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Toshiaki Ishizuka, Takashi Hinata and Yasuhiro Watanabe

postischemic neovascularization by 1.5-fold as compared to those from untreated diabetic mice ( Ebrahimian et al . 2006 ). The effects of hyperglycemia or hypoxia have been associated with increased levels of reactive oxygen species (ROS; Waypa et al . 2001

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Chao Li, Bin Yang, Zhihao Xu, Eric Boivin, Mazzen Black, Wenlong Huang, Baoyou Xu, Ping Wu, Bo Zhang, Xian Li, Kunsong Chen, Yulian Wu and Gina R Rayat

). Oxidative stress is associated with increased production of oxidizing species or a significant decrease in the effectiveness of antioxidant defenses ( Schafer & Buettner 2001 , Fleury et al . 2002 ). Exposure to high levels of reactive oxygen species (ROS

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George Bikopoulos, Aurelio da Silva Pimenta, Simon C Lee, Jonathan R Lakey, Sandy D Der, Catherine B Chan, Rolando Bacis Ceddia, Michael B Wheeler and Maria Rozakis-Adcock

clusters from the islets of all donors revealed the induction of genes involved in reactive oxygen species (ROS) activity, inflammation, and immunity. This provides evidence that chronic exposure of human islets to FFA activates inflammatory and metabolic

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Parveen Abidi, Haiyan Zhang, Syed M Zaidi, Wen-Jun Shen, Susan Leers-Sucheta, Yuan Cortez, Jiahuai Han and Salman Azhar

differences in absorbance at wavelength 570 nm minus 690 nm using a microplate reader. Measurement of ROS Oxidant-induced intracellular reactive oxygen species (ROS) generation and oxidative stress was monitored by measuring changes in fluorescence resulting

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Palaniappan Murugesan, Muthusamy Balaganesh, Karundevi Balasubramanian and Jagadeesan Arunakaran

in vivo ( Murugesan et al. 2005 b ). During normal metabolism, cells produce reactive oxygen species (ROS) that can damage DNA, protein, and lipids. In steroidogenic cells, ROS are produced by the electron transport chain. In addition, ROS are also

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E Meimaridou, M Goldsworthy, V Chortis, E Fragouli, P A Foster, W Arlt, R Cox and L A Metherell

receptor on a B6/Balbc mix background . Molecular and Cellular Endocrinology 300 32 – 36 . ( https://doi.org/10.1016/j.mce.2008.10.027 ) 19022343 10.1016/j.mce.2008.10.027 Diemer T Allen JA Hales KH Hales DB 2003 Reactive oxygen

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Gen Chen, Xiangjuan Chen, Chao Niu, Xiaozhong Huang, Ning An, Jia Sun, Shuai Huang, Weijian Ye, Santie Li, Yingjie Shen, Jiaojiao Liang, Weitao Cong and Litai Jin

. CAT indicates catalase; HO1, heme oxygenase 1; NQO1, NAD(P)H dehydrogenase (quinone 1); ROS, reactive oxygen species. A full color version of this figure is available at https://doi.org/10.1530/JOE-18-0457 . In summary, our findings indicate

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Hiranya Pintana, Wanpitak Pongkan, Wasana Pratchayasakul, Nipon Chattipakorn and Siriporn C Chattipakorn

oxygen species (ROS), mitochondrial membrane potential change (ΔΨm) and mitochondrial swelling were also determined. Brain mitochondrial ROS assay Brain mitochondrial ROS were measured using dichloro-hydrofluoresceindiacetate (DCFHDA) fluorescent dye

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Marika Bogdani, Angela M Henschel, Sanjay Kansra, Jessica M Fuller, Rhonda Geoffrey, Shuang Jia, Mary L Kaldunski, Scott Pavletich, Simon Prosser, Yi-Guang Chen, Åke Lernmark and Martin J Hessner

tissues, such as kidney or liver, islets possess lower levels of the antioxidant enzymes superoxide dismutase (SOD) and catalase ( Lenzen 2008 ) and may be more susceptible to redox imbalances arising from overproduction of reactive oxygen species (ROS

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CJ Newton, D Bilko, S Pappa and SL Atkin

The oestrogen receptor is fundamental to the growth and survival of the rat pituitary tumour cell line, GH(3). Our previous studies have shown that antioestrogens such as RU 58668 and ZM 182780 will reduce the rate of cell division and also induce cell death. Death of these cells in response to antioestrogen treatment appears to be due to a heightened sensitivity to reactive oxygen species (ROS). As part of a study to determine the cross-talk between steroid receptor systems in these cells, we have observed that the glucocorticoid, dexamethasone (Dex), inhibits antioestrogen-induced cell death. Cell death induced by H(2)O(2) is enhanced by ZM 182780 and this effect is also blocked by Dex. As apoptotic cell death in a number of systems involves an early loss of mitochondrial membrane potential (DeltaPsi(m)), we have performed detailed studies on the time-course of DeltaPsi(m) loss in relation to the loss in cell membrane function. These studies have indicated that a loss of DeltaPsi(m) parallels a loss of cell membrane function - this is more characteristic of necrosis than of apoptosis. From microscopic observations of these cells in response to H(2)O(2), it has been noted that early cell membrane blebbing, induced by H(2)O(2), is blocked in the presence of ZM 182780. Cell membrane blebbing can precede necrosis as well as apoptosis and it is thought to involve cytoskeletal changes, for which localised glycolytic reactions provide ATP. These observations, together with those showing that removal of glucose, but not inhibition of mitochondrial function, enhances ROS-induced cell death, prompted studies on the glycolytic pathway. As a strong candidate mechanism, it would appear that, via an effect on one of the rate-limiting glycolytic enzymes, glyceraldehyde-3-phosphate dehydrogenase, Dex is able to overcome the antioestrogen-enhanced loss of glycolytic function following exposure of cells to ROS. This report contributes to the growing body of evidence showing that glucocorticoids provide a survival advantage to both normal and tumour cell types.