Abstract
Despite Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) -induced Oxidative Stress (OxS) being well documented in different organs, the molecular pathways underlying placental OxS in late-pregnancy women with SARS-CoV-2 infection are poorly understood. Herein, we performed an observational study to determine whether placentae of women testing positive for SARS-CoV-2 during the third trimester of pregnancy showed redox-related alterations involving Catalase (CAT) and Superoxide Dismutase (SOD) antioxidant enzymes as well as placenta morphological anomalies relative to a cohort of healthy pregnant women. Next, we evaluated if placental redox-related alterations and mitochondria pathological changes were correlated with the presence of maternal symptoms. We observed ultrastructural alterations of placental mitochondria accompanied by increased levels of oxidative stress markers Thiobarbituric Acid Reactive Substances (TBARS) and Hypoxia Inducible Factor-1 α (HIF-1α) in SARS-CoV-2 women during the third trimester of pregnancy. Importantly, we found an increase in placental CAT and SOD antioxidant enzymes accompanied by physiological neonatal outcomes. Our findings strongly suggest a placenta-mediated OxS inhibition in response to SARS-CoV-2 infection, thus contrasting the cytotoxic profile caused by Coronavirus Disease 2019 (COVID-19).
Highlights
A cause–effect relationship between abnormal placental response, maternal COVID-19 severity, and neonatal outcome has not been established to date
Kruskal–Wallis test and Mann–Whitney U-test with a Bonferroni correction were used. This is the first report of alterations of placental mitochondria associated with increased levels of oxidative stress markers Thiobarbituric Acid Reactive Substances (TBARS) and Hypoxia Inducible Factor-1 α (HIF-1α) in women with SARS-CoV-2 infection during the third trimester of pregnancy
Our results were associated with an increase in placental Superoxide Dismutase (SOD) and CAT anti-oxidant enzymatic activities accompanied by physiological neonatal outcomes providing clues for a compensatory adaptation of the placenta to maintain its physiological abilities and to protect fetal growth
Summary
A cause–effect relationship between abnormal placental response, maternal COVID-19 severity, and neonatal outcome has not been established to date. Inflammatory changes in SARS-CoV-2-positive placentae are commonly reported. The prevalence of chronic villitis of unknown origin is higher in placentae delivered by COVID-19 patients than in those of healthy controls [1]. The extent to which the vertical transmission of SARS-CoV-2 occurs and the timing of such transmission are unclear. SARS-CoV-2 intrapartum transmission is possible [2], low incidence rates of in utero transmission [3–6] and early and late adverse obstetric outcomes [7,8] suggest that the placenta may play a critical role in modulating maternal response to SARS-CoV-2 infection. The main variable is placental permissibility to SARS-CoV-2 entry mechanisms initiated by spike protein (S) attachment
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