Mendonca 2014 Abstract IOC 2014-04 Schroecken

From Bioblast
Mendonca AP, Rodrigues MF, Amoedo ND, Oliveira MF (2014) Effects of iron on mitochondrial physiology of central nervous system cell lines. Mitochondr Physiol Network 19.02.


Mendonca AP, Rodrigues MF, Amoedo ND, Oliveira MF (2014)

Event: MiPNet19.02 IOC88

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 Β΅M 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 Β± 1.7 vs. 7.6 Β± 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 Β± 3.4 vs. 1.6 Β± 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 Β± 0.6 vs. 8.0 Β± 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.

β€’ O2k-Network Lab: BR Rio de Janeiro Oliveira MF

Labels: MiParea: Respiration 

Tissue;cell: Nervous system, Other cell lines, Neuroblastoma 

Coupling state: LEAK, OXPHOS, ET 

HRR: Oxygraph-2k 


Institute of Medical Biochemistry, Federal University of Rio de Janeiro, Brazil

Financial support: FAPERJ, CNPq.

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