Oxidative Stress and Cerebral Vascular Tone: The Role of Reactive Oxygen and Nitrogen Species.
Michele SalvagnoElda Diletta StercheleMario ZaccarelliMrakic-Sposta SimonaIan James WelsbyCostantino BalestraFabio Silvio TacconePublished in: International journal of molecular sciences (2024)
The brain's unique characteristics make it exceptionally susceptible to oxidative stress, which arises from an imbalance between reactive oxygen species (ROS) production, reactive nitrogen species (RNS) production, and antioxidant defense mechanisms. This review explores the factors contributing to the brain's vascular tone's vulnerability in the presence of oxidative damage, which can be of clinical interest in critically ill patients or those presenting acute brain injuries. The brain's high metabolic rate and inefficient electron transport chain in mitochondria lead to significant ROS generation. Moreover, non-replicating neuronal cells and low repair capacity increase susceptibility to oxidative insult. ROS can influence cerebral vascular tone and permeability, potentially impacting cerebral autoregulation. Different ROS species, including superoxide and hydrogen peroxide, exhibit vasodilatory or vasoconstrictive effects on cerebral blood vessels. RNS, particularly NO and peroxynitrite, also exert vasoactive effects. This review further investigates the neuroprotective effects of antioxidants, including superoxide dismutase (SOD), vitamin C, vitamin E, and the glutathione redox system. Various studies suggest that these antioxidants could be used as adjunct therapies to protect the cerebral vascular tone under conditions of high oxidative stress. Nevertheless, more extensive research is required to comprehensively grasp the relationship between oxidative stress and cerebrovascular tone, and explore the potential benefits of antioxidants as adjunctive therapies in critical illnesses and acute brain injuries.
Keyphrases
- cerebral ischemia
- oxidative stress
- reactive oxygen species
- hydrogen peroxide
- subarachnoid hemorrhage
- dna damage
- induced apoptosis
- resting state
- white matter
- cell death
- brain injury
- functional connectivity
- blood brain barrier
- liver failure
- ischemia reperfusion injury
- diabetic rats
- respiratory failure
- climate change
- drug induced
- risk assessment
- signaling pathway
- intensive care unit
- endoplasmic reticulum stress
- living cells
- human health
- mechanical ventilation
- electron transfer