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1.
Saad S. Al-Shehri Christine L. Knox Helen G. Liley David M. Cowley John R. Wright Michael G. Henman Amitha K. Hewavitharana Bruce G. Charles Paul N. Shaw Emma L. Sweeney John A. Duley 《PloS one》2015,10(9)
Introduction
Xanthine oxidase (XO) is distributed in mammals largely in the liver and small intestine, but also is highly active in milk where it generates hydrogen peroxide (H2O2). Adult human saliva is low in hypoxanthine and xanthine, the substrates of XO, and high in the lactoperoxidase substrate thiocyanate, but saliva of neonates has not been examined.Results
Median concentrations of hypoxanthine and xanthine in neonatal saliva (27 and 19 μM respectively) were ten-fold higher than in adult saliva (2.1 and 1.7 μM). Fresh breastmilk contained 27.3±12.2 μM H2O2 but mixing baby saliva with breastmilk additionally generated >40 μM H2O2, sufficient to inhibit growth of the opportunistic pathogens Staphylococcus aureus and Salmonella spp. Oral peroxidase activity in neonatal saliva was variable but low (median 7 U/L, range 2–449) compared to adults (620 U/L, 48–1348), while peroxidase substrate thiocyanate in neonatal saliva was surprisingly high. Baby but not adult saliva also contained nucleosides and nucleobases that encouraged growth of the commensal bacteria Lactobacillus, but inhibited opportunistic pathogens; these nucleosides/bases may also promote growth of immature gut cells. Transition from neonatal to adult saliva pattern occurred during the weaning period. A survey of saliva from domesticated mammals revealed wide variation in nucleoside/base patterns.Discussion and Conclusion
During breast-feeding, baby saliva reacts with breastmilk to produce reactive oxygen species, while simultaneously providing growth-promoting nucleotide precursors. Milk thus plays more than a simply nutritional role in mammals, interacting with infant saliva to produce a potent combination of stimulatory and inhibitory metabolites that regulate early oral–and hence gut–microbiota. Consequently, milk-saliva mixing appears to represent unique biochemical synergism which boosts early innate immunity. 相似文献2.
Background
Peroxidase represents a heterogeneous group of distinct enzyme family that plays extremely diverse biological functions. Ascorbate peroxidase from Leishmania major (LmAPX) has been shown to be central to the redox defense system of Leishmania. To investigate further its exact physiological role in Leishmania, we attempted to create LmAPX -knockout mutants by gene replacement in L. major strains.Methodology/Principal Findings
The null mutant cell culture contains a higher percentage of metacyclic and apoptotic cells compared to both wild type and LmAPX overexpressing cells. Flowcytometric analysis reveals the presence of a higher concentration of intracellular H2O2, indicative of increased oxidative stress in parasites lacking LmAPX. IC50 value for exogenously added H2O2 shows that deletion of LmAPX in L. major renders the cell more susceptible to H2O2. Real time PCR studies demonstrate an elevated mRNA level of non-selenium glutathione peroxidase in LmAPX null mutant cell line, suggesting that these enzymes were induced to compensate the LmAPX enzyme. The null mutant cells exhibit hypervirulence after infection with macrophages as well as inoculation into BALB/c mice; in contrast, overexpressing cells show avirulence.Conclusions/Significance
Collectively, these data provide strong evidence that LmAPX is an important factor for controlling parasite differentiation and survival within macrophages. 相似文献3.
