It has been proposed that the high serum myoinositol promotes fetal growth and affects development of lung surfactant. However, it is unclear how the extracellular myoinositol becomes available in specific cells and whether there are developmental differences in myoinositol uptake. In the present study the mechanisms and perinatal development of intracellular myoinositol uptake into rabbit lung cells were investigated. Lung slices, lung explants, and type II alveolar cells were used. Evidence of saturable, sodium- and energy-dependent, and of non-saturable, sodium- and energy-independent myoinositol uptake was found. The nonsaturable uptake decreased by 67% during spontaneous maturation, as studied in lung slices. Beta-methasone (0.2 mg/kg days 26.3 and 27.3, to the doe) decreased by 65% the nonsaturable myoinositol uptake in 28-day-old fetuses. However, the saturable uptake revealed only small changes during perinatal development. The effect of extracellular myoinositol on surfactant phospholipid synthesis was evaluated in lung explants from 28-day-old fetuses, cultured for 2 days. In the presence of 10(-6) M dexamethasone the concentration of extracellular myoinositol, required for half-maximal inhibition of surfactant phosphatidylglycerol incorporation was higher than in explants grown without the hormone (approximately 0.4 versus 0.2 mM). However, in the microsomal fraction the phosphatidylglycerol incorporation was always inhibited by as low as 4 microM myoinositol. Myoinositol was taken up by isolated type II cells preferably by nonsaturable mechanism. The phosphatidylglycerol incorporation was less sensitive to extracellular myoinositol in adult than in fetal cells.(ABSTRACT TRUNCATED AT 250 WORDS)