Crosstalk Between Oxidative Stress and Mitochondrial Damage: Focus on Amyotrophic Lateral Sclerosis.

Viviana Greco, Patrizia Longone, Alida Spalloni, Luisa Pieroni, Andrea Urbani

Research output: Chapter in Book/Report/Conference proceedingChapter

12 Citations (Scopus)


Proteins oxidation by reactive species is implicated in the aetiology or progression of a panoply of disorders and diseases such as neurodegenerative disorders. It is becoming increasingly evident that redox imbalance in the brain mediates neurodegeneration. Free radicals, as reactive species of oxygen (ROS) but also reactive nitrogen species (RNS) and reactive sulfur species (RSS), are generated in vivo from several sources. Within the cell the mitochondria represent the main source of ROS and mitochondrial dysfunction is both the major contributor to oxidative stress (OS) as well its major consequence. To date there are no doubts that a condition of OS added to other factors as mitochondrial damage in mtDNA or mitochondrial respiratory chain, may contribute to trigger or amplify mechanisms leading to neurodegenerative disorders. In this chapter, we aim at illustrate the molecular interplay occurring between mitochondria and OS focusing on Amyotrophic Lateral Sclerosis, describing a phenotypic reprogramming mechanism of mitochondria in complex neurological disorder.
Original languageEnglish
Title of host publicationMitochondria in Health and in Sickness
Number of pages12
Publication statusPublished - 2019

Publication series



  • Amyotrophic Lateral Sclerosis
  • Mitochondrial damage
  • Oxidative stress
  • Reactive Oxygen Species
  • Reactive species
  • Redox proteomics


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