Experimental apoptosis provides clues about the role of mitochondrial changes in neuronal death

Patrizia Fattoretti, Carlo Bertoni-Freddari, Rina Recchioni, Belinda Giorgetti, Marta Balietti, Yessica Grossi, Moreno Solazzi, Tiziana Casoli, Giuseppina Di Stefano, Fiorella Marcheselli

Research output: Chapter in Book/Report/Conference proceedingConference contribution


A quantitative morphometric study has been carried out in human neuroblastoma SK-N-BE 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), volume fraction occupied by mitochondria/μm 3 of cytoplasm (volume density: Vv), and average mitochondrial volume (V) were calculated for both COX-positive and -negative organelles. The ratio (R) of the cytochemical precipitate area to the overall area of each mitochondrion 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 nonsignificant 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 fraction of small mitochondria provides an adequate amount of ATP for progression of the programmed cell death and these more efficient organelles appear to represent a reactive response to the loss of metabolically impaired mitochondria. 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.

Original languageEnglish
Title of host publicationAnnals of the New York Academy of Sciences
Number of pages10
Publication statusPublished - Dec 2006

Publication series

NameAnnals of the New York Academy of Sciences
ISSN (Print)00778923
ISSN (Electronic)17496632


  • Apoptosis
  • Cytochrome oxidase activity
  • Mitochondrial metabolic competence
  • Mitochondrial structural dynamics
  • Morphometry
  • SK-N-BE cells

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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