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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 . ( ) 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 . 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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M Vega, I Carrasco, T Castillo, J L Troncoso, L A Videla, and L Devoto


To evaluate the effect of reactive oxygen species in human corpus luteum function, we investigated whether hydrogen peroxide (H2O2) affects the in vitro luteal cell production of steroids. H2O2 treatment (1·0–100 μm) of mid and late luteal cell cultures elicited a dose-dependent decrease in basal progesterone production. However, treatment of mid luteal cells with a low concentration of H2O2 0·01 μm) significantly stimulated progesterone secretion (P<0·05). In addition, H2O2 (100 μm) markedly inhibited human chorionic gonadotropin (hCG)-stimulated progesterone and estradiol secretion. cAMP production was enhanced (2·4-fold, P<0·05) by hCG treatment of luteal cells. The addition of H2O2 (0·1–100 μm) to hCG-stimulated luteal cell cultures elicited a decrease in cAMP concentration (P<0·05) and in the specific binding of radiolabeled hCG by luteal cells. Progesterone and estradiol production stimulated by dibutyryl cAMP were significantly inhibited by H2O2 (P<0·05). These findings suggest that H2O2 interferes with basal steroid production and, in hCG-stimulated conditions, it may inactivate the gonadotropin–receptor complex. The anti-steroidogenic action of H2O2 therefore raises the possibility of a modulatory role of H2O2 in human luteal steroidogenesis.

Journal of Endocrinology (1995) 147, 177–182