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Cun Li, Thomas J McDonald, Guoyao Wu, Mark J Nijland, and Peter W Nathanielsz

-W Jeong JK Dietrich MO Ruan H-B Kim E Suyama S Kelly K Gyengesi E Arbiser JL 2011 Peroxisome proliferation-associated control of reactive oxygen species sets melanocortin tone and feeding in diet-induced obesity . Nature Medicine

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Morag J Young and Amanda J Rickard

cell stiffness, which, in turn, reduces NO release ( Oberleithner 2005 ). Increased production of reactive oxygen species (ROS) by endothelial NO synthase (eNOS) uncoupling contributes to the pathology in angiotensin II and DOCA

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Wanpitak Pongkan, Hiranya Pintana, Thidarat Jaiwongkam, Sasiwan Kredphoo, Sivaporn Sivasinprasasn, Siriporn C Chattipakorn, and Nipon Chattipakorn

impairment begins at an intracellular level, in which overproduction of reactive oxygen species (ROS) leads to increased oxidative stress and impaired insulin signaling cascade ( Valle et al . 2011 ). This impairment can cause energy insufficiency in the

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R Vinayagamoorthi, Zachariah Bobby, and M G Sridhar

insulin resistance is not clearly known. Elevated levels of fatty acids are known to cause the production of reactive oxygen species (ROS) and oxidative stress ( Carisson et al . 1999 , Rao & Reddy 2001 ). Many studies have shown that the ROS induces

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Alice S Green, Paul J Rozance, and Sean W Limesand

enhancement, and lines ending with bars represent inhibition of the defined processes. ER, endoplasmic reticulum; ROS, reactive oxygen species; Caα1D, voltage-gated calcium channel α1D. β-cell deficiencies in animal models of IUGR In addition to obvious

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Alvaro Souto Padron, Ruy Andrade Louzada Neto, Thiago Urgal Pantaleão, Maria Carolina de Souza dos Santos, Renata Lopes Araujo, Bruno Moulin de Andrade, Monique da Silva Leandro, João Pedro Saar Werneck de Castro, Andrea Claudia Freitas Ferreira, and Denise Pires de Carvalho

Caillou B Talbot M Ameziane-El-Hassani R Lacroix L Lagent-Chevallier O Al Ghuzlan A Roos D Bidart JM Virion A 2010 Intracellular expression of reactive oxygen species-generating NADPH oxidase NOX4 in normal and cancer thyroid

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Shuai Li and Wipawee Winuthayanon

outcome. After the shedding of the cumulus cells, the embryo depends on tubal fluid and internal antioxidant activities to gain protection against reactive oxygen species (ROS)-induced stress ( Fig. 3 ). Two major systems are involved in this process: non

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M G Gnanalingham, A Mostyn, D S Gardner, T Stephenson, and M E Symonds

subject of intense debate ( Nedergaard & Cannon 2003 ), with postulated roles in energy balance ( Buemann et al. 2001 ), reactive oxygen species (ROS) production ( Negre-Salvayre et al. 1997 ) and apoptosis ( Voehringer et al. 2000 ), as summarised

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Daniel E Francés, María T Ronco, Juan A Monti, Paola I Ingaramo, Gerardo B Pisani, Juan P Parody, José M Pellegrino, Paloma Martín Sanz, María C Carrillo, and Cristina E Carnovale

compounds as an estimation of LPO ( Ohkuwa et al . 1995 , Winiarska et al . 2004 ). On the other hand, it was established that hyperglycemia increases mitochondrial reactive oxygen species (ROS) production, which could represent a key event in the

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E Bucris, A Beck, S Boura-Halfon, R Isaac, Y Vinik, T Rosenzweig, S R Sampson, and Y Zick

oxidative stress than other cell types. Several studies indicate that treatment of cultured cells with insulin, or hyperinsulinemia induced in animal models, promotes the generation of reactive oxygen species (ROS) ( Mukherjee et al . 1978 , May & de Haen