SERUM PAF ACETYLHYDROLASE INCREASES DURING NEONATAL MATURATION
SERUM PAF ACETYLHYDROLASE INCREASES DURING NEONATAL MATURATION
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DOI：
10.1016/0090-6980(90)90030-y
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发表时间：
1990-06-01
影响因子：
2.9
通讯作者：
DONOVAN, M
中科院分区：
文献类型：
--
作者：
CAPLAN, M;HSUEH, W;DONOVAN, M
乙酰水解酶是一种不稳定酸的43kd蛋白质，可催化有效的磷脂炎性介质--血小板激活因子(PAF)降解为其生物活性非活性代谢物lysoPAG。PAG的半衰期较短，因此乙酰水解酶在其调节中起着重要作用。由于先前的工作表明PAF可能参与某些新生儿疾病，如坏死性小肠结肠炎，我们研究了年龄对乙酰水解酶活性的影响。用放射性标记的PAF和测定反应产物来定量血清乙酰水解酶活性。前瞻性采集70名受试者的血清样本，年龄从4小时到48岁不等。新生儿(3周)的乙酰水解酶活性低于所有其他年龄段(8.2±-)。1.4nmole/ml/min vs 30.0.+-。1.6nmole/ml/min，p<；.01)。此外，从0天到6周，酶活性与日龄的自然对数呈线性关系(r=0.65，p<；.001)。出生6周时，乙酰水解酶活性接近年龄较大的儿童和成人。足月儿和早产儿的新生儿乙酰水解酶活性相似(8.6.+-)。1.9nmole/ml/min与7.2.+-.2.4nmole/ml/min，p=NS)。我们的结论是，在人类新生儿中，乙酰水解酶的活性很低，并在生命的前6周增加。这些结果表明，新生儿可能处于由PAF介导的病理生理过程的风险增加。
Acetylhydrolase is an acid-labile, 43 kd protein that catalyzes the degradation of platelet activating factor (PAF), a potent phospholipid inflammatory mediator, to its biologically inactive metabolite lysoPAG. PAG has a short half-life, thus acetylhydrolase plays an important role in its regulation. Since previous work suggests that PAF may be involved in certain neonatal diseases such as necrotizing enterocolitis, we studied the effect of age on acetylhydrolase activity. Serum acetylhydrolase activity was quantified using radio-labelled PAF and measuring reaction products. Serum samples were obtained prospectively from 70 subjects ranging in age from 4 hr to 48 yr. Acetylhydrolase activity was lower for newborns (< 3 wk) than all other age ranges (8.2 .+-. 1.4 nmole/ml/min vs 30.0 .+-. 1.6 nmole/ml/min, p < .01). Furthermore, enzyme activity increased linearly with respect to the natural logarithm of age from 0 days to 6 weeks (r = 0.65, p < .001). By 6 weeks of life acetylhydrolase activity approached values of older children and adults. Newborn acetylhydrolase activity was similar between term and preterm infants (8.6 .+-. 1.9 nmole/ml/min vs 7.2 .+-. 2.4 nmole/ml/min, p = NS). We conclude that acetylhydrolase activity is low in human neonates and increases during the first 6 weeks of life. These results suggest that newborn infants may be at increased risk for pathophysiologic processes mediated by PAF.