Preeclampsia

What is preeclampsia?

Preeclampsia is a serious pregnancy complication characterized by high blood pressure and signs of damage to other organ systems, most commonly the liver and kidneys. It usually begins after 20 weeks of pregnancy in women whose blood pressure had been normal. Left untreated, preeclampsia can lead to serious, even fatal, complications for both the mother and the baby.

 

Preeclampsia is thought to occur due to problems with the placenta, which supplies the baby with nutrients and oxygen during pregnancy. Factors that may increase the risk of developing preeclampsia include:

 

• First pregnancy
• History of preeclampsia or high blood pressure in previous pregnancies
• Obesity
• Multiple pregnancies (twins, triplets, etc.)
• Being younger than 20 or older than 40
• Certain medical conditions, such as chronic hypertension, diabetes, kidney disease, or autoimmune disorders

 

The exact cause of preeclampsia is not known, but it is believed to involve problems with the development of the placenta and the interaction between the mother’s immune system and the placenta. These problems can lead to reduced blood flow to the placenta, oxidative stress, inflammation, and release of substances into the maternal bloodstream that affect blood vessel function and cause high blood pressure.

 

What is the relationship between preeclampsia and oxidative stress?

The relationship between preeclampsia and oxidative stress is an area of active research, and while the exact mechanisms are not fully understood, there is evidence to suggest that oxidative stress plays a significant role in the pathogenesis of preeclampsia.

 

• Placental Dysfunction: Oxidative stress is believed to contribute to abnormalities in placental function, which play a central role in the development of preeclampsia. During pregnancy, the placenta undergoes rapid growth and extensive vascularization to support the growing fetus. Dysregulation of oxidative stress pathways within the placenta can lead to inadequate blood flow, impaired placental development, and the release of pro-inflammatory and vasoconstrictive factors into the maternal circulation, contributing to the development of hypertension and other symptoms of preeclampsia.

 

• Endothelial Dysfunction: Oxidative stress can impair endothelial function, which refers to the ability of the cells lining blood vessels to regulate vascular tone and maintain vascular integrity. In preeclampsia, endothelial dysfunction is a hallmark feature and contributes to the widespread vascular abnormalities observed in the condition, including vasoconstriction, increased vascular permeability, and thrombosis. Elevated levels of oxidative stress markers have been found in the endothelial cells of women with preeclampsia, suggesting a direct role for oxidative stress in endothelial dysfunction.

 

• Inflammation: Oxidative stress can trigger inflammatory responses within the placenta and maternal circulation, leading to the release of pro-inflammatory cytokines, chemokines, and other mediators of inflammation. Chronic low-grade inflammation is believed to be involved in the pathogenesis of preeclampsia and contributes to endothelial dysfunction, vascular damage, and systemic complications. Oxidative stress and inflammation can create a vicious cycle, as inflammation can further increase oxidative stress and exacerbate tissue damage.

 

• Oxidative Damage: Increased oxidative stress in preeclampsia results in the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which can damage cellular structures such as lipids, proteins, and DNA. Oxidative damage to the placenta, endothelium, and other tissues may contribute to the pathophysiology of preeclampsia by disrupting cellular function, impairing vascular homeostasis, and promoting tissue injury and dysfunction.

 

Overall, oxidative stress is believed to be a key contributor to the development and progression of preeclampsia, acting through multiple pathways to promote placental dysfunction, endothelial dysfunction, inflammation, and oxidative damage.