- Email: [email protected]
Catalase localization in Duchenne-Becker patients’ erythrocytes
S102
D. Rossin et al. / Free Radical Biology and Medicine 108 (2017) S18–S107
E-mail address: [email protected] (A. Korac)
P-243
Acknowledgements
Mitochondrial respiratory profile in human dermal fibroblast treated with HMG-coa reductase inhibitor
Serbian Ministry of Education, Science and Technological Development, Grant #173055P. http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.326
Fabio Marcheggiani 2, Julia Weise 3, Anja Knott 3, Alexandra Vogelsang 3, Luca Tiano 1 1
242
Cerebral protection during fetal-to-neonatal transition under hypoxic atmosphere Isabel Torres-Cuevas 1, Elena Cubells 2, Justo Escobar 3, Jose Manuel Verdugo 4, Miguel Asensi 5, Maximo Vento 2,6 1
Neonatal Research Group, Health Research Institute La Fe, Valencia, Spain 2 Neonatal Research Group, Health Research Institute La Fe, Valencia, Spain 3 Neonatal Research Group, Health Research Institute La Fe, Valencia, Spain 4 Comparative Neurobiology, Department of biology, University of Valencia, Valencia, Spain 5 Department of Physiology, University of Valencia, Valencia, Spain 6 Division of Neonatology, University and Polytechnic Hospital La Fe, Valencia, Spain Keywords: Hypoxia; oxidative stress; biomarkers; brain; mitochondria
Newborn asphyxia is a complication during the perinatal period. The use of O2 for resuscitation has been broadly used in clinic. However, it has been demonstrated that oxygen overexposure induces oxidative stress (OS). We speculate that delaying postnatal in the extrauterine oxygenation status would preserve reducing equivalents, enhance redox adaptation, and protect oxyregulator tissues. The objective is evaluated OE status, induced by FetalNeonatal Transition (FNT) under different FiO2 conditions, in brain. FiO2 in pregnant mice was reduced from 21% to 14% or not the night before of delivery (G19). 8 hours after birth both group were led to room air (Hx14/21 and Nx21/21 groups) or hyperoxia (FiO2 ¼ 100%) (Hx14/100 and Nx21/100 groups) and reset to 21% after 1 hour. The pups were sacrificed P1. We have determinated OS biomarkers (GSH/GSSG, Cysteine/ Cystine, Homocysteine/ Homocystine), protein (m-tyr and o-tyr/Phe, 3NO2-tyr and 3Cltyr/tyr), and DNA (8OH-dG/2-dG) damage by HPLC-MS/MS and we have done a mitocondrial morphology study using ME. The results show a higher OS in the Nx21/100 group compared to the Hx14/ 100 group that decreases. The group Hx14/21 and Hx14/100 present a better mitochondrialcharacteristics compared to environmental conditions and their subsequent reoxygenation. Our results support that FNT under hypoxic conditions could be protective to face a possible event of newborn resuscitation. E-mail address: [email protected] (I. Torres-Cuevas) Acknowledgements
PFIS FI12/00109 grant from the Health Institute Carlos III (Spanish Ministry of Economy and Competitiveness) and PI14/ 0443 grant and RD12/0026/0012 grant both from the health Institute Carlos III (Spanish Ministry of Economy and Competitiveness) http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.327
Department of Life and Environmental Sciences, Polytechnic University of Marche, Italy 2 Department of Clinical and Dental Sciences, Polytechnic University of Marche, Italy 3 Research and Development, Beiersdorf AG, Hamburg, Germany
Coenzyme Q10 is a endogenous isoprenilated quinone with antioxidant and bioenergetic activity. Its cellular levels and oxidative status are effected in ageing and synthetic rate is influenced by simvastatin, a widely used lipid lowering drug inhibiting HMGcoA reductase, a key enzyme in the mevalonate pathway. In light of its central role in mitochondrial bioenergetic and its relevance to the senescence process we evaluated how CoQ10 deprivation affected mitochondrial respiration in terms of oxygen consumption rate (OCR), evaluated using extracellular flux analyzer Seahorse bioscience, either in basal condition or following the incubation of selective inhibitors of different respiratory complexes. Human dermal fibroblast incubated at sublethal concentration of simvastatin, in the range 0.6 – 10 μM for 72 hours, showed a significant decrease in basal mitochondrial respiration at all tested concentrations associated with a significant decrease in ATP production. Moreover, at concentration higher than 2.5 μM significant decrease of maximal respiration and spare respiratory capacity suggest a decrease of the mitochondrial mass and/or poor ETC integrity that parallelled CoQ10 deprivation stressing the role of this molecule in cellular bioenergetics. Overall the data support the use of this experimental model for the study of age-related CoQ10 decrease in human skin. E-mail address: [email protected] (F. Marcheggiani) http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.328
P-244
Impact of lipo- and glucotoxic stress on proteolytic systems in murine liver Tobias Jung 1, Ioanna Korovila 1, Christiane Ott 1,3, Richard Kehm 1,2, Tilman Grune 1,2,3 1
German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Germany 2 German Center for Diabetes Research (DZD), Munich-Neuherberg 85764, Germany 3 German Center for Cardiovascular Research (DZHK), Berlin 13357, Germany Keywords: Metabolic syndrome; liver; proteasomal system; inflammation; glucotoxicity; lipotoxicity
Metabolic syndrome (MS) is a chronic pathology characterized (amongst others) by dysregulated plasma glucose and high serum triglycerides. One of the central organs affected is the liver, causing increasing fat accumulation and inflammation.
