Can amniotic fluid protect developing fetal lungs against the harmful effects of oxidative stress?

Abstract

Background/aim Preterm births cause fetuses to be born without completing the development of their organs. Due to this undesirable situation, it is the pulmonary tissue which has to be most exposed to harmful effects of extrauterine environment. Early disappearance of the prophylactic and constructive effects of amniotic fluid (AF) on developing tissues, such as pulmonary tissue, facilitates the formation of pulmonary morbidities resulting from oxygen. Setting out from this knowledge, we wanted, in addition to assessing the beneficent effects of AF on pulmonary tissue, to study the importance of AF in morbidities of this tissue thought to originate from oxygen. Materials and methods In this experimental study, while the study group was made up of the fetuses of pregnant rats exposed to hyperbaric oxygen, (hyperoxic pregnant rat fetuses-HPRF), the control group was formed of the fetuses of the rats pregnant in the usual room setting (normoxic pregnant rat fetuses-NPRF). The pulmonary and hepatic tissues taken from the fetuses of these pregnant rats on the 21st day of their pregnancy were compared biochemically and histologically. For biochemical assessment, total glutathione (tGSH), catalase (CAT), malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α) values and for histopathological assessment, apoptosis, alveolar wall count (AWC), vena centralis count (VCC) were included. Results Statistical significance was found in the pulmonary tissue values of tGSH on behalf of NPRF, and MDA on behalf of HPRF (p < 0.05). In liver tissue, statistical significance was detected in tGSH and CAT values in favor of NPRF and in MDA, and TNF-α values in favor of HPRF (p < 0.05). Conclusion Our study has demonstrated that AF protects the pulmonary tissue from the harmful effects of oxygen in the intrauterine period. In addition, our data have suggested that the pulmonary tissue’s being deprived of the useful effects of AF owing to premature birth may be an important trigger in the occurrence of the pulmonary morbidities thought to result from oxygen.