euthanized. Kidneys were collected and submitted to the following analyses: catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH) and TBARS. The data were tested for significant differences by ANOVA and Kruskal-Wallis test (p<0.05). For CAT, GPx and TBARS no differences among the groups were observed. A dose-response effect was observed for GSH. In summary, only few changes in the antioxidant parameters in relation with the level of administered fluoride were observed. Key words: Fluoride, Antioxidants, kidney Financial Support: Fapesp Proc. 2012/19499-2

235 Effect of Argine for mTOR Signaling Pathway in Intestinal Epithelial Restitution Hiroshi Ichikawa1, Tomohisa Takagi2, Mayuko Oka3, and Yukiko Minamiyama3 1Doshisha University, Japan, 2Kyoto Prefectural University of Medicine, Japan, 3Kyoto Prefectural University, Japan Arginine enhances mucosal restitution, and regulates the immune response, protein synthesis and other multiple physiological events through mammalian target of rapamycin (mTOR)/p70 (S6) kinase pathway and produces nitric oxide. We studied detailed mechanism of cells. Rat intestinal epithelial (RIE) cells were cultured in serum and arginine-free medium with increasing arginine concentrations and rapamycin. Proliferation was evaluated by MTT-assay. Migration was measured by wound healing model experiment. mTOR/p70 (S6) kinase pathway was analyzed by western blot. Our results show that low arginine level decreased proliferation and migration, but over 50 μM of arginine significantly improved the suppression of proliferation. Cell migration was not affected by the addition of rapamycin. Furthermore, arginine increased cell proliferation through mTOR/p70 (S6) kinase pathway. However the mechanism of cell proliferation that mediated by mTOR/p70 (S6) kinase seemed to be influenced by not only arginine but also other nutritional conditions.

236 Fructose-Derived Advanced Glycation End-Products Evoke Skeletal Muscle Damage in Mice by Multiple Interference with SCAP-SREBP Pathway Raffaella Mastrocola1, Debora Nigro1, Fausto Chiazza2, Massimo Collino2, and Manuela Aragno1 1Dept. of Clinical and Biological Sciences, University of Turin, Italy, 2Dept. of Drug Science and Technology, University of Turin, Italy Advanced Glycation End-Products (AGEs) are derived from the reaction between reducing sugars and proteins, and exert key role in the pathogenesis of diabetes complications. We previously demonstrated that a fructose-enriched diet evoked a drastic increase in AGEs which contributed to hepatosteatosis by interfering with the SCAP-SREBP pathway that regulates the de novo lipogenesis. Although skeletal muscle is one of the main tissues involved in diet-induced metabolic derangements, informations about diet-derived AGEs impact on muscle are completely lacking.

In the present study C57Bl/6J mice were fed a standard diet (SD) or a 60% fructose diet (HFRT) for 12 weeks. Two subgroups of SD and HFRT mice received pyridoxamine (120 mg/kg/day), an AGE-inhibitor compound, in the drinking water. At the end of protocol HFRT mice had altered plasma lipid profile, although without evident increased body weight or glucose homeostasis alterations, compared to SD mice. Conversely, we found dramatic alterations in glucose and lipid metabolism in gastrocnemius muscle of HFRT featured by a fiber type shift towards oxidative metabolism, accompanied by SDH, SIRT-1 and PGC-increase, and a marked hyperactivation of the SCAP-SREBP signaling with consequent intramyocellular lipids accumulation. We detected high levels of AGEs in both plasma and gastrocnemius muscle of HFRT mice and this increase was associated with upregulation of the AGE receptor RAGE, and impaired expression of glyoxalase and AGE-R1, two AGE-detoxifying systems. The use of pyridoxamine counteracted almost completely the fructose-induced metabolic derangements in gastrocnemius. Overall, these results demonstrate the existence of multiple pathways by which AGEs interfere with SREBP signaling and metabolic processes and provide new insights into the role of fructose-derived AGEs in tissue damage.

237 Antioxidant Activity of a Medicinal Plant Extract from the Brazilian Forest: Myracrodruon Urundeuva Alessandra Cury Machado1, Lais G Pieroni2, Flávia Godoy Iano1, Anne Lígia Dokkedal2, and Rodrigo Cardoso de Oliveira1 1University of São Paulo, Brazil, 2UNESP, Brazil Myracrodruon urundeuva (Aroeira: popular name) is a tree, original from Brazil and others countries of the South America, whose leaves have been studied with therapeutic purpose in dentistry and medicine, due to its antimicrobial and anti-inflammatory potential, and ability to accelerate the repair process. However, to date, there has been no study about the antioxidant activity of Myracrodruon urundeuva. Therefore the purpose of this study was to analyze the antioxidant activity of a medicinal extract from this Brazilian plant, through DPPH (2,2-diphenyl-1-picrylhydrazyl) assay. The ability to scavenge DPPH radical was measured in these experiments by the discoloration of the solution. The original extract has been fractionated: n-butanol, ethanol and methanol fractions. All fractions of the extracts of Aroeira were evaluated through antioxidant assay, in vitro, DPPH. Gallic acid and quercetin were used as standards and the experiments were in triplicate. All of the fractions of Myracrodruon urundeuva (n-butanol, ethanol and methanol fractions) showed strong antioxidant activity (IC50

-1) in the DPPH free radical assay. The n-butanol fraction may also be highlighted, because it showed the lowest result of IC50 (IC50

-1). This specie, Myracrodruon urundeuva, traditionally used in popular medicine in Brazil, showed good results in this assay and may be a promising source for the development of natural antioxidants and future candidates for phytochemical, pharmacological, cytotoxicity studies in related pathologies. Keywords: antioxidant potential, DPPH, Myracrodruon urundeuva

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