D. Rossin et al. / Free Radical Biology and Medicine 108 (2017) S18–S107
E-mail address: [email protected] (A. Korac)
P-243
Acknowledgements
Mitochondrial respiratory profile in human dermal fibroblast treated with HMG-coa reductase inhibitor
Serbian Ministry of Education, Science and Technological Development, Grant #173055P. http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.326
Fabio Marcheggiani 2, Julia Weise 3, Anja Knott 3, Alexandra Vogelsang 3, Luca Tiano 1 1
242
Cerebral protection during fetal-to-neonatal transition under hypoxic atmosphere Isabel Torres-Cuevas 1, Elena Cubells 2, Justo Escobar 3, Jose Manuel Verdugo 4, Miguel Asensi 5, Maximo Vento 2,6 1
Neonatal Research Group, Health Research Institute La Fe, Valencia, Spain 2 Neonatal Research Group, Health Research Institute La Fe, Valencia, Spain 3 Neonatal Research Group, Health Research Institute La Fe, Valencia, Spain 4 Comparative Neurobiology, Department of biology, University of Valencia, Valencia, Spain 5 Department of Physiology, University of Valencia, Valencia, Spain 6 Division of Neonatology, University and Polytechnic Hospital La Fe, Valencia, Spain Keywords: Hypoxia; oxidative stress; biomarkers; brain; mitochondria
Newborn asphyxia is a complication during the perinatal period. The use of O2 for resuscitation has been broadly used in clinic. However, it has been demonstrated that oxygen overexposure induces oxidative stress (OS). We speculate that delaying postnatal in the extrauterine oxygenation status would preserve reducing equivalents, enhance redox adaptation, and protect oxyregulator tissues. The objective is evaluated OE status, induced by FetalNeonatal Transition (FNT) under different FiO2 conditions, in brain. FiO2 in pregnant mice was reduced from 21% to 14% or not the night before of delivery (G19). 8 hours after birth both group were led to room air (Hx14/21 and Nx21/21 groups) or hyperoxia (FiO2 ¼ 100%) (Hx14/100 and Nx21/100 groups) and reset to 21% after 1 hour. The pups were sacrificed P1. We have determinated OS biomarkers (GSH/GSSG, Cysteine/ Cystine, Homocysteine/ Homocystine), protein (m-tyr and o-tyr/Phe, 3NO2-tyr and 3Cltyr/tyr), and DNA (8OH-dG/2-dG) damage by HPLC-MS/MS and we have done a mitocondrial morphology study using ME. The results show a higher OS in the Nx21/100 group compared to the Hx14/ 100 group that decreases. The group Hx14/21 and Hx14/100 present a better mitochondrialcharacteristics compared to environmental conditions and their subsequent reoxygenation. Our results support that FNT under hypoxic conditions could be protective to face a possible event of newborn resuscitation. E-mail address: [email protected] (I. Torres-Cuevas) Acknowledgements
PFIS FI12/00109 grant from the Health Institute Carlos III (Spanish Ministry of Economy and Competitiveness) and PI14/ 0443 grant and RD12/0026/0012 grant both from the health Institute Carlos III (Spanish Ministry of Economy and Competitiveness) http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.327
Department of Life and Environmental Sciences, Polytechnic University of Marche, Italy 2 Department of Clinical and Dental Sciences, Polytechnic University of Marche, Italy 3 Research and Development, Beiersdorf AG, Hamburg, Germany
Coenzyme Q10 is a endogenous isoprenilated quinone with antioxidant and bioenergetic activity. Its cellular levels and oxidative status are effected in ageing and synthetic rate is influenced by simvastatin, a widely used lipid lowering drug inhibiting HMGcoA reductase, a key enzyme in the mevalonate pathway. In light of its central role in mitochondrial bioenergetic and its relevance to the senescence process we evaluated how CoQ10 deprivation affected mitochondrial respiration in terms of oxygen consumption rate (OCR), evaluated using extracellular flux analyzer Seahorse bioscience, either in basal condition or following the incubation of selective inhibitors of different respiratory complexes. Human dermal fibroblast incubated at sublethal concentration of simvastatin, in the range 0.6 – 10 μM for 72 hours, showed a significant decrease in basal mitochondrial respiration at all tested concentrations associated with a significant decrease in ATP production. Moreover, at concentration higher than 2.5 μM significant decrease of maximal respiration and spare respiratory capacity suggest a decrease of the mitochondrial mass and/or poor ETC integrity that parallelled CoQ10 deprivation stressing the role of this molecule in cellular bioenergetics. Overall the data support the use of this experimental model for the study of age-related CoQ10 decrease in human skin. E-mail address: [email protected] (F. Marcheggiani) http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.328
P-244
Impact of lipo- and glucotoxic stress on proteolytic systems in murine liver Tobias Jung 1, Ioanna Korovila 1, Christiane Ott 1,3, Richard Kehm 1,2, Tilman Grune 1,2,3 1
German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), Germany 2 German Center for Diabetes Research (DZD), Munich-Neuherberg 85764, Germany 3 German Center for Cardiovascular Research (DZHK), Berlin 13357, Germany Keywords: Metabolic syndrome; liver; proteasomal system; inflammation; glucotoxicity; lipotoxicity
Metabolic syndrome (MS) is a chronic pathology characterized (amongst others) by dysregulated plasma glucose and high serum triglycerides. One of the central organs affected is the liver, causing increasing fat accumulation and inflammation.