Protective effect of maternal prenatal melatonin administration on rat pups born to mothers submitted to constant light during gestation

Cisternas, Carla D.; Compagnucci, Maurizio; Conti, Nathalie; Ponce, Rubén Hugo; Vermouth, Nelia T.

doi:10.1590/s0100-879x2010007500083

Cited by 19 publications

(18 citation statements)

References 37 publications

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“…It is known that prenatal stress initiated before day 11 of gestation disrupts the maternal melatonin rhythm [Persengiev et al, 1991] and could consequently affect the synchronization of fetal suprachiasmatic nucleus. The fetus is exposed to the maternal melatonin rhythm, and hence indirectly to light/dark information [Cisternas et al, 2010]. However, exposure to light at night suppresses the nocturnal peak of maternal melatonin, depriving the fetus of a light/ dark signal [Torres-Farfán et al, 2006].…”

Section: Discussionmentioning

confidence: 99%

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Prenatal Exposure to Continuous Constant Light Alters Endochondral Ossification of the Tibiae of Rat Pups

Fontanetti

Nervegna

Vermouth

et al. 2014

Cells Tissues Organs

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Clinical and experimental studies suggest that prenatal exposure to stress can impact the growth and development of offspring. The effect of prenatal exposure to constant light, applied as a chronic stressor, on endochondral ossification of the tibiae of 3-day-old and 15-day-old pups was histomorphometrically evaluated. Pregnant rats were divided into 2 groups: mothers chronically exposed to a 12:12-hour light/light cycle (LL) and control mothers maintained on a 12:12-hour light/dark cycle on days 10-20 of pregnancy. On postnatal days 3 and 15, the pups were weighed and euthanized. The tibiae were resected and histologically processed to obtain sections for hematoxylin and eosin staining (HE) and tartrate-resistant acid phosphatase (TRAP) histochemistry, in order to perform histomorphometric determinations. The data were statistically analyzed. A significant decrease in hypertrophic cartilage thickness was observed in the tibiae of the 3-day-old (LL: 0.134 ± 0.02 vs. controls: 0.209 ± 0.023 mm; p < 0.01) and 15-day-old (LL: 23.32 ± 3.98 vs. controls: 22.96 ± 1.93 mm; p < 0.05) prenatally stressed pups. The subchondral bone volume was significantly lower in the tibiae of the 3-day-old LL pups (38.83 ± 6.14%) than in the controls (62.83 ± 10.67%; p < 0.01). The decrease in subchondral bone volume and hypertrophic cartilage thickness shows that the normal growth process of the tibia is impaired in prenatally stressed pups.

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Section: Discussionmentioning

confidence: 99%

“…days 10-20 of gestation. The constant-light model was validated in previous studies performed at our laboratory demonstrating that constant light initiated on day 10 of gestation interrupts maternal fetal synchronization, which begins on days 11-12 of gestation [Bellavía et al, 1996;Cisternas et al, 2010;Fontanetti et al, 2013].…”

Section: Animal Groupsmentioning

confidence: 95%

Prenatal Exposure to Continuous Constant Light Alters Endochondral Ossification of the Tibiae of Rat Pups

Fontanetti

Nervegna

Vermouth

et al. 2014

Cells Tissues Organs

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“…As shown in Table 1, a variety of early-life insults have been reported to cause developmental programming of adult diseases. These environmental and nutritional insults include maternal undernutrition [42], N G -nitro- l -arginine-methyester (L-NAME) induced preeclampsia [43], high-fructose consumption [63], prenatal hypoxia [64], glucocorticoid exposure [33,36,37,38,39,40,65], high-fat diet [40], and constant light exposure [66]. These insults induce a number of programming effects on adult offspring including hypertension, reduced nephron number, cognition deficit, behavior dysfunction, obesity, and liver steatosis.…”

Section: Melatonin As a Reprogramming Therapy In Animal Models Of mentioning

confidence: 99%

“…Thus, the influence of melatonin on adult offspring should be considered as reprogramming instead of direct effects. So far, a few mechanisms, including oxidative stress [42,43,63,65], epigenetic regulation [38,39,40], reduction in nephron numbers [39], and alterations of the RAS [40] have been linked to the reprogramming effects of melatonin.…”

Section: Melatonin As a Reprogramming Therapy In Animal Models Of mentioning

confidence: 99%

Developmental Programming of Adult Disease: Reprogramming by Melatonin?

Tain

Huang

Hsu

2017

IJMS

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Adