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M H2O2 (m + h2o2)
Selected AbstractsAqueous photolysis of 8:2 fluorotelomer alcoholENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 8 2005Suzanne A. Gauthier Abstract The 8:2 fluorotelomer alcohol (8:2 FTOH) was photodegraded in aqueous hydrogen peroxide solutions, synthetic field water (SFW) systems, and Lake Ontario (Canada) water samples. It was found to undergo indirect photolysis, with the data suggesting that the hydroxyl radical was the main degradation agent and that nitrate promoted photolysis whereas dissolved organic carbon inhibited it. The half-lives of 8:2 FTOH were 0.83 ± 0.20 h (10 mM H2O2), 38.0 ± 6.0 h (100 ,M H2O2), 30.5 ± 8.0 to 163.1 ± 3.0 h (SFW systems), and 93.2 ± 10.0 h (Lake Ontario). No significant loss of the parent compound by direct photolysis could be observed. The major monitored products were the 8:2 fluorotelomer aldehyde, the 8:2 fluorotelomer acid (8:2 FTCA), and perfluorooctanoate (PFOA); the minor monitored products were the 8:2 fluorotelomer unsaturated acid (8:2 FTUCA) and perfluorononanoate (PFNA). The intermediates, 8:2 FTCA and 8:2 FTUCA, were photodegraded to verify the degradation pathway, and a mechanism for the photolysis was proposed whereby the end products of the photolysis pathway were PFOA (major) and PFNA (minor). [source] Role of mitogen-activated protein kinases in the mechanism of oxidant-induced cell swelling in cultured astrocytesJOURNAL OF NEUROSCIENCE RESEARCH, Issue 11 2010M. Moriyama Abstract Cytotoxic brain edema, usually a consequence of astrocyte swelling, is an important complication of stroke, traumatic brain injury, hepatic encephalopathy, and other neurological disorders. Although mechanisms underlying astrocyte swelling are not fully understood, oxidative stress (OS) has generally been considered an important factor in its pathogenesis. To better understand the mechanism(s) by which OS causes cell swelling, we examined the potential involvement of mitogen-activated protein kinases (MAPKs) in this process. Cultures exposed to theoxidant H2O2 (10, 25, 50 ,M) for different time periods (1,24 hr) significantly increased cell swelling in a triphasic manner. Swelling was initially observed at 10 min (peaking at 30 min), which was followed by cell shrinkage at 1 hr. A subsequent increase in cell volume occurred at approximately 6 hr, and the rise lasted for at least 24 hr. Cultures exposed to H2O2 caused the activation of MAPKs (ERK1/2, JNK and p38-MAPK), whereas inhibition of MAPKs diminished cell swelling induced by 10 and 25 ,M H2O2. These findings suggest that activation of MAPKs is an important factor in the mediation of astrocyte swelling following oxidative stress. © 2010 Wiley-Liss, Inc. [source] Application of the comet assay to measure DNA damage induced by UV radiation in the hydrophyte, Spirodela polyrhizaPHYSIOLOGIA PLANTARUM, Issue 3 2007Lei Jiang The single-cell gel electrophoresis or comet assay is now widely used to detect DNA damage in animal cells induced by radiation or chemicals. Here, we apply the comet assay to measure ultraviolet (UV)-B-induced DNA damage in plant cells. The accepted animal cell protocol for the comet assay was modified to adapt it to plant cells. The major modifications were conversion of the plant cells to protoplasts and the use of T4 endonuclease V. As a positive control hydrogen peroxide was applied. Significant DNA damage was detected at 100 ,M H2O2. This type of DNA damage was not affected by T4 endonuclease V treatment, which implies that the mechanism of H2O2 -induced DNA damage was different from UV-B-induced DNA damage. Our results also indicate that both UV-A and UV-B radiation can induce DNA single-strand breaks in plant cells, while UV-B was more effective than UV-A for inducing pyrimidine dimer formation. [source] Proteomic profiling and identification of cofilin responding to oxidative stress in vascular smooth musclePROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 24 2006Chang-Kwon Lee Abstract We used 2-DE and MALDI-TOF/TOF to identify proteins of vascular smooth muscle cells whose expression was or was not altered by exposure to 500,,M H2O2 for 30,min. We detected more than 800 proteins on silver-stained gels of whole protein extracts from rat aortic smooth muscle strips. Of these proteins, 135 clearly unaffected and 19 having levels altered by exposure to H2O2 were identified. Protein characterization revealed that the most prominent vascular smooth muscle proteins were those with antioxidant, cytoskeletal structure, or muscle contraction. In addition, cofilin, an isoform of the actin depolymerizing factor family, shifted to its basic site on the 2-DE gel as a result of H2O2 treatment. In Western blot analysis of proteins from A7r5 aortic smooth muscle cells, the phosphorylation, but not the expression, of cofilin was decreased by H2O2 in a dose-dependent manner. The H2O2 -induced dephosphorylation of cofilin and apoptosis was inhibited by Na3VO4, an inhibitor of protein tyrosine phosphatase (PTP). These results suggest that cofilin is one of the proteins regulated by H2O2 treatment in vascular smooth muscle, and has an important role in the induction of vascular apoptosis through PTP-dependent mechanisms. [source] Peroxisome Proliferation in Foraminifera Inhabiting the Chemocline: An Adaptation to Reactive Oxygen Species Exposure?,THE JOURNAL OF EUKARYOTIC MICROBIOLOGY, Issue 3 2008JOAN M. BERNHARD ABSTRACT. Certain foraminiferal species are abundant within the chemocline of marine sediments. Ultrastructurally, most of these species possess numerous peroxisomes complexed with the endoplasmic reticulum (ER); mitochondria are often interspersed among these complexes. In the Santa Barbara Basin, pore-water bathing Foraminifera and co-occurring sulfur-oxidizing microbial mats had micromolar levels of hydrogen peroxide (H2O2), a reactive oxygen species that can be detrimental to biological membranes. Experimental results indicate that adenosine triphosphate concentrations are significantly higher in Foraminifera incubated in 16 ,M H2O2 than in specimens incubated in the absence of H2O2. New ultrastructural and experimental observations, together with published results, lead us to propose that foraminiferans can utilize oxygen derived from the breakdown of environmentally and metabolically produced H2O2. Such a capability could explain foraminiferal adaptation to certain chemically inhospitable environments; it would also force us to reassess the role of protists in biogeochemistry, especially with respect to hydrogen and iron. The ecology of these protists also appears to be tightly linked to the sulfur cycle. Finally, given that some Foraminifera bearing peroxisome,ER complexes belong to evolutionarily basal groups, an early acquisition of the capability to use environmental H2O2 could have facilitated diversification of foraminiferans during the Neoproterozoic. [source] 3241: Effect of glutaredoxin 2 gene knockout on lens epithelial cells against oxidative stressACTA OPHTHALMOLOGICA, Issue 2010M LOU Purpose The mitochondrial glutaredoxin 2 (Grx2) is known to possess both dethiolase and peroxidase activities, and has shown an ability to protect cells from oxidative stress-induced apoptosis in the human lens epithelial cells. In this study, we further studied the function of Grx2 by using Grx2 knockout mouse lens epithelial (MLE) cells as a model. Methods Primary culture of MLE cells was established from the lenses of wild-type (WT) and Grx2-knockout (Grx2 KO) mice. Cells were probed for ,A-crystallin and Grx2 by Western blot analysis while cell viability was examined by WST-8 assay. Glutathione (GSH) level, Grx2 and Complex I activities, and lactate dehydrogenase (LDH) release were determined by spectrophotometric assays. Reactive oxygen species was detected using DCF-DA fluorescein with a cell sorter. Apoptosis was quantified by flow cytometry. Results Both primary cell cultures were confirmed to be lens epithelial cells by the presence of ,A-crystallin. Western blotting showed normal expression of Grx2 in WT cells but absent in Grx2 KO cells. Both cell types showed similar morphology and growth rate with same level of GSH pool and complex 1 activity in the mitochondrial fraction. However, KO cells were more sensitive to oxidative stress (100 ,M H2O2 for 6 h) and exhibited lower cell viability and more LDH leakage in comparison with the WT cells. In addition, knockdown of Grx2 weakened the cell's ability to detoxify H2O2 and enhanced the H2O2-induced inactivation of complex I in the electron transport chain. Conclusion Grx2 can protect MLE cells from H2O2-induced cell injury, and the mechanism of this protection is likely associated with its ability to detoxify H2O2 and its preservation of complex I activity in the mitochondria. [source] Preconditioning protects the retinal pigment epithelium cells from oxidative stress-induced cell deathACTA OPHTHALMOLOGICA, Issue 1 2009Rajesh K. Sharma Abstract. Purpose:, The cytotoxic effects of oxidative stress, which play an important role in ocular diseases, are well known. In this study, we investigated the effect of non-lethal doses of oxidative stress on various cell functions, namely cell viability, cell attachment and cell migration in a widely used retinal pigment epithelium (RPE) cell line (ARPE-19). Methods:, A single exposure to various concentrations of hydrogen peroxide (H2O2) was used to establish a dose response for H2O2 -induced cell death. Other cellular responses, such as changes in cell attachment and migration, were monitored after exposure to increasing doses. Finally, the effects of preconditioning cells with increasing non-lethal doses of H2O2, with and without a subsequent exposure to lethal doses of H2O2, were determined. Results:, The optimum dose for inducing cell death in ARPE-19 cells was between 900 and 1000 ,m H2O2. Preconditioning the cells with 1, 10 and 50 ,m of H2O2 provided a dose-dependent protection against cell death induced by a lethal dose (900,1000 ,m) of H2O2. Preconditioning with higher doses caused cells to become more susceptible to the cytotoxic effects of the lethal dose. Although H2O2 increased cell attachment in lower doses, it induced a dose-dependent inhibition of cell attachment to the substrate in higher doses. H2O2 did not affect cell migration in sub-lethal doses. Conclusion:, Preconditioning RPE cells with limited exposure to non-lethal oxidative stress confers significant protection against subsequent H2O2 -induced cell death. It also affects cell attachment in a dose-specific manner. This finding may help in understanding the pathogenesis of diseases in which oxidative stress plays an important role and in determining the suitability of certain treatment strategies, in particular RPE transplantation in the treatment of age-related macular degeneration. [source] | ||||||||||