Objective — to investigate bioactive substances, such as specific markers of preterm labor and fetal growth restriction, in amniotic fluid. Subject and methods. The investigation enrolled 123 pregnant women aged 20—39 years at 34—40 weeks’ gestation. Group 1 included 42 patients with premature births at 34—37 weeks of pregnancy; Group 2 consisted of 34 pregnant women having fetal growth restriction. A control group was represented by 47 pregnant women with the physiological course of pregnancy and labor. All the pregnant women underwent standard clinical, laboratory, and instrumental examinations. The amniotic fluid obtained by a catheter in the first stage of labor was used to determine the cellular bioregulators of uterine contractility and fetal growth restriction. The investigators estimated the levels of cholesterol, α-fetoprotein, cachectin, annexin, and vascular endothelial growth factor A with the analyzer kits, NO-synthase from the higher NO from L-arginine in presence of NADPH. The activity of secretory phospholipase and NF-κB p65 subunit was determined by enzyme immunoassay of NO3 and NO2, by applying the classic Griss reaction. Results. The investigators revealed the molecular mechanisms for the development of preterm labor, which consisted in modifying the amniotic fluid levels of cachectin and nitric oxide, and the mechanism of fetal growth restriction resulting from the impaired arrival of fetal cholesterol, the major component of cell membranes. Conclusion. The degree of endocrine disorders should be estimated even in early pregnancy in order to prevent preterm labor. The features of the development of fetal growth restriction, which were found on the basis of cholesterol transport impairment and cachectin and nitric oxide levels in amniotic fluid during preterm labor, can serve as a rationale for optimizing therapy for threatened preterm labor and fetal growth restriction.