derived from 2-acetyl-4-aminoresorcinol proposed may have antioxidant activity due to the hydroxyl groups they contain. It is also possible to act as NADPH oxidase inhibitors since they have structural relationship and also possess Resveratrol, and anhydrocarbon chain with a carboxyl group as other inhibitors. the synthesized compound was 2-acetyl -4- aminoresorcinol, and from it the derived succinic, glutaric and phthalic compounds, characterized by mass spectrometry. the determination of antioxidant capacity was performed with ABTS, DPPH, and FRAP assays, so as Fenton reaction.

Mechanism of Surgical Adhesion Suppression by an Oxychlorine Free Radical Scavenger Cleva Villanueva1, Juan Manuel Zavala Rodriguez1, Rosa Amalia Bobadilla Lugo1, Saul Rojas Hernandez1, Rafael Campos Rodriguez1, and Robert David Kross2 1Instituto Politecnico Nacional, Mexico, 2Kross Link Laboratories, United States We have previously shown that proprietary oxychlorine solutions (OS) decrease surgical adhesion formation and scavenge superoxide. Since Macrophage 2 (M2) plays an important role in wound healing, and probably on adhesion formation, the goal of the study was to evaluate the effect of such OS on early macrophage polarization. Male Wistar rats were subjected to a surgical adhesion model. the abdominal cavities of half the animals were washed at the end of the surgery with isotonic saline solution (control) and the other half with an OS containing 100 ppm of chlorine dioxide. Three animals per group were sacrificed at 0, 1, 3, 6, 12 and 24 hrs after surgery. Nitric oxide (NO) and Interleukin 10 (IL-10) (markers of M1 and M2 macrophages respectively) were measured in the peritoneal liquid (colorimetric and ELISA methods, respectively). in the control group, IL-10 significantly (p<0.01) increased 3 hrs after surgery (peak) and it fell thereafter, whereas NO slightly increased only in the first hour. OS stopped the increase of IL-10 and significantly increased (p<0.01) NO from one to 6 hrs after surgery. It is concluded that the OS effect could be at least partially explained by its early modification of macrophage polarization during the surgical adhesion formation process. Supported by grant SIP20130842.

N-acetylcysteine amide (NACA) Prevents Retinal Degeneration Induced by Sodium Iodate in C57BL/6 Mice Hsiu-Jen Wang1, Shakila B. Tobwala1, Deniel Lindgren2, Robert S. Aronstam1, Humeyra Karacal3, and Nuran Ercal1 1Missouri University of Science & Technology, United States, 2Ocuscience, United States, 3Washington University, United States Age-related macular degeneration (AMD) is the leading cause of blindness in the elderly. AMD is a degenerative condition that begins in and progresses to the retinal pigment epithelium (RPE) and, ultimately, the overlying

photoreceptors. Since oxidative stress is strongly implicated in the pathogenesis of AMD, we hypothesized that N-acetylcysteine amide (NACA), a novel thiol antioxidant, would retard progression of retinal degeneration. in order to assess whether NACA had a significant impact on prevention of sodium iodate (NaIO3)-induced (50mg/kg) retinal degeneration, we utilized 2-month-old C57BL/6 mice which were divided into a control group, a NACA-only group, a NaIO3-induced retinal degeneration group, and a NACA-treated retinal degeneration group. We measured the degrees of photoreceptor cell death and function in the mice using both an electroretinogram (ERG) and analysis of photoreceptor histology, the thickness of the outer nuclear layer (ONL). Our results indicated that treatment with NACA eye drops significantly prevented the reduction in mean peak amplitude of scotopic and photopic waves and reduction in ONL thickness induced by sodium iodate. NACA demonstrated preservation of visual potential and the photoreceptor function in the NaIO3-induced retinal degeneration. in addition, NACA was able to increase the retinal glutathione (GSH) levels in NaIO3 treated mice. These results illustrated that NACA can prevent photoreceptor degeneration and loss of visual potential in vivo and, therefore, this nontoxic and potent antioxidant should be considered for the treatment of AMD.

The NADPH Oxidase Nox4 is a Novel Target for Anti-Angiogenic Therapy Valeska Weinberger1, Nina Henke2, Ralf P. Brandes1, and Katrin Schröder1 1Institute for Cardiovascular Physiology, Goethe-University Frankfurt am Main, Germany, 2Institute of Biochemistry I, Goethe-University Frankfurt am Main, Germany Angiogenesis is a pre-requisite for tumor progression as it facilitates a sufficient nutrient supply to the tumor which in turn allows further growth. Tumor angiogenesis is in part mediated by the vascular endothelial growth factor VEGF but if VEGF signaling is blocked other angiogenic factors substitute for it. Thus, interference with the upstream hypoxia signaling in tumors is potentially a more successful approach. the constitutively active NADPH oxidase Nox4 is an important source of H2O2 and has been suggested to be induced by hypoxia and impacts on gene expression. on such basis, we hypothesized that blockade of Nox4 may limit angiogenic responses in tumors. The process was studied using the chemical carcinogen 3-methylcholanthrene (MCA) in wild-type and Nox knockout mice. MCA induced fibrosarcoma in WT, Nox1y/-, Nox2y/- and Nox4y/-

mice. Histological analysis for vessel density using anti-CD31 staining showed a massive reduction in tumor vascularization in Nox4y/-. in contrast to that the angiogenic response in the Nox1 knockout mice was increased, whereas knockout of Nox2 had no effect on vessel density. Accordingly, serum from Nox4y/- mice exhibited a reduced pro-migratory effect on human umbilical vein endothelial cells. as underlying mechanisms we identified a lack of hypoxia signaling in Nox4y/- mice. Hypoxia- inducible factor 1-alpha (HIF1- in the tumors was attenuated as was the expression of the -dependent genes VEGF-A, glucose transporter 1 and adrenomedullin. as Nox4 generates H2O2, and as -prolylhydroxylases, an the effect. Thus, Nox4 is a novel target for anti-angiogenic therapy and due to that possibly a suitable approach for tumor treatment.

doi: 10.1016/j.freeradbiomed.2013.10.734

doi: 10.1016/j.freeradbiomed.2013.10.735

doi: 10.1016/j.freeradbiomed.2013.10.736

doi: 10.1016/j.freeradbiomed.2013.10.737