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

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

Risultato della ricerca: Contributo in libroChapter

12 Citazioni (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.
Lingua originaleEnglish
Titolo della pubblicazione ospiteMitochondria in Health and in Sickness
Numero di pagine12
Stato di pubblicazionePubblicato - 2019

Serie di pubblicazioni



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


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