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Updated: Aug 11, 2025
The Serial Anesthesia Array for the High-Throughput Investigation of Volatile Agents Using Drosophila melanogaster
Published on: February 24, 2023
Long-term sevoflurane exposure resulted in temporary rather than lasting cognitive impairment in Drosophila
Ziming Liu1, Xuanyi Pan1, Jiguang Guo2
1Department of Anesthesiology, Affiliated Hospital of Hebei University, Baoding 071000, Hebei, China.
Insights
Sevoflurane anesthesia in young Drosophila caused temporary brain cell death and memory issues. These effects resolved over time, indicating no permanent neurotoxicity from early sevoflurane exposure.
Area of Science:
- Neuroscience
- Toxicology
- Developmental Biology
Background:
- Sevoflurane is a common inhaled anesthetic in pediatric surgery.
- Concerns exist regarding its potential neurotoxicity to developing brains.
- Evidence on permanent cognitive deficits from pediatric anesthesia remains debated.
Purpose of the Study:
- To investigate the lifetime neurotoxicity of early, prolonged sevoflurane exposure.
- Utilizing Drosophila melanogaster as a short-life-cycle animal model.
- To assess long-term cognitive and cellular effects.
Main Methods:
- Exposure of young Drosophila to 3% sevoflurane for 6 hours.
- Assessment of learning and memory using the T-maze assay.
- Evaluation of apoptosis, ATP, ROS levels, and gene expression in fly heads.
Main Results:
- Sevoflurane exposure induced transient neuroapoptosis and cognitive deficits within the first week.
- These impairments resolved over the fly's lifespan, showing no permanent damage.
- Changes in caspase, Bcl-2, ATP, and ROS levels were observed during the transient phase, with antioxidant gene expression correlating with ROS levels.
Conclusions:
- Early, prolonged sevoflurane anesthesia in Drosophila leads to transient, not permanent, neurotoxicity.
- The observed brain damage and cognitive deficits are temporary and reversible.
- Antioxidant mechanisms may play a role in recovery from sevoflurane-induced impairment.
Abstract:
Sevoflurane is the primary inhaled anesthetic used in pediatric surgery. It has been the focus of research since animal models studies found that it was neurotoxic to the developing brain two decades ago. However, whether pediatric general anesthesia can lead to permanent cognitive deficits remained a subject of heated debate. Therefore, our study aims to determine the lifetime neurotoxicity of early long-time sevoflurane exposure using a short-life-cycle animal model, Drosophila melanogaster. To investigate this question, we measured the lifetime changes of two-day-old flies' learning and memory abilities after anesthesia with 3 % sevoflurane for 6 h by the T-maze memory assay. We evaluated the apoptosis, levels of ATP and ROS, and related genes in the fly head. Our results suggest that 6 h 3 % sevoflurane exposure at a young age can only induce transient neuroapoptosis and cognitive deficits around the first week after anesthesia. But this brain damage recedes with time and vanishes in late life. We also found that the mRNA level of caspases and Bcl-2, ROS level, and ATP level increased during this temporary neuroapoptosis process. And mRNA levels of antioxidants, such as SOD2 and CAT, increased and decreased simultaneously with the rise and fall of the ROS level, indicating a possible contribution to the recovery from the sevoflurane impairment. In conclusion, our results suggest that one early prolonged sevoflurane-based general anesthesia can induce neuroapoptosis and learning and memory deficit transiently but not permanently in Drosophila.
