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Preeclampsia (PE) is a pregnancy-specific syndrome with multisystem involvement which leads to fetal, neonatal, and maternal morbidity and mortality. A model of salt-loaded pregnant rats has been previously studied, sharing several pathological characteristics of preeclamptic women. In this study, it was compared the effects of the treatment with an oral magnesium salt, magnesium gluconate (Mg-gluconate), on the osmotic fragility of red blood cells, lipid peroxidation, and PMCA activity of placental homogenates and red blood cell ghosts in salt-loaded pregnant rats. Mg-gluconate has a higher antioxidant capacity than MgSO

Preeclampsia is a pregnancy-specific syndrome with multisystem involvement which leads to foetal, neonatal, and maternal morbidity and mortality. This syndrome is characterized by the onset of clinical signs and symptoms and delivery before (early-onset preeclampsia, eoPE), or after (late-onset preeclampsia, loPE), the 34 weeks of gestation. Preeclampsia is a mitochondrial disorder where its differential involvement in eoPE and loPE is unclear. Mitochondria regulate cell metabolism and are a significant source of reactive oxygen species (ROS). The syncytiotrophoblast in eoPE and loPE show altered mitochondrial structure and function resulting in ROS overproduction, oxidative stress, and cell damage and death. Mitochondrial dysfunction in eoPE may result from altered expression of several molecules, including dynamin-related protein 1 and mitofusins, compared with loPE where these factors are either reduced or unaltered. Equally, mitochondrial fusion/fission dynamics seem differentially modulated in eoPE and loPE. It is unclear whether the electron transport chain and oxidative phosphorylation are differentially altered in these two subgroups of preeclampsia. However, the activity of complex IV (cytochrome c oxidase) and the expression of essential proteins involved in the electron transport chain are reduced, leading to lower oxidative phosphorylation and mitochondrial respiration in the preeclamptic placenta. Interventional studies in patients with preeclampsia using the coenzyme Q10, a key molecule in the electron transport chain, suggest that agents that increase the antioxidative capacity of the placenta may be protective against preeclampsia development. In this review, the mitochondrial dysfunction in both eoPE and loPE is summarized. Therapeutic approaches are discussed in the context of contributing to the understanding of mitochondrial dysfunction in eoPE and loPE.

SARS-CoV-2 causes coronavirus disease 2019 (COVID-19) also in pregnant women. Infection in pregnancy leads to maternal and placental functional alterations. Pregnant women with vascular defects such as preeclampsia show high susceptibility to SARS-CoV-2 infection by undefined mechanisms. Pregnant women infected with SARS-CoV-2 show higher rates of preterm birth and caesarean delivery, and their placentas show signs of vasculopathy and inflammation. It is still unclear whether the foetus is affected by the maternal infection with this virus and whether maternal infection associates with postnatal affections. The SARS-CoV-2 infection causes oxidative stress and activation of the immune system leading to cytokine storm and next tissue damage as seen in the lung. The angiotensin-converting-enzyme 2 expression is determinant for these alterations in the lung. Since this enzyme is expressed in the human placenta, SARS-CoV-2 could infect the placenta tissue, although reported to be of low frequency compared with maternal lung tissue. Early-onset preeclampsia (eoPE) shows higher expression of ADAM17 (a disintegrin and metalloproteinase 17) causing an imbalanced renin-angiotensin system and endothelial dysfunction. A similar mechanism seems to potentially account for SARS-CoV-2 infection. This review highlights the potentially common characteristics of pregnant women with eoPE with those with COVID-19. A better understanding of the mechanisms of SARS-CoV-2 infection and its impact on the placenta function is determinant since eoPE/COVID-19 association may result in maternal metabolic alterations that might lead to a potential worsening of the foetal programming of diseases in the neonate, young, and adult.

The role of oxidative stress in the physiopathology of human pregnancy is of particular interest. Pregnancy is well-known to increase the oxidative stress, mainly produced by a normal systemic inflammatory response, which results in high amounts of circulating reactive oxygen species (ROS) and reactive nitrogen species (RNS). Both ROS and RNS play an important role as secondary messengers in many intracellular signalling cascades. However, they can also exert critical effects on pathological processes involving the pregnant woman. ROS, RNS and antioxidants establish a balance that determines the oxidation status of animals and humans. This review focuses on the mechanism of oxidative stress in pregnancy as well as its involvement and consequences on the human pregnancy-specific clinical syndrome preeclampsia. Organización Mundial de la Salud H9/181/R427 Fondo Nacional de Ciencia Tecnología e Innovación (FONACIT) F-2005000222 Agencia Española de Cooperación Internacional para el Desarrollo (AECID) C/024225/09, D/031187/10, A1/036123/11 Junta de Andalucía CTS-584 Fondo Nacional de Desarrollo Científico y Tecnológico (FONDECYT) 1150377, 11150083

Objective: To evaluate the osmotic fragility of red blood cells and the level of lipid peroxidation, the Ca2+-ATPase activity of red cell ghosts and placental homogenates from salt-loaded pregnant rats.Methods: Salt-loaded pregnant rats received 1.8% NaCl solution ad libitum as a beverage for seven days, starting on 15th day of pregnancy. Then, it was evaluated the level of lipid peroxidation and the Ca2+-ATPase activity of placental homogenates and red blood cell ghosts from control and experimental rats. Furthermore, the osmotic fragility of the red blood cells was evaluated by measuring the lysis of these cells when incubated with a NaCl solution with different osmolarities.Results: It was found that placental homogenates and red blood cell ghosts from experimental pregnant rats showed an increased level of lipid peroxidation and a lowered Ca2+-ATPase activity, as compared to control pregnant rats. They also presented an increased osmotic fragility of their red blood cells.Conclusions: Salt-loa...

To evaluate the osmotic fragility of red blood cells and the level of lipid peroxidation, the Ca(2+)-ATPase activity of red cell ghosts and placental homogenates from salt-loaded pregnant rats.Salt-loaded pregnant rats received 1.8% NaCl solution ad libitum as a beverage for seven days, starting on 15th day of pregnancy. Then, it was evaluated the level of lipid peroxidation and the Ca(2+)-ATPase activity of placental homogenates and red blood cell ghosts from control and experimental rats. Furthermore, the osmotic fragility of the red blood cells was evaluated by measuring the lysis of these cells when incubated with a NaCl solution with different osmolarities.It was found that placental homogenates and red blood cell ghosts from experimental pregnant rats showed an increased level of lipid peroxidation and a lowered Ca(2+)-ATPase activity, as compared to control pregnant rats. They also presented an increased osmotic fragility of their red blood cells.Salt-loaded pregnant rats showed, similar to preeclamptic women, an increased level of lipid peroxidation and a lowered Ca(2+)-ATPase activity in placental and red blood cells membranes, as well as an increased osmotic fragility of the red blood cells.