Visit our Expo - Redox and Inflammation signaling 2012

Session XII : Cell death and neurodegenerative diseases Poster XII, 13
Mitochondrial metabolic competence in the early stages of neuronal cell death
Patrizia Fattoretti, Carlo Bertoni-Freddari, *Rina Recchioni, Belinda Giorgetti, Marta
Balietti, Yessica Grossi, Moreno Solazzi, Tiziana Casoli, Giuseppina Di Stefano,
*Fiorella Marcheselli
Neurobiology of Aging Laboratory and *Centre of Cytology, INRCA Research
Department, Via Birarelli 8, 60121 Ancona, Italy Email: p.fattoretti@inrca.it
A quantitative morphometric study has been carried out in human neuroblastoma SKNBE
cells to evaluate the ultrastructural features and the metabolic efficiency of mitochondria
involved in the early steps of apoptosis. In mitochondria from control and apoptotic cells
cytochrome oxidase (COX) activity was estimated by preferential cytochemistry. Number of
mitochondria (numeric density: Nv) and volume fraction occupied by mitochondria/cubic
micron of cytoplasm (volume density: Vv) and average mitochondrial volume (V) were
calculated on both COX positive and negative organelles. The ratio (R) of the cytochemical
precipitate area (CPA) to the overall area of each mitochondrion (MA) was evaluated on COX
positive organelles to estimate the inner mitochondrial membrane fraction actively involved
in cellular respiration. Following apoptotic stimulus, the whole mitochondrial population
showed a significant increase of Nv and Vv, while V was significantly decreased. In COX
positive organelles higher values of Nv were found, V appeared significantly reduced and Vv
was unchanged. R was increased at a not significant extent in apoptotic cells. COX positive
mitochondria accounted for 21% and 35% of the whole population in control and in apoptotic
cells, respectively. These findings document that in the early stages of apoptosis the increased
numeric density of mitochondria of small size provides an adequate amount of ATP for
progression of the programmed cell death process. In turn, an increased fraction of small and
more efficient mitochondria appears to represent a reactive response to the loss of
metabolically-impaired organelles. A better understanding of the mitochondrial role in
neuronal apoptosis may suggest potential interventions to prevent the extensive nerve cell
death typical of neurodegenerative diseases.
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