Edit Abstract: Mendonca 2014 Abstract IOC 2014-04 Schroecken

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Abstract:	Intracerebral hemorrhage (ICH) accounts for approximately 15% of the annual 5.7 million deaths worldwide caused by stroke. The ICH pathophysiology comprises a complex chain of events starting with blood–brain barrier disruption and infiltration of blood derived products (BDPs) into the brain parenchyma, resulting in a progressive edema, inflammation, oxidative stress and neurotoxicity. Some of the BDPs, such as iron, plays a central role in the CNS cell toxicity. Neurons and astrocytes are morphologically, functionally and metabolically distinct CNS cells and previous evidence from our group indicated that neurons were not only more efficient in BDPs uptake, but also more susceptible to these blood components, when compared to astrocytes. Considering that mitochondria represents an important source of reactive oxygen species (ROS), we hypothesized that mitochondrial function of CNS cells would be differently affected by iron exposure. Here, we investigated the effects of iron exposure to neuroblastoma (SH-SY5Y) and glioblastoma (U-138) cell lines mitochondrial physiology assessed by high resolution respirometry (HRR) analyses. We observed that 50 µM iron for 24h caused no changes in viability for both cell lines. Comparative HRR analyses of both cell lines without iron exposure revealed that respiratory rates associated to oxidative phosphorylation (OXPHOS) in neuroblastoma are significantly higher, when compared to glioblastoma (13.7 ± 1.7 vs. 7.6 ± 1.3 nmoles O2/min/106 cells, p<0.01). Also, the coupling of electron transport system (ET-pathway) to OXPHOS was higher in neuroblastoma than in glioblastoma cell lines (slopes 0.674 vs. 0.196). Interestingly, the reserve respiratory capacity was significantly higher in glio than in neuroblastomas (16.7 ± 3.4 vs. 1.6 ± 1.2 nmoles O2/min/106 cells, p<0.01). Exposure to iron caused any effects on glioblastoma mitochondrial metabolic parameters, but it significantly decreased the leak respiration in neuroblastoma (11.1 ± 0.6 vs. 8.0 ± 1.0 nmoles O2/min/106 cells, p<0.01). We conclude that mitochondrial physiology is distinct among the two cell lines tested, and that iron modulates mitochondrial inner membrane permeability of neuroblastomas, which may contribute to neurotoxicity associated to this metal.
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MiP areas:	Gender Respiration Instruments;methods mt-Biogenesis;mt-density mt-Structure;fission;fusion mt-Membrane mtDNA;mt-genetics nDNA;cell genetics Genetic knockout;overexpression Comparative MiP;environmental MiP Developmental biology Exercise physiology;nutrition;life style mt-Medicine Patients Pharmacology;toxicology mt-Awareness
Pathological states:	COPD Aging;senescence Alzheimer's Autism Cancer Cardiovascular Diabetes Inherited Infectious Myopathy Neurodegenerative Obesity Parkinson's Sepsis Other
Stress conditions:	Hypoxia Cell death Cryopreservation Ischemia-reperfusion Permeability transition Oxidative stress;RONS Temperature Mitochondrial disease
Organism:	Pig Human Mouse Rat Guinea pig Bovines Horse Dog Rabbit Cat Other mammals Chicken Zebrafish Drosophila Artemia Caenorhabditis elegans Saccharomyces cerevisiae Birds Reptiles Amphibians Fishes Chelicerates Crustaceans Hexapods Myriapods Annelids Molluscs Nematodes Other invertebrates Fungi Plants Protists Eubacteria Archea Algae
Tissues;cells:	Fat Heart Skeletal muscle Nervous system Liver Kidney Lung;gill Islet cell;pancreas;thymus Endothelial;epithelial;mesothelial cell Blood cells Genital Other cell lines CHO HEK HeLa Neuroblastoma Fibroblast HUVEC Macrophage-derived Lymphocyte Platelet Stem cells
Preparations:	SMP Intact organism Intact organ Permeabilized cells Permeabilized tissue Homogenate Isolated mitochondria Chloroplasts Enzyme Oxidase;biochemical oxidation Intact cells
Enzymes:	Complex I Adenine nucleotide translocase Complex II;succinate dehydrogenase Complex III Complex IV;cytochrome c oxidase Complex V;ATP synthase Inner mt-membrane transporter Marker enzyme Supercomplex TCA cycle and matrix dehydrogenases Uncoupling protein
Regulation:	pH Aerobic glycolysis ADP ATP ATP production AMP Calcium Coupling efficiency;uncoupling Cyt c Flux control Inhibitor Ion;substrate transport mt-Membrane potential Oxygen kinetics PCr;Cr Phosphate Redox state Substrate Temperature Threshold;excess capacity Uncoupler Fatty acid Amino acid Q-junction effect
Coupling:	ET LEAK ROUTINE OXPHOS
Pathways:	F N S Gp DQ CIV NS Other combinations ROX
High-resolution respirometry:	pH Oxygraph-2k TIP2k O2k-Fluorometer NO TPP Ca O2k-Spectrophotometer O2k-Manual O2k-Protocol Theory NextGen-O2k
Event:	A1 A2 A3 A4 B1 B2 B3 B4 C1 C2 C3 C4 D1 D2 D3 D4 E1 E2 Oral Poster P-flash Review
Additional labels:	(separate values by colon)

Free text: Any additional information (e.g. affiliations of authors). ==Affiliation== Institute of Medical Biochemistry, Federal University of Rio de Janeiro, Brazil Financial support: FAPERJ, CNPq.

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