Ya-Dan Wen Hong Wang Sok-Hong Kho Suguro Rinkiko Xiong Sheng Han-Ming Shen Yi-Zhun Zhu 《PloS one》2013,8(2)
Background
Hydrogen sulfide (H2S) has been shown to have cytoprotective effects in models of hypertension, ischemia/reperfusion and Alzheimer''s disease. However, little is known about its effects or mechanisms of action in atherosclerosis. Therefore, in the current study we evaluated the pharmacological effects of H2S on antioxidant defenses and mitochondria protection against hydrogen peroxide (H2O2) induced endothelial cells damage.Methodology and Principal Findings
H2S, at non-cytotoxic levels, exerts a concentration dependent protective effect in human umbilical vein endothelial cells (HUVECs) exposed to H2O2. Analysis of ATP synthesis, mitochondrial membrane potential (ΔΨm) and cytochrome c release from mitochondria indicated that mitochondrial function was preserved by pretreatment with H2S. In contrast, in H2O2 exposed endothelial cells mitochondria appeared swollen or ruptured. In additional experiments, H2S was also found to preserve the activities and protein expressions levels of the antioxidants enzymes, superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase in H2O2 exposed cells. ROS and lipid peroxidation, as assessed by measuring H2DCFDA, dihydroethidium (DHE), diphenyl-l-pyrenylphosphine (DPPP) and malonaldehyde (MDA) levels, were also inhibited by H2S treatment. Interestingly, in the current model, D, L-propargylglycine (PAG), a selective inhibitor of cystathionine γ-lyase (CSE), abolished the protective effects of H2S donors.Innovation
This study is the first to show that H2S can inhibit H2O2 mediated mitochondrial dysfunction in human endothelial cells by preserving antioxidant defences.Significance
H2S may protect against atherosclerosis by preventing H2O2 induced injury to endothelial cells. These effects appear to be mediated via the preservation of mitochondrial function and by reducing the deleterious effects of oxidative stress. 相似文献4.
Effect of exogenous hydrogen peroxide on enzymatic and nonenzymatic antioxidants in leaves of young pea plants treated with paraquat 总被引:1,自引:0,他引:1
Irina Moskova Dessislava Todorova Vera Alexieva Sergei Ivanov Iskren Sergiev 《Plant Growth Regulation》2009,57(2):193-202
The effects of exogenously applied hydrogen peroxide on the antioxidant system of pea plants were investigated. Ten-day-old
pea seedlings were sprayed with 2.5 mM H2O2 and 24 h later with 0.2 mM PQ. Samples were taken 0, 2 and 5 h after the start of illumination. The protective effect of
H2O2 was evaluated by monitoring of parameters related to the damage caused by PQ. The treatment with PQ led to a severe leakage
of electrolytes from leaf tissues. Malondialdehyde level increased in PQ treated plants, but remained unchanged in H2O2 pre-treated ones after 5 h of illumination. Increased catalase and glutathione-S-transferase activity was observed in pea
plants treated with H2O2 and PQ. Ascorbate peroxidase activity decreased significantly after paraquat application, but pre-treatment with H2O2 prevented ascorbate peroxidase inhibition to some extent. Increased guaiacol peroxidase activity was detected after H2O2 application. PQ application caused a drastic decline in the levels of thiol-group bearing compounds, reduced glutathione
and ascorbate, while the quantity of oxidized glutathione and dehydroascorbate were increased. The results presented on changes
in enzymatic and nonenzymatic antioxidants suggest that preliminary H2O2 application to pea plants treated with PQ, alleviates the toxic effects of the herbicide. 相似文献
5.
Mitoxantrone (MH2X), an anthraquinone-type anti-cancer agent used clinically in the treatment of human malignancies, is oxidatively activated by the peroxidase/H2O2 enzyme system. In contrast to the enzymatic mechanisms of drug oxidation, the chemical transformations of MH2X are not well described. In this study, MH2X metabolites, produced by the horseradish, lacto- or lignin peroxidase (respectively HRP, LPO and LIP)/H2O2 system, were investigated by steady-state spectrokinetic and HPLC-MS methods. At an equimolar mitoxantrone/H2O2 ratio, the efficacy of the enzyme-catalyzed oxidation of mitoxantrone decreased in the following order: LPO > HRP > LIP, which accorded with the decreasing size of the substrate access channel in the enzyme panel examined. In all cases, the central drug oxidation product was the redox-active cyclic metabolite, hexahydronaphtho-[2,3-f]-quinoxaline-7,12-dione (MH2), previously identified in the urine of mitoxantrone-treated patients. As the reaction progressed, data gathered in this study suggests that further oxidation of the MH2 side-chains occurred, yielding the mono- and dicarboxylic acid derivatives respectively. Based on the available data a further MH2 derivative is proposed, in which the amino-alkyl side-chain(s) are cyclised. With increasing H2O2 concentrations, these novel MH2 derivatives were oxidised to additional metabolites, whose spectral properties and MS data indicated a stepwise destruction of the MH2 chromophore due to an oxidative cleavage of the 9,10-anthracenedione moiety. The novel metabolites extend the known sequence of peroxidase-induced mitoxantrone metabolism, and may contribute to the cytotoxic effects of the drug in vivo. Based on the structural features of the proposed MH2 oxidation products we elaborate on various biochemical mechanisms, which extend the understanding of mitoxantrone’s pharmaceutical action and its clinical effectiveness with a particular focus on peroxidase-expressing solid tumors, such as breast carcinoma. 相似文献
6.
