Keywords
Oxygen Free Radicals
Placenta
oxidative stress
Obesity
Mitochondrial morphology
How to Cite
Abstract
Background: In obesity, mitochondrial dysfunction and increased oxidative stress are observed, characterized by changes in the structure of mitochondria, accumulation of mutations in mitochondrial DNA, and an overproduction of reactive oxygen species (ROS), which results in an inefficient response in ATP production.
Purpose: The main objective of this research was to evaluate the levels of oxidative stress and its impact on mitochondrial morphology in term placentas of obese pregnant women.
Methodology: Analytical retrospective cross-sectional cohort study. 30 placenta samples were obtained from full-term pregnant women with no previous pathological history who attended an IPS in Cali. They were divided into three study groups: Control group, CO=10 (BMI 18.5kg/m2- 24.9kg/m2); Pregestational obesity, OP=10 BMI >30 kg/m2; Gestational obesity, OG= 10 (BMI?29.9kg/m2 with increase>13kg). The analysis of oxidative stress damage was evaluated by means of anti-Nitrotyrosine (NT) antibody; Mitochondrial morphology was analyzed with TEM (Transmission Electron Microscopy).
Results: NT residues were present in greater quantities in the placentas of mothers with obesity, compared to the control group (CO:11.64+-0.40; OG: 14.7+- 0.92; OP:17.44+- 2.13; p?0.02). The mitochondria present in the terminal villi of the syncytiotrophoblast of the OP and OG groups showed changes in their number, size and shape. In addition, alterations in the mitochondrial cristae, loss of the internal and external mitochondrial membranes and fragmentation of mitochondria in the cytoplasm of the placental cell were identified.
Conclusions: Maternal obesity caused significant changes in oxidative stress levels, evaluated by nitrotyrosine residues, as well as severe damage in mitochondrial morphology. These changes could negatively affect the metabolism of biomolecules and placental functioning, inducing a persistent inflammatory process mediated by oxygen free radicals.
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