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Serum PAF acetylhydrolase increases during neonatal maturation.
Prostaglandins
|June 1, 1990
Summary
Neonatal serum acetylhydrolase activity, crucial for regulating inflammatory platelet-activating factor (PAF), is significantly lower in newborns. Activity increases rapidly within the first six weeks of life, suggesting infants may be more susceptible to PAF-mediated diseases.
Area of Science:
- Biochemistry
- Immunology
- Neonatology
Background:
- Platelet-activating factor (PAF) is a potent inflammatory mediator.
- Acetylhydrolase degrades PAF to its inactive form, lysoPAF, playing a key role in PAF regulation.
- Low acetylhydrolase activity may increase susceptibility to PAF-related neonatal diseases like necrotizing enterocolitis.
Purpose of the Study:
- To investigate the effect of age on serum acetylhydrolase activity in human subjects.
- To determine if acetylhydrolase activity differs between newborns and older individuals.
- To assess the developmental trajectory of acetylhydrolase activity in early life.
Main Methods:
- Serum samples were collected from 70 subjects aged 4 hours to 48 years.
- Acetylhydrolase activity was measured using radio-labelled PAF and quantifying reaction products.
- Statistical analysis was performed to compare activity across different age groups and correlate it with age.
Main Results:
- Serum acetylhydrolase activity was significantly lower in newborns (less than 3 weeks) compared to all other age groups (8.2 nmole/ml/min vs 30.0 nmole/ml/min).
- Enzyme activity showed a linear increase with the natural logarithm of age from birth to 6 weeks (r=0.65, p<0.001).
- Newborn acetylhydrolase activity was comparable between term and preterm infants.
Conclusions:
- Human neonatal serum acetylhydrolase activity is markedly low.
- Activity increases substantially during the first six weeks of life, approaching adult levels.
- Neonates may have an elevated risk for pathophysiological conditions mediated by PAF due to lower acetylhydrolase levels.