Brightness and shadows of mitochondrial ROS in the brain

Daniel Jimenez-Blasco1, Angeles Almeida2, Juan P Bolaños1

  • 1Instituto de Biología Funcional y Genómica (IBFG), Universidad de Salamanca, CSIC, Salamanca, Spain; Instituto de Investigación Biomédica de Salamanca (IBSAL), Hospital Universitario de Salamanca, Universidad de Salamanca, CSIC, Salamanca, Spain; Centro de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable (CIBERFES), Madrid, Spain.

PubMed

Insights

Mitochondrial reactive oxygen species (mROS) are crucial for astrocyte function, despite higher levels than neurons. Reduced astrocytic mROS leads to neuronal damage and organismal harm.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Mitochondrial reactive oxygen species (mROS) are typically viewed as harmful byproducts.
  • Astrocytes exhibit significantly higher mROS levels than neurons, yet these are vital for cellular metabolism and behavior.

Approach:

  • Discusses intrinsic mechanisms of higher mROS production in astrocyte mitochondria.
  • Identifies specific molecular targets of beneficial mROS in astrocytes.
  • Explains how diminished astrocytic mROS results in elevated neuronal mROS and subsequent damage.

Key Points:

  • Astrocytes generate mROS at a much higher rate than neurons due to specific mitochondrial respiratory chain mechanisms.
  • Beneficial mROS in astrocytes target specific molecules essential for maintaining cellular homeostasis.
  • A decrease in astrocytic mROS disrupts neuronal function, leading to oxidative stress and damage.

Conclusions:

  • The dual role of ROS in the brain, both beneficial and detrimental, is clarified at molecular and organismal levels.
  • This review aims to resolve the apparent controversy surrounding ROS in brain function and pathology.

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