Brehier A, Rooney S A
Exp Lung Res. 1981 Nov;2(4):273-87. doi: 10.3109/01902148109052323.
We measured the rate of choline incorporation into phosphatidylcholine in lung slices; the glucogen content of the lung; and the activities of pulmonary cholinephosphate cytidylyltransferase, cholinephosphotransferase and phosphatidate phosphatase in the mouse during late fetal and early postnatal development. We also examined the effect of maternal dexamethasone administration on these parameters of fetal lung maturation. There was a development increase in the rate of choline incorporation between 17 days gestation (term is 19 days) and the immediate newborn period. There was also a developmental decrease in the glycogen content of the lung but this did not occur until 18 days. There was a developmental increase in the activities of cholinephosphate cytidylytransferase and phosphatidate phosphatase but little change in the activity of cholinephosphotransferase. Dexamethasone doubled the rate of choline incorporation into phosphatidylcholine at 17 and 18 days gestation. It decreased the glycogen content of the fetal lung by 74% at 18 and 19 days, but had no effect at 16 and 17 days. Dexamethasone increased the activity of pulmonary cholinephosphate cytidylyltransferase by 37% and that of cholinephosphotransferase by 27% at 17 days. It increased the activity of phosphatidate phosphatase by 25% at 16 days and by 32% at 19 days. These data show that the normal development profile of these parameters of fetal lung maturation in the mouse, as well as the effects of glucocorticoids thereon, are generally similar to those in the rabbit and rat. However, stimulation of cholinephosphotransferase by glucocorticoids has not been generally observed in other species. Furthermore, since the changes in the rate of choline incorporation precede those in glycogen depletion, the data suggest that the relationship between phospholipid synthesis and glycogen degradation is not simply that of precursor to product.
我们测定了肺切片中胆碱掺入磷脂酰胆碱的速率、肺中的糖原含量,以及在胎儿后期和出生后早期发育阶段小鼠肺中胆碱磷酸胞苷转移酶、胆碱磷酸转移酶和磷脂酸磷酸酶的活性。我们还研究了母体给予地塞米松对这些胎儿肺成熟参数的影响。在妊娠17天(足月为19天)至刚出生期间,胆碱掺入速率呈发育性增加。肺中的糖原含量也呈发育性下降,但直到18天才出现这种情况。胆碱磷酸胞苷转移酶和磷脂酸磷酸酶的活性呈发育性增加,而胆碱磷酸转移酶的活性变化不大。地塞米松使妊娠17天和18天时胆碱掺入磷脂酰胆碱的速率增加了一倍。它在妊娠18天和19天时使胎儿肺中的糖原含量降低了74%,但在16天和17天时没有影响。地塞米松在妊娠17天时使肺胆碱磷酸胞苷转移酶的活性增加了37%,使胆碱磷酸转移酶的活性增加了27%。它在妊娠16天时使磷脂酸磷酸酶的活性增加了25%,在19天时增加了32%。这些数据表明,小鼠胎儿肺成熟这些参数的正常发育情况,以及糖皮质激素对其的影响,通常与兔子和大鼠相似。然而,糖皮质激素对胆碱磷酸转移酶的刺激在其他物种中一般未观察到。此外,由于胆碱掺入速率的变化先于糖原消耗的变化,数据表明磷脂合成与糖原降解之间的关系并非简单的前体与产物的关系。