₂O₂ were evaluated. Our results show that HUVECs incubated with 200 μM H₂O₂ had significantly decreased the viability of endothelial cells, which was accompanied with apparent cell apoptosis, the activation of caspase-3 and the upregulation of p53 expression, which was known to play a key role in H₂O₂-induced cell apoptosis. However, pretreatment with tanshinone IIA (3–10 μM) resulted in a significant resistance to H₂O₂-induced apoptosis. In addition, pretreatment with tanshinone IIA decreased the activity of caspase-3 and p53 expression. Tanshinone IIA also induced activating transcription factor (ATF) 3 expression; while knockdown of ATF-3 with ATF-3 siRNAsignificantly reduced tanshinone IIA's protective effect. In conclusion, the present study shows that tanshinone IIA can protect endothelial cells against oxidative injury induced by H₂O₂, suggesting that this compound may constitute a promising intervention against cardiovascular disorders and ATF-3 may play an important role in this process.

The present study evaluates the anti-oxidative stress activity of Vaccinium bracteatum Thunb. fruit extract (VBFW) to identify the mechanisms responsible for its antidepressant-like effects. To evaluate the antidepressant and anti-oxidant effects of VBFW, malondialdehyde (MDA), serotonin transporter (SERT), and monoamine oxidase A (MAO-A) levels were measured in a mouse model of chronic restraint stress (CRS). The underlying mechanisms preventing oxidative stress and neuronal apoptosis were investigated using in vitro models of hydrogen peroxide (H₂O${}_2)$-induced neuronal damage. The results showed that VBFW treatment (200mg/kg) significantly reduced MDA, SERT, and MAO-A levels in the prefrontal cortex of CRS mice. Furthermore, VBFW (30$\mu$g/mL) exhibited protective effects against H₂O₂-induced cell death via inhibition of the H₂O₂-induced increase in Bax and decrease in Bcl-2 levels within the mitochondria of SH-SY5Y cells. Furthermore, VBFW (10 and 30$\mu$g/mL) exerted protective effects against H₂O₂-induced cell death through inhibition of key mitochondria-associated apoptotic proteins such as cytochrome c, caspase-3 and PARP. Additionally, VBFW (10 and 30$\mu$g/mL) could improve the activity of anti-oxidant enzymes (such as SOD and catalase) in H₂O₂-treated SH-SY5Y cells. These results suggest that the antidepressant and anti-oxidant effects of VBFW might be mediated by the regulation of SERT and MAO-A, and possibly associated with regulation of oxidative stress-induced apoptosis.

A method was developed to conveniently and rapidly determine hydrogen peroxide (H₂O₂) in food. The glassy carbon electrode (GCE) modified with agmatine sulfate (AS) easily anchoring nickel ion was attached to AS with polyamine structure. As a result, more Ni${}^{2+}$ was obtained and transformed to Ni(OH)₂/NiOOH on the AS–GCE, which caused the electrode to own much better electrocatalytic performance on H₂O₂. Based on these, the content of H₂O₂ in thin sheet of bean curd sample was detected with standard addition method, by which good results were obtained.

The following topics are under this section:

• Repurposing of Waste
• Brain Tumours: Identifying Patients for Targeted Therapy
• Metabolic Imaging

The oxidation of p-toluidine in acetonitrile by hydrogen peroxide is a very slow reaction which produces 4,4'-dimethylazoxybenzene as the product. The presence of functionalized multiwalled carbon nanotubes (CNT) in the above reaction produces 4,4'-dimethylazobenzene. The reactions have been followed by GC/MS, which show the following mass nos.: 226,92 (without CNT) and 210,120,92,28 (with CNT). UV-VIS absorption spectroscopy shows maximum corresponding to 4,4'-dimethylazobenzene at 444 nm. The rate of formation of 4,4'-dimethylazobenzene has been determined as 0.0093 s^-1.

Aniline is oxidized to nitrosobenzene as the initial product, which undergoes further oxidation to nitrobenzene. The nitrosobenzene formation is catalyzed by functionalized multiwalled carbon nanotubes (CNT) followed by a coupling reaction between nitrosobenzene and aniline to produce azobenzene. This coupling requires close proximity of the reactants. It proceeds rapidly resulting in the UV-VIS absorption spectrum showing maxima at 327 nm and 425 nm. The nitrosobenzene yield in the presence of CNTs is controlled by the amount present in the medium. As the reaction is not catalyzed by unfunctionalized CNTs or graphitic particles, the uniqueness of the functionalized multiwalled CNTs in this catalysis suggests a nanodimensional reaction pathway.

The cuprous oxide nanoparticles were prepared with glucose as reducing agent by a wet-chemical method. The composition and structure of the catalysts were characterized with XRD and SEM analysis. The catalytic activity and stability of the catalyst for the H₂O₂ reduction were studied using the curves of cyclic voltammetry and chronoamperometry. The results showed that the crystal structure of the synthesized Cu₂O was the pure cubic phase and the crystallite size was about 19.5 nm. The Cu₂O powder was spherical and the average diameter of the spheres is about 1.0 μm. The Cu₂O nanoparticles were active for H₂O₂ electroreduction and the current density was about 30 mA cm^-2 at E = -0.4 V.