Background
Because H2O2 is generated by various oxidase-catalyzed reactions, a highly sensitive determination method of H2O2 is applicable to measurements of low levels of various oxidases and their substrates such as glucose, lactate, glutamate, urate, xanthine, choline, cholesterol and NADPH. We propose herein a new, highly sensitive method for the measurement of H2O2 and glucose using fluorescence correlation spectroscopy (FCS).Methodology/Principal Findings
FCS has the advantage of allowing us to determine the number of fluorescent molecules. FCS measures the fluctuations in fluorescence intensity caused by fluorescent probe movement in a small light cavity with a defined volume generated by confocal illumination. We thus developed a highly sensitive determination system of H2O2 by FCS, where horseradish peroxidase (HRP) catalyzes the formation of a covalent bond between fluorescent molecules and proteins in the presence of H2O2. Our developed system gave a linear calibration curve for H2O2 in the range of 28 to 300 nM with the detection limit of 8 nM. In addition, by coupling with glucose oxidase (GOD)-catalyzed reaction, the method allows to measure glucose in the range of 80 nM to 1.5 µM with detection limit of 24 nM. The method was applicable to the assay of glucose in blood plasma. The mean concentration of glucose in normal human blood plasma was determined to be 4.9 mM.Conclusions/Significance
In comparison with commercial available methods, the detection limit and the minimum value of determination for glucose are at least 2 orders of magnitude more sensitive in our system. Such a highly sensitive method leads the fact that only a very small amount of plasma (20 nL) is needed for the determination of glucose concentration in blood plasma. 相似文献7.
8.
9.
Mouse and human spermatozoa, but not rabbit spermatozoa, have long been known to be sensitive to loss of motility induced by exogenous H2O2. Recent work has shown that loss of sperm motility in these species correlates with the extent of spontaneous lipid peroxidation. In this study, the effect of H2O2 on this reaction in sperm of the three species was investi gated. The rate of spontaneous lipid peroxidation in mouse and human sperm is markedly enhanced in the presence of 1-5 mM H2O2, while the rate in rabbit sperm is unaffected by H2O2. The enhancement of lipid peroxidation, the rate of reaction of H2O2 with the cells, the activity of sperm glutathione peroxidase, and the endogenous glutathione content are highest in mouse sperm, intermediate in human sperm, and very low in rabbit sperm. Inac tivation of glutathione peroxidase occurs in the presence of H2O2 due to complete conver sion of endogenous glutathione to GSSG: No GSH is available as electron donor substrate to the peroxidase. Inactivation of glutathione peroxidase by the inhibitor mercaptosucci nate has the same effect on rate of lipid peroxidation and loss of motility in mouse and human sperm as does H2O2. This implies that H2O2 by itself at 1-5 mM is not intrinsically toxic to the cells. With merceptosuccinate, the endogenous glutathione is present as GSH in mouse and human sperm, indicating that the redox state of intracellular glutathione by itself plays little role in protecting the cell against spontaneous lipid peroxidation. Mouse and human sperm also have high rates of superoxide production. We conclude that the key intermediate in spontaneous lipid peroxidation is lipid hydroperoxide generated by a chain reaction initiated by and utilizing superoxide. Removal of this hydroperoxide by gluta thione peroxidase protects these sperm against peroxidation; inactivation of the peroxidase allows lipid hydroperoxide to increase and so increases the peroxidation rate. Rabbit sperm have low rates of superoxide reaction due to high activity of their superoxide dismutase; lack of endogenous glutathione and low peroxidase activity does not affect their rate or lipid peroxidation. As a result, these sperm are not affected by either H2O2 or mercapto-succinate. These results lead us to postulate a mechanism for spontaneous lipid peroxida tion in mammalian sperm which involves reaction of lipid hydroperoxide and O2 as the rate-determining step. 相似文献
10.
