Increased low-density lipoprotein susceptibility to oxidation in pregnancies and fetal growth restriction.
OBJECTIVE
Atherosis and placental infarction have been observed in pregnancies complicated by fetal growth restriction (FGR). Low-density lipoprotein (LDL) oxidation plays a central role in the pathogenesis of atherosclerosis; therefore, it could be involved in the placental alterations observed in FGR. The aims of the present study were to estimate LDL susceptibility to oxidation in pregnancies complicated by FGR and to evaluate their relationship with fetal growth and placental hormone secretion.


METHODS
A cohort prospective study was carried out in 50 women with uncomplicated pregnancies and 55 women with FGR. Blood was drawn at 15, 24, and 32 weeks of gestation. Low-density lipoprotein oxidation was initiated by the addition of CuCl2 and formation of conjugated dienes was monitored. Cholesterol, triglycerides, vitamin E, estradiol, progesterone, and placental lactogen were determined.


RESULTS
Women with FGR showed a lag phase (minutes from addition of CuCl2) similar to the control group in the first trimester of pregnancy (85.3 +/- 3.3 versus 81.3 +/- 5.6). But in the second and third trimester, they showed a lower lag phase than the control group: 69.6 +/- 3.6 versus 84.4 +/- 3.5 (P < .05) and 69.9 +/- 3.4 versus 95.6 +/- 3.4 (P < .001). During the third trimester, pregnancies complicated with FGR showed lower levels of estradiol, progesterone, and human placental lactogen than those in the control group. In the third trimester, a positive correlation was found between the lag phase and the birth weight (P = .001) and with the plasma levels of estradiol (P = .002).


CONCLUSIONS
Fetal growth restriction is associated with an increased LDL susceptibility to oxidation, a process that could damage the placenta, leading to alterations in placental endocrine function and fetal weight. Pregnancies complicated by fetal growth restriction show an increased LDL susceptibility to oxidation, a process that may lead to placental dysfunction and growth delay.
Sánchez-Vera
Isabel
I
School of Medicine, Universidad San Pablo-CEU, Madrid, Spain.
Bonet
Bartolomé
B
Viana
Marta
M
Quintanar
Amalia
A
López-Salva
Antonio
A
D000328:Adult; D002784:Cholesterol / Q000097:blood; D015331:Cohort Studies; D003300:Copper; D004958:Estradiol / Q000097:blood; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism*; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism*; D010084:Oxidation-Reduction; D010928:Placental Lactogen / Q000097:blood; D011247:Pregnancy; D011374:Progesterone / Q000097:blood; D011446:Prospective Studies; D014280:Triglycerides / Q000097:blood; D014810:Vitamin E / Q000097:blood
D008077:Lipoproteins, LDL; D014280:Triglycerides; D014810:Vitamin E; D011374:Progesterone; D004958:Estradiol; D003300:Copper; D010928:Placental Lactogen; D002784:Cholesterol; C028419:cuprous chloride