Propofol anesthesia in children does not induce sister chromatid exchanges in lymphocytes
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Published on: June 11, 2017
Thorsten K W Krause1, Lars Jansen, Jens Scholz
1Department of Anesthesiology, University Hospital Hamburg-Eppendorf, Martinistr 52, 20246 Hamburg, Germany. tkrause@uke.uni-hamburg.de
Insights
Propofol anesthesia in children did not show genotoxic effects, as measured by sister chromatid exchanges (SCE). This study found no significant increase in SCE rates following propofol-based anesthesia in pediatric patients.
Area of Science:
- Anesthesiology
- Genetics
- Pediatrics
Background:
- Propofol is a common anesthetic for children, but its genotoxic potential is not well-understood.
- Sister chromatid exchanges (SCE) in T-lymphocytes serve as a biomarker for genotoxicity.
Purpose of the Study:
- To investigate the genotoxic effects of propofol-induced total intravenous anesthesia in children.
- To assess SCE formation in pediatric T-lymphocytes following propofol anesthesia.
Main Methods:
- 40 pediatric patients (ASA I-III) received propofol and alfentanil for anesthesia.
- Blood samples were collected pre- and post-anesthesia for SCE analysis.
- 25 T-lymphocyte metaphases per sample were analyzed for SCE frequencies.
Main Results:
- Total intravenous anesthesia with propofol did not alter SCE rates in pediatric T-lymphocytes.
- No statistically significant differences in SCE were observed before and after anesthesia.
- Slightly higher SCE rates in girls were not statistically significant compared to boys.
Conclusions:
- Propofol anesthesia under the studied conditions did not induce genotoxicity in children.
- Short-term exposure to propofol during pediatric anesthesia showed no observable genotoxic effects.
Background:
Propofol is frequently used for general anesthesia in children although little is known about possible genotoxic effects in humans. We investigated the formation of sister chromatid exchanges (SCE) in metaphase chromosomes of T-lymphocytes of children as a marker for possible genotoxocity following total intravenous anesthesia with propofol for minor surgical procedures.
Methods:
40 children ASA classification I-III were included (ASA I n=34, ASA II n=5, ASA III n=1) in the study. Anesthesia was induced by propofol (3mg/kg) and alfentanil. Succinylcholine or rocuronium were administered for muscle relaxation. After tracheal intubation anesthesia was maintained by continuous propofol infusion at 12 mg/(kgh). Blood samples were drawn before induction and after termination of anesthesia. Following a 72 h cell culture period, 25 T-lymphocyte metaphases per blood sample for all children were analyzed for SCE frequencies.
Results:
Total intravenous anesthesia with propofol on children did not influence SCE rates in metaphase chromosomes of T-lymphocytes. No SCE differences could be detected between blood samples before initiation and after termination of anesthesia (Wilcoxon signed rank test). Slightly elevated SCE rates were obtained in T-lymphocytes of girls compared to boys, but these differences did not reach statistical significance.
Conclusions:
Propofol anesthesia under the chosen conditions did not induce the formation of SCE in children in vivo. No genotoxic effect of a short term exposure to propofol during pediatric anesthesia had been observed.
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