Alexey V. Sokolov Elena T. Zakahrova Valeria A. Kostevich Valeria R. Samygina Vadim B. Vasilyev 《Biometals》2014,27(5):815-828
Copper-containing plasma protein ceruloplasmin (Cp) forms a complex with lactoferrin (Lf), an iron-binding protein, and with the heme-containing myeloperoxidase (Mpo). In case of inflammation, Lf and Mpo are secreted from neutrophil granules. Among the plasma proteins, Cp seems to be the preferential partner of Lf and Mpo. After an intraperitoneal injection of Lf to rodents, the “Cp–Lf” complex has been shown to appear in their bloodstream. Cp prevents the interaction of Lf with protoplasts of Micrococcus luteus. Upon immunoprecipitation of Cp, the blood plasma becomes depleted of Lf and in a dose-dependent manner loses the capacity to inhibit the peroxidase activity of Mpo, but not the Mpo-catalyzed oxidation of thiocyanate in the (pseudo)halogenating cycle. Antimicrobial effect against E. coli displayed by a synergistic system that includes Lf and Mpo–H2O2–chloride, but not thiocyanate, as the substrate for Mpo is abrogated when Cp is added. Hence, Cp can be regarded as an anti-inflammatory factor that restrains the halogenating cycle and redirects the synergistic system Mpo–H2O2–chloride/thiocyanate to production of hypothiocyanate, which is relatively harmless for the human organism. Structure and functions of the “2Cp–2Lf–Mpo” complex and binary complexes Cp–Lf and 2Cp–Mpo in inflammation are discussed. 相似文献
11.
Asrin Rahimi Iraj Amiri Amaneh Mohammadi Roushandeh Zoleikha Golipour Choshali Zohreh Alizadeh Tayebeh Artimani Saeid Afshar Sara Soleimani Asl 《Biotechnology letters》2018,40(3):609-615
Objective
To investigate the effect of H2O2 on the migration and antioxidant defense of mesenchymal stem cells (MSCs) and the neurotrophic effects of H2O2-treated MSCs on spinal cord injury (SCI).Results
Sublethal concentrations of H2O2 decreased cell migration and expression of CXCR4 and CCR2 as well as Nrf2 expression in MSCs. In the second phase, transplantation of treated and untreated MSCs to SCI caused minor changes in locomotor dysfunction. There was a significantly difference between cell-treated and spinal cord injury groups in expression of BDNF (brain-derived neurotrophic factor). Transplantation of H2O2-treated cells caused an increase in BDNF expression compared to non-treated cells.Conclusion
Transplantation of H2O2-treated stem cells may have protective effects against SCI through by increasing neurotrophic factors.12.
Background
A potentially lethal flux of hydrogen peroxide (H2O2) is continuously generated during aerobic metabolism. It follows that aerobic organisms have equipped themselves with specific H2O2 dismutases and H2O2 reductases, of which catalase and the alkyl hydroperoxide reductase (AhpR) are the best-studied prokaryotic members. The sequenced Haemophilus influenzae Rd genome reveals one catalase, designated HktE, and no AhpR. However, Haemophilus influenzae type b strain Eagan (Hib), a causative agent of bacterial sepsis and meningitis in young children, disrupted in its hktE gene is not attenuated in virulence, and retains the ability to rapidly scavenge H2O2. This redundancy in H2O2-scavenging is accounted for by peroxidatic activity which specifically uses glutathione as the reducing substrate. 相似文献13.
