heart. Systolic blood pressure was measured by non-invasive plethysmography or telemetry. Gene and protein expression were identified by real-time PCR and Western blot analysis. Superoxide level were determined by lucigenine – enhanced chemiluminis- cence. Enzyme activities were detected using radioactivity and spectrophotometric assay. Results and Conclusion: In NO-deficient models (1) we found that hypertension and antioxidant response in young rats was regu- lated mainly through peripheral regulation (vessels and heart), while in adult rats the main changes were observed in neuronal regulation of brainstem and RVLM. In DOX model of cardiomyo- pathy (2) we observed that increase in superoxide level corelated with development of hypertension and with Akt kinase activation and decrease of antioxidant response and SOD activities in animal hearts. Finally in hypertension treated models SHR(3a) and MS(3b) of adult rats we found that PPAR gama agonist PIO affected blood pressure and redox signaling in rats with metabolic syndrome, but not in SHR-model. Hovewer in young SHR we found that PIO treatment influenced blood pressure decrease and improved re- dox- sensitive regulation. Supported by APVV-0348-12 and VEGA 02/0129/14. http://dx.doi.org/10.1016/j.freeradbiomed.2016.04.144 P-82 A "multi-omic" investigation of the effects of long wavelength ultraviolet light on primary human keratinocytes Marie-Sophie Narzt 1,2 , Ionela M. Nagelreiter 1,2 , Valery N. Bochkov 3 , Julie Latreille 4 , Maria Fedorova 5 , Zhixu Ni 5 , Manuel Filzwieser 2 , Haihong Qin 1 , Lucia Terlecki 2,6 , Matthias Hackl 7 , Johannes Grillari 2,6 , Lucian Beer 8 , Martin Bilban 9 , Erwin Tschachler 1 , Florian Gruber 1,2 1 Department of Dermatology Medical University of Vienna, Austria 2 Christian Doppler Laboratory for Biotechnology of Skin Aging, Austria 3 Department of Pharmaceutical Chemistry, University of Graz, Austria 4 ChanelPB, Pantin, France 5 Institute of Bioanalytical Chemistry, Faculty of Chemistry and Mi- neralogy, Universität Leipzig, Germany 6 VIBT-BOKU Vienna, Austria 7 TAmiRNA Vienna, Austria 8 Department of Biomedical Imaging and Image-guided Therapy, Medical University of Vienna, Austria 9 Core Facility Genomics, Medical University of Vienna, Austria Long wavelength ultraviolet (UVA) light is the dominant en- vironmental oxidative stressor for the skin and a major factor for skin aging. UVA exposure of dermal fibroblasts leads to oxidation of membrane phospholipids and these can induce Nrf2 activation and autophagy as stress responses. The role of keratinocytes, the major epidermal cell type, in the initial events of UVA mediated photoaging is not well understood. The aim of this study was to assess how this stressor would affect the generation of oxidized lipids as potential stress messengers and the accompanying changes in the mRNA and microRNA transcriptome and in protein expression. We studied the oxidized phospholipidome of cultured primary keratinocytes immediately or after 24 hour recovery post stress (UVA or UV- oxidized phosopholipids, UVPL) using HPLC-MS/MS. We then investigated the transcriptomic response of these cells 7 hours after the stress on mRNA level using microarrays and microRNA levels using deep sequencing. Further, we assessed protein regulation using a proteome profiler antibody array 24 hours post stress. HPLC-MS/MS showed that 173 distinct lipid species within the human keratinocytes were significantly increased immediately after UVA exposure of which 141 species were also increased in UVPL - treated cells. 120 UVA generated lipid species had declined to their baseline values after 24 h. In parallel, gene ontology and pathway analysis of global mRNA expression of keratinocytes showed that the 81 mRNAs induced both by UVA and UVPL could be attributed to the action of upstream reg- ulators Nrf2, the unfolded protein response, and PPAR signaling. Among the upregulated genes we found mitochondrial phos- pholipases, peroxiredoxins and other enzymes capable of meta- bolizing isoprostanoid-PL and other lipid mediators correlated to (skin) aging. The Nrf2 regulated thioredoxin-1 and Nrf2 in- dependent superoxid dismutase- 2 were confirmed on protein level as co-induced genes. This suggests that UV-induced phos- pholipids initiate a transcriptional response that not only induces synthesis of antioxidant stress response genes but also enzymes to specifically metabolize and detoxify bioactive oxidized membrane lipids. http://dx.doi.org/10.1016/j.freeradbiomed.2016.04.145 P-83 Disulfide stress in carbon monoxide poisoning Merve Ergin 1 , Mustafa Caliskanturk 2 , Almila Senat 3 , Onur Akturk 1 , Ozcan Erel 3 1 25 Aralik State Hospital, Department of Biochemistry, Gaziantep, Turkey 2 25 Aralik State Hospital, Department of Emergency Medicine, Gaziantep, Turkey 3 Yildirim Beyazit University, Faculty of Medicine, Department of Biochemistry, Ankara, Turkey Aims: Carbon monoxide is the most common cause of lethal poi- soning around the world. The purpose of this study was to in- vestigate the homeostasis between thiol-disulfide couples in acute carbon monoxide poisoning. Methods: This case control study consisted of 43 subjects that were diagnosed with carbon monoxide poisoning and 35 healthy individuals. Thiol-disulfide paired tests were examined using the recently developed method. Results: Patients with carbon monoxide poisoning had sig- nificantly higher levels of serum disulfide levels than controls (20.7 7 5.03 vs 16.43 7 3.97, p ¼ 0.001). Native thiol levels were 344.29 7 62.29 μmol/L in the patient group and 475 7 49.01 μmol/L in healthy group (p o 0.001) and total thiol levels were 385.71 7 66.92 μmol/L in the carbon monoxide poisoning group and 507.87 7 50.54 μmol/L in the control group (p o 0.001).The disulfide / native thiol percent ratios and disulfide / total thiol percent ratios were significantly higher and native thiol / total E. Chiaradia et al. / Free Radical Biology and Medicine 96 (2016) S32–S69 S67