Efeitos morfológicos e de lipoperoxidação da restrição alimentar aguda durante a gestação de camundongos

Abstract

The Food Restriction (FR) of pregnant female require alternatives measures are taken to maintain the conceptus through the metabolism of trophoblast cells during early pregnancy or mature placenta. Within this context, the effects of acute FR in the area of maternal-fetal interface were studied from morphological, cytochemical, immunocytochemical and lipid peroxidation analysis as well as its effects on fetuses and neonates. For this purpose, virgin Swiss mice were placed for mating with adult males of the same lineage and the morning of observation of vaginal plug was considered as the first day of pregnancy (dop). The pregnant females were organized into 5 experimental groups, Group I: FR 7th to 8th dop followed by euthanasia; Group II: FR from the 14th to 15th dop followed by euthanasia; Group III: FR from the 14th to 15th dop followed by return of feed until the 18th dop and euthanasia; Group IV: FR 7th to 8th dop followed by return of feed and evaluation of offspring. Group V: FR from the 14th to 15th dop followed by return of feed and evaluation of offspring. In groups I, II and III, ovaries, uterus, sites of embryonic development (SED) and fetal (SFD), as well as placentas and fetuses were evaluated at the time of collection and processed for paraffin embedding is destined for coloring with H&E, reaction with PAS, DBA lectin cytochemistry and immunocytochemistry for caspase-3. Some SED and SFD were destined to evaluation lipid peroxidation and protein mass. Groups IV and V were destined for physical examination of offspring by quantification of neonates, measurement of crown-rump length and body mass verification. According to the results, the acute FR, while not causing significant morphological changes in group I increased the amount of uNK cells, apoptosis in the embryonic, trophoblast and decidual cells, depletion of glycogen and increased protein mass of the SED and of lipid peroxidation in SED and maternal liver. In group II, the FR resulted in edema formation in the spongiotrophoblast region, deficient growth of the labyrinth trophoblast layer, reduced glycogen stores, increased apoptosis in the cells of glycogen, death and cell degeneration in the placenta, increased phagocytic activity of trophoblastic giant cells (TGCs), increased tissue turnover, decreased differentiation of uNK3 cells into uNK4 cells and increased placental lipid peroxidation. The analysis of group III showed that return of feed can reverse some changes evidenced, but yet was noticed an increase of apoptosis in placental cells and the presence of residual bodies in the TGCs. Despite all the changes entailed by FR, with the reestablishment of feeding, the number of offspring of groups IV and V showed no reduction, although neonates of group IV have experienced intrauterine growth restriction (IUGR). The results of this study indicate that acute FR leads a series of changes in metabolism in order to supply gestational maternal food shortages through alternative routes of energy harvesting in an attempt to maintain the integrity of the fetus and that the damage caused by FR during pregnancy can be minimized with the free provision of food, but still be associated with the occurrence of IUGR.