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Neonatal Anesthesia and Oxidative Stress
David A Gascoigne1, Mohammed M Minhaj2, Daniil P Aksenov1,2
1Department of Radiology, NorthShore University HealthSystem, Evanston, IL 60201, USA.
Insights
Neonatal anesthesia can disrupt the brain's redox balance, leading to oxidative stress. This imbalance, particularly from long-term pathways, may contribute to later neurodevelopmental issues in children.
Area of Science:
- Neuroscience
- Anesthesiology
- Biochemistry
Background:
- Neonatal anesthesia poses risks to brain redox balance due to immature antioxidant systems.
- Oxidative stress, an imbalance between reactive oxygen species (ROS) and antioxidants, is linked to adverse effects of early anesthetic exposure.
- Potential consequences include learning deficits and behavioral abnormalities.
Purpose of the Study:
- To review mechanisms of anesthetic agents and ROS production.
- To explore pathways of neonatal anesthesia-induced oxidative stress.
- To assess the relationship between neonatal anesthesia and oxidative stress.
Main Methods:
- Literature review of anesthetic agents' mechanisms.
- Analysis of key reactive oxygen species (ROS) production pathways.
- Examination of primary antioxidant systems.
- Exploration of immediate, short-term, and long-term oxidative stress pathways.
Main Results:
- Oxidative stress is evident during and immediately after neonatal anesthesia.
- Short-term oxidative stress pathways appear to have a limited temporal effect.
- Long-term pathways can lead to lasting neurodevelopmental alterations.
Conclusions:
- Neonatal anesthesia significantly impacts brain redox balance.
- Long-term oxidative stress pathways present a critical concern for neurodevelopment.
- Further research is needed to mitigate these risks.
Abstract:
Neonatal anesthesia, while often essential for surgeries or imaging procedures, is accompanied by significant risks to redox balance in the brain due to the relatively weak antioxidant system in children. Oxidative stress is characterized by concentrations of reactive oxygen species (ROS) that are elevated beyond what can be accommodated by the antioxidant defense system. In neonatal anesthesia, this has been proposed to be a contributing factor to some of the negative consequences (e.g., learning deficits and behavioral abnormalities) that are associated with early anesthetic exposure. In order to assess the relationship between neonatal anesthesia and oxidative stress, we first review the mechanisms of action of common anesthetic agents, the key pathways that produce the majority of ROS, and the main antioxidants. We then explore the possible immediate, short-term, and long-term pathways of neonatal-anesthesia-induced oxidative stress. We review a large body of literature describing oxidative stress to be evident during and immediately following neonatal anesthesia. Moreover, our review suggests that the short-term pathway has a temporally limited effect on oxidative stress, while the long-term pathway can manifest years later due to the altered development of neurons and neurovascular interactions.