Many studies have investigated the role of oxidative stress on cardiovascular system in the brainstem of spontaneously hypertensive rats (SHR). However, we do not know yet if catalase inhibition influences cardiopulmonary reflex (Bezol-Jarisch reflex). Thus, we aimed to evaluate the effects of central catalase inhibition on cardiopulmonary reflex in SHR. Males Wistar Kyoto (WKY) rats and SHR were implanted with a stainless steel guide cannula into the fourth cerebral ventricle (4th V). The femoral artery and vein were cannulated for mean arterial pressure (MAP) and heart rate (HR) measurement and drug infusion, respectively. The cardiopulmonary reflex was tested with phenylbiguanide (PBG, 8 μg/kg, bolus, i.v.). Cardiopulmonary reflex was evaluated before and 15 minutes after 3-amino-1,2,4-triazole (ATZ, 0.01 g/100 μL) injection into the 4th V. Vehicle treatment did not change basal MAP and HR and cardiopulmonary reflex responses in SHR and WKY rats. Central ATZ increased hypotensive (p = 0.038) responses without influencing the bradycardic reflex (p = 0.287) in WKY rats. In SHR, ATZ increased hypotension (p = 0.0004) and bradycardic (p = 0.04) responses to i.v. PBG. No changes were observed regarding basal MAP and HR after ATZ injection in SHR and WKY rats. We suggest central catalase inhibition affects cardiopulmonary reflex with more intensity in SHR compared to WKY rats.

Highly sensitive catalase electrodes for sensing hydrogen peroxide have been fabricated based on polypyrrole films with microcontainers. The microcontainers have a cup-like morphology and are arranged in a density of 4000 units cm^-2. Catalase was immobilized into the polypyrrole films with microcontainers (Ppy-mc), which were coated on a Pt substrate electrode. The catalase/Ppy-mc/Pt electrode showed linear response to hydrogen peroxide in the range of 0–18 mmol/L at a potential of -0.3 V (versus SCE). Its sensitivity was measured to be approximately 3.64 μA (mmol/L)^-1 cm^-2, which is about two times that of the electrode fabricated from a flat Ppy film (catalase/Ppy-flat/Pt electrode). The electrode is highly selective for hydrogen peroxide and its sensitivity is interfered by potential interferents such as ascorbic acid, urea and fructose. Furthermore, such catalase electrodes showed long-term storage stability of 15 days under dry conditions at 4°C.

Liquid phase catalytic selective hydroxylation of phenol to catechol and hydroquinone was carried out in the presence of metalloporphyrins using hydrogen peroxide as oxidant and water as solvent. Five kinds of metal tetra(p-chlorophenyl)porphrin (T(p-Cl)PPMCl, M = Fe, Co, Mn, Cu, Zn) were studied. It was found that T(p-Cl)PPFeCl had high catalytic activity and diphenol selectivity for the hydroxylation of phenol to catechol and hydroquinone. The influence of various reaction parameters, namely, reaction temperature, solvent, ratio of substrate and oxidant, substrate concentration, the amount of catalyst, reaction time and pH value were investigated systematically. When water was used as solvent (10 mL), the optimum conditions were following: pH = 7, the concentration of phenol was 0.3 g/mL, the molar ratio of phenol and H₂O₂ was 1/2, the molar ratio of catalyst and phenol was 7/100000, the reaction temperature was 65°C and the reaction time was 1.5 h. Under above optimum conditions, the phenol conversion was up to 55.1%, and the selectivity of diphenol was almost up to 99.9%, the molar turnover numbers of the catalyst was about 7500. A possible mechanism was also proposed.

The complex N,N',N″,N‴-tetramethyl-tetra-3,4-pyridinoporphyrazinocobalt(II) ([Co^IITMPz[4+])⁴⁺ adsorbed on a graphite electrode undergoes spontaneous reduction, forming a surface containing Co^I. Five reversible surface peaks are observed at low pH, two of which are two-electron concerted processes. At high pH, one of these two-electron processes splits into two one-electron waves. Both oxidation and reduction of the central metal can be observed, along with successive reduction steps involving the porphyrazine ligand. Notable is the marked shift to positive potentials of these processes, relative to unsubstituted cobalt phthalocyanine, due to the positive charge localized on the porphyrazine. The electrocatalytic activity of this complex modified electrode toward the reduction of hydrogen peroxide is also reported. We demonstrate that a series of different surfaces exist which are obtained by variation of pH and polarization potential and that these surfaces possess differing electrocatalytic activity. Surfaces inactive to hydrogen peroxide can exist at potentials more negative than active surfaces even though the driving force for peroxide reduction will be greater for the former.

Transformation of methane, the most abundant and the least reactive compound of natural gas to valuable products is one of the most difficult chemical problems of great practical importance. In Nature, methane monooxygenase enzymes transform methane to methanol in water under physiological conditions. However, chemical analogs for such a transformation are unknown. Here, we show the mild and efficient aqueous oxidation of methane by hydrogen peroxide, an ecologically and biologically relevant oxidant catalyzed by supported μ-nitrido diiron phthalocyanine dimer, (FePc^tBu₄)₂N. This bio-inspired complex containing a stable Fe–N–Fe motif catalyzes the oxidation of methane to methanol which is further transformed to formaldehyde and formic acid as is demonstrated using ¹³CH₄ and ¹⁸O labelling. (FePc^tBu₄)₂N-H₂O₂ system shows a high activity in the oxidation of benzene to phenol which occurs via formation of benzene oxide and exhibits NIH shift typically accociated with biological oxidation. Mechanistic features of oxidation of methane and benzene as well as detected intermediate hydroperoxo- and high valent oxo diiron complexes support an O-atom transfer reaction mechanism relevant to bio-oxidation.