Mohammed Freewan Martin D. Rees Tito S. Sempértegui Plaza Elias Glaros Yean J. Lim Xiao Suo Wang Amanda W. S. Yeung Paul K. Witting Andrew C. Terentis Shane R. Thomas 《The Journal of biological chemistry》2013,288(3):1548-1567
The heme enzyme indoleamine 2,3-dioxygenase (IDO) is a key regulator of immune responses
through catalyzing l-tryptophan (l-Trp) oxidation. Here, we show that
hydrogen peroxide (H2O2) activates the peroxidase function of IDO to
induce protein oxidation and inhibit dioxygenase activity. Exposure of IDO-expressing
cells or recombinant human IDO (rIDO) to H2O2 inhibited dioxygenase
activity in a manner abrogated by l-Trp. Dioxygenase inhibition correlated with
IDO-catalyzed H2O2 consumption, compound I-mediated formation of
protein-centered radicals, altered protein secondary structure, and opening of the distal
heme pocket to promote nonproductive substrate binding; these changes were inhibited by
l-Trp, the heme ligand cyanide, or free radical scavengers. Protection by
l-Trp coincided with its oxidation into oxindolylalanine and kynurenine and the
formation of a compound II-type ferryl-oxo heme. Physiological peroxidase substrates,
ascorbate or tyrosine, enhanced rIDO-mediated H2O2 consumption and
attenuated H2O2-induced protein oxidation and dioxygenase
inhibition. In the presence of H2O2, rIDO catalytically consumed
nitric oxide (NO) and utilized nitrite to promote 3-nitrotyrosine formation on IDO. The
promotion of H2O2 consumption by peroxidase substrates, NO
consumption, and IDO nitration was inhibited by l-Trp. This study identifies IDO
as a heme peroxidase that, in the absence of substrates, self-inactivates dioxygenase
activity via compound I-initiated protein oxidation. l-Trp protects against
dioxygenase inactivation by reacting with compound I and retarding compound II reduction
to suppress peroxidase turnover. Peroxidase-mediated dioxygenase inactivation, NO
consumption, or protein nitration may modulate the biological actions of IDO expressed in
inflammatory tissues where the levels of H2O2 and NO are elevated
and l-Trp is low. 相似文献
14.
Enhanced Killing of Acanthamoeba Cysts with a Plant Peroxidase-Hydrogen Peroxide-Halide Antimicrobial System
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The activity of H2O2 against the resistant cyst stage of the pathogenic free-living amoeba Acanthamoeba was enhanced by the addition of KI and either horseradish peroxidase or soybean peroxidase or, to a lesser degree, lactoperoxidase. This resulted in an increase in the cysticidal activity of 3% (wt/vol) H2O2, and there was >3-log killing in 2 h, compared with the 6 h required for comparable results with the peroxide solution alone (P < 0.05). With 2% H2O2, enhancement was observed at all time points (P < 0.05), and total killing of the cyst inoculum occurred at 4 h, compared with 6 h for the peroxide alone. The activity of sublethal 1% H2O2 was enhanced to give 3-log killing after 8 h of exposure (P < 0.05). No enhancement was obtained when KCl or catalase was used as a substitute in the reaction mixtures. The H2O2 was not neutralized in the enhanced system during the experiments. However, in the presence of a platinum disk used to neutralize H2O2 in contact lens care systems, the enhanced 2% H2O2 system gave 2.8-log killing after 6 h or total cyst killing by 8 h, and total neutralization of the H2O2 occurred by 4 h. In contrast, 2% H2O2 alone resulted in <0.8-log killing of cysts in the presence of the platinum disk due to rapid (<1 h) neutralization of the peroxide. Our observations could result in significant improvement in the efficacy of H2O2 contact lens disinfection systems against Acanthamoeba cysts and prevention of acanthamoeba keratitis. 相似文献
15.
