Abstract

Oxidative stress (OS) plays a pivotal role in placental development; however, abnormal loads in oxidative stress molecules may overwhelm the placental defense mechanisms and cause pathological situations. The environment in which the mother evolves triggers an exposure of the placental tissue to chemical, physical, and biological agents of OS, with potential pathological consequences. Here we shortly review the physiological and developmental functions of OS in the placenta, and present a series of environmental pollutants inducing placental oxidative stress, for which some insights regarding the underlying mechanisms have been proposed, leading to a recapitulation of the noxious effects of OS of environmental origin upon the human placenta.

Highlights

  • The mechanistic studies that we present seem to demonstrate that the impact of environmental pollutants upon the health risk is genuine and that the generation of oxidative stress in the placenta is a sensible and truthful mediator of placental diseases

  • In the STOX1 mouse model of preeclampsia, we have shown previously that oxidative/nitrosative stress is a major cause of the onset of the disease [153,154], corroborating the importance of this pathway in hypertensive disorders of pregnancy [155,156]

  • Specific environmental pollutants are produced en masse for novel technological developments, for instance, connected to the upsurge of electric vehicles in many countries, leading to an exponential production of batteries that may release novel molecules in our environment

Read more

Summary

Introduction

The placenta is an extraembryonic annex that develops as a major interface between the mother and the fetus in mammals. CTB are mononucleated cells that can fuse and differentiate into STB, a syncytium where nuclei share the same cytoplasm Both cell types are organized in highly branched (up to 16 degrees of ramification) tree-like structures called placental villi, which are embedded in spaces filled by maternal blood, constituting the intervillous space or lacunae (Figure 1). NOplugs stimulates, at the same time, VEGF functions as athe pro-angiogenic molecule Once these plugs these are removed around week 12 of pregnancy, maternal blood bathes the lacunae, alare removed around week of pregnancy, the maternal blood bathes the lacunae, allowing lowing the interchange of nutrients and gases between the mother and the foetus. OS induces the oxygen expression of antioxidants such as supermitochondrial and the release of reactive species (ROS) and reactive nitrogen oxide dismutase catalase (CAT),the glutathione peroxidase (GPx).such. Inducible growth factor (PIGF) implicated expression in endothelial growth and angiogenesis

What Is the Origin of Oxidative Stress in the Placenta?
What Are the Antioxidant Mechanisms in the Placenta?
Mechanisms of Oxidative Stress Induction by Environmental Pollutants
Exposure to Environmental Metals
Cadmium
Mercury and Methyl-Mercury
Chromium
Exposure to Tobacco
Exposure to Airborne Particulate Matter
Exposure to Vexing Biomolecules and Riling Toxins
Exposure to Organometallic Molecules and Endocrine Disrupters
Plastic Modifiers
Findings
Final Considerations and Conclusions
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call