Maternal Serum Melatonin Increases During Pregnancy and Falls Immediately After Delivery Implicating the Placenta as a Major Source of Melatonin

Ejaz, Haroon; Figaro, Juliana K.; Woolner, Andrea; Thottakam, Bensita Mary Viju Jose; Galley, Helen F.

doi:10.3389/fendo.2020.623038

Cited by 34 publications

(30 citation statements)

References 33 publications

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“…However, maternal blood and placenta melatonin concentrations of women are variable. Some authors report higher hormone concentration in the blood (Ejaz et al, 2021) and tissue (Lanoix et al, 2012), while others show lower levels (Bouchlariotou et al, 2014) similar to those valours found in blood and placenta in this study and colostrum (Morceli et al, 2013) from diabetic mothers.…”

Section: Discussionsupporting

confidence: 90%

Melatonin Hormone Acts on Cells of Maternal Blood and Placenta From Diabetic Mothers

et al. 2022

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Changes in glucose metabolism of diabetic mothers affect immunological components, proinflammatory factors, and placental hypervascularization that can induce cell death. The hormone melatonin has been identified as a potential modulating agent. The aim of this study was to analyze the oxidative process and the apoptosis in maternal blood and placental cells modulated by melatonin from diabetic mothers. The groups were 40 pregnant women divided into non-diabetic (ND) and type 2 diabetes mellitus (T2DM) groups. Blood and placental cells were obtained by density gradient and maintained in culture treated or not with melatonin (100 ng/mL) for 24 h (37°C, 5% CO2). Oxidative stress was evaluated by superoxide release and CuZn superoxide dismutase (SOD). Apoptosis was assessed by flow cytometry. Maternal hyperglycemia increased superoxide release and apoptosis in MN cells from maternal blood and reduced SOD level and SOD/O2- ratio. Melatonin reduced oxidative stress and apoptosis rates in MN cells in the blood of diabetic mothers. There was a reduction in SOD and SOD/O2- ratio in the placental extravillous layer, and melatonin restored the concentrations of this enzyme. There was greater superoxide release, reduced SOD/O2- ratio, and apoptosis in MN cells placental villous layer. Melatonin increased apoptosis rates in the placental villous layer from hyperglycemic mothers. These data suggest that hyperglycemia altered the processes oxidative in blood and placenta from hyperglycemic mothers. These changes reflected in the mechanisms of induction of apoptosis, especially in the vascularized layers of the placenta, and were modulated by melatonin.

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Section: Discussionsupporting

confidence: 90%

Melatonin Hormone Acts on Cells of Maternal Blood and Placenta From Diabetic Mothers

et al. 2022

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“…This endogenous synthesis of melatonin diminished with aging and made elderly patient more susceptible to infections or others inflammatory and neurodegenerative diseases 30 , 31 . Other life circumstances may modify this phenomenon like pregnancy 32 . Therefore, future research are needed to explore which innate and environmental factors influence this synthesis, the role of endogenous melatonin in the neonatal brain protection and the potential interaction with exogenous melatonin.…”

Section: Discussionmentioning

confidence: 99%

Partial protective effects of melatonin on developing brain in a rat model of chorioamnionitis

Favrais

Saliba

Savary

et al. 2021

Sci Rep

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Melatonin has shown promising neuroprotective effects due to its anti-oxidant, anti-inflammatory and anti-apoptotic properties, making it a candidate drug for translation to humans in conditions that compromise the developing brain. Our study aimed to explore the impact of prenatal melatonin in an inflammatory/infectious context on GABAergic neurons and on oligodendrocytes (OLs), key cells involved in the encephalopathy of prematurity. An inflammatory/infectious agent (LPS, 300 μg/kg) was injected intraperitoneally (i.p.) to pregnant Wistar rats at gestational day 19 and 20. Melatonin (5 mg/kg) was injected i.p. following the same schedule. Immunostainings focusing on GABAergic neurons, OL lineage and myelination were performed on pup brain sections. Melatonin succeeded in preventing the LPS-induced decrease of GABAergic neurons within the retrospenial cortex, and sustainably promoted GABAergic neurons within the dentate gyrus in the inflammatory/infectious context. However, melatonin did not effectively prevent the LPS-induced alterations on OLs and myelination. Therefore, we demonstrated that melatonin partially prevented the deleterious effects of LPS according to the cell type. The timing of exposure related to the cell maturation stage is likely to be critical to achieve an efficient action of melatonin. Furthermore, it can be speculated that melatonin exerts a modest protective effect on extremely preterm infant brains.

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“…Melatonin was originally identified as a hormone released from the pineal gland at night but not during the day and was known as the “dark hormone” that promoted sleep 46 . Melatonin is now known to be synthesized and released, but not in a circadian rhythm, from other tissues such as retina, bone marrow, gastrointestinal tract, and placenta 47–49 . When ingested by humans, it is regarded as having a good safety profile established over the last 50 years 50,51 .…”

Section: Therapeutic Options For Activating Nrf2 In “Long Covid” Subj...mentioning

confidence: 99%

“LONG COVID”—A hypothesis for understanding the biological basis and pharmacological treatment strategy

Jarrott

Head

Pringle

et al. 2022

Pharmacology Res & Perspec

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Infection of humans with SARS‐CoV‐2 virus causes a disease known colloquially as “COVID‐19” with symptoms ranging from asymptomatic to severe pneumonia. Initial pathology is due to the virus binding to the ACE‐2 protein on endothelial cells lining blood vessels and entering these cells in order to replicate. Viral replication causes oxidative stress due to elevated levels of reactive oxygen species. Many (~60%) of the infected people appear to have eliminated the virus from their body after 28 days and resume normal activity. However, a significant proportion (~40%) experience a variety of symptoms (loss of smell and/or taste, fatigue, cough, aching pain, “brain fog,” insomnia, shortness of breath, and tachycardia) after 12 weeks and are diagnosed with a syndrome named “LONG COVID.” Longitudinal clinical studies in a group of subjects who were infected with SARS‐CoV‐2 have been compared to a non‐infected matched group of subjects. A cohort of infected subjects can be identified by a battery of cytokine markers to have persistent, low level grade of inflammation and often self‐report two or more troubling symptoms. There is no drug that will relieve their symptoms effectively. It is hypothesized that drugs that activate the intracellular transcription factor, nuclear factor erythroid‐derived 2‐like 2 (NRF2) may increase the expression of enzymes to synthesize the intracellular antioxidant, glutathione that will quench free radicals causing oxidative stress. The hormone melatonin has been identified as an activator of NRF2 and a relatively safe chemical for most people to ingest chronically. Thus, it is an option for consideration of re‐purposing studies in “LONG COVID” subjects experiencing insomnia, depression, fatigue, and “brain fog” but not tachycardia. Appropriately designed clinical trials are required to evaluate melatonin.

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Maternal Serum Melatonin Increases During Pregnancy and Falls Immediately After Delivery Implicating the Placenta as a Major Source of Melatonin

Cited by 34 publications

References 33 publications

Melatonin Hormone Acts on Cells of Maternal Blood and Placenta From Diabetic Mothers

Melatonin Hormone Acts on Cells of Maternal Blood and Placenta From Diabetic Mothers

Partial protective effects of melatonin on developing brain in a rat model of chorioamnionitis

“LONG COVID”—A hypothesis for understanding the biological basis and pharmacological treatment strategy

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