Objective
To evaluate the impact of mesenchymal stem cells (MSCs) against hepatic I/R injury and explore the role of N-acetyltransferase 8 (NAT8) in the process.Methods
We investigated the potential of injected MSCs systemically via the tail vein in healing injuried liver of the SD rat model of 70% hepatic I/R injury by measuring the biochemical and pathologic alterations. Subsequently, we evaluated the expression levels of NAT8 by western blotting in vivo. Concurrently, hydrogen peroxide (H2O2)-induced apoptosis in the human normal liver cell line L02 was performed in vitro to evaluate the protective effects of MSC conditioned medium (MSC-CM) on L02 cells. In addition, we downregulated and upregulated NAT8 expression in L02 cells and induced apoptosis by using H2O2 to study the protective role of NAT8.Results
MSCs implantation led to a significant reduced liver enzyme levels, an advanced protection in the histopathological findings of the acutely injured liver and a significantly lower percentage of TUNEL-positive cells, which were increased after I/R injury. In vitro assays, MSC-CM inhibited hepatocyte apoptosis induced by H2O2. Moreover, overexpression or downregulation of NAT8 prevented or aggravated hepatocyte apoptosis induced by H2O2, respectively.Conclusions
MSC transplantation provides support to the I/R-injured liver by inhibiting hepatocellular apoptosis and stimulating NAT8 regeneration. 相似文献16.
Takanori Maruta Takahiro Inoue Masahiro Noshi Masahiro Tamoi Yukinori Yabuta Kazuya Yoshimura Takahiro Ishikawa Shigeru Shigeoka 《Biochimica et Biophysica Acta (BBA)/General Subjects》2012
Background
Reactive oxygen species (ROS) are not only cytotoxic compounds leading to oxidative damage, but also signaling molecules for regulating plant responses to stress and hormones. Arabidopsis cytosolic ascorbate peroxidase 1 (APX1) is thought to be a central regulator for cellular ROS levels. However, it remains unclear whether APX1 is involved in plant tolerance to wounding and methyl jasmonate (MeJA) treatment, which are known to enhance ROS production.Methods
We studied the effect of wounding and MeJA treatment on the levels of H2O2 and oxidative damage in the Arabidopsis wild-type plants and knockout mutants lacking APX1 (KO-APX1).Results
The KO-APX1 plants showed high sensitivity to wounding and MeJA treatment. In the leaves of wild-type plants, H2O2 accumulated only in the vicinity of the wound, while in the leaves of the KO-APX1 plants it accumulated extensively from damaged to undamaged regions. During MeJA treatment, the levels of H2O2 were much higher in the leaves of KO-APX1 plants. Oxidative damage in the chloroplasts and nucleus was also enhanced in the leaves of KO-APX1 plants. These findings suggest that APX1 protects organelles against oxidative stress by wounding and MeJA treatment.General significance
This is the first report demonstrating that H2O2-scavenging in the cytosol is essential for plant tolerance to wounding and MeJA treatment. 相似文献17.
Potential roles for cyclic and pseudocyclic electron flow in C4 plants are to provide ATP for the C4 cycle and, under excess light, to down-regulate PS II activity through membrane energization. Intact mesophyll chloroplasts of maize were used to evaluate forms of electron transport including the Mehler peroxidase reaction (linear electron flow to O2, formation of H2O2 which is reduced by ascorbate, and linear flow linked to reduction of oxidized ascorbate). Addition of H2O2 to isolated chloroplasts in the light in the presence of an uncoupler induced Photosystem (PS) II activity, as determined from increases in photochemical quenching of chlorophyll fluorescence (qp) and the quantum yield of PS II. H2O2 also induced dissipation of energy by thylakoid membrane energization and non-photochemical fluorescence quenching (qn), which was inhibited by addition of an uncoupler. These effects of H2O2 on qp and qn were inhibited by addition of KCN, an inhibitor of ascorbate peroxidase. The results suggest that H2O2 is reduced via ascorbate, and that the oxidized ascorbate is then reduced by linear electron flow contributing to photochemistry and thylakoid membrane energization. Evidence for function of pseudocyclic electron flow via the Mehler peroxidase reaction was obtained with only oxygen as an electron acceptor, as well as in the presence of oxaloacetate a natural electron acceptor in C4 photosynthesis. KCN decreased qp and PS II yield in the absence and presence of oxaloacetate and, in the former case, it severely reduced q_n. KCN also decreased pH formation across the thylakoid membrane based on its decrease in the light-induced quenching of 9-aminoacridine fluorescence, particularly in the absence of oxaloacetate. Antimycin A, an inhibitor of cyclic electron flow, also diminished pH formation. These results provide evidence for shared energization of thylakoid membranes by the Mehler peroxidase reaction, cyclic electron flow, and linear electron flow linked to the C4 pathway. 相似文献
18.
Seahyoung Lee Ina Yun Onju Ham Se-Yeon Lee Chang Yeon Lee Jun-Hee Park Jiyun Lee Hyang-Hee Seo Eunhyun Choi Ki-Chul Hwang 《Biological research》2015,48(1)
Background
Low survival rate of transplanted cells compromises the efficacy of cell therapy. Hexokinase II (HKII) is known to have anti-apoptotic activity through its interaction with mitochondria. The objective was to identify miRNAs targeting HKII and investigate whether miRNA-mediated modulation of HKII could improve the survival of mesenchymal stem cells (MSCs) exposed to H2O2. The expression of HKII in MSCs exposed to H2O2 was evaluated, and HKII-targeting miRNA was screened based on miRNA-target prediction databases. The effect of H2O2 on the expression of the selected HKII-targeting miRNA was examined and the effect of modulation of the selected HKII-targeting miRNA using anti-miRNA on H2O2-induced apoptosis of MSC was evaluated.Results
H2O2 (600 μM) induced cell death of MSCs and decreased mitochondrial HKII expression. We have identified miR-181a as a HKII-targeting miRNA and H2O2 increased the expression of miR-181a in MSCs. Delivery of anti-miR-181a, which neutralizes endogenous miR-181a, significantly attenuated H2O2-induced decrease of HKII expression and disruption of mitochondrial membrane potential, improving the survival of MSCs exposed to H2O2.Conclusions
These findings suggest that H2O2-induced up-regulation of miR-181a contributes to the cell death of MSCs by down-regulating HKII. Neutralizing miR-181a can be an effective way to prime MSCs for transplantation into ischemic tissues. 相似文献19.
Sevil Altınkılıç Mustafa Nazıroğlu Abdülhadi Cihangir Uğuz Ramazan Özcankaya 《The Journal of membrane biology》2010,235(3):211-218
Oxidative stress is a critical route of damage in various psychological disorders such as schizophrenia, although fish oil
and risperidone (RISP) induce antioxidant effects in the human body. However, the mechanisms behind these effects remain elusive.
We investigated the effects of fish oil and RISP in the PC12 cell line by evaluating Ca2+ mobilization, lipid peroxidation (LP) and antioxidant levels. PC12 cells were divided into eight flasks: control, fish oil,
RISP, H2O2, fish oil + H2O2, RISP + H2O2, fish oil + RISP and fish oil + RISP + H2O2. Cells were incubated with fish oil and RISP for 24 and 48 h, respectively. Then, cells were exposed to H2O2 for 15 min before analysis. Ca2+ release and LP levels were higher in the H2O2 group than in the control, RISP and fish oil groups, although their levels were decreased by incubation of cells in fish
oil and RISP. Glutathione peroxidase activity, reduced glutathione and vitamin C levels in the cells were lower in the H2O2 group than in the control, RISP and fish oil groups, although levels were higher in cells incubated with fish oil and RISP
than in those in the H2O2 groups. In conclusion, these results indicate that RISP and fish oil induced protective effects on oxidative stress in PC12
cells by modulating cytosolic Ca2+ release and antioxidant levels. 相似文献
20.
Comparative proteomics analysis of the root apoplasts of rice seedlings in response to hydrogen peroxide 总被引:2,自引:0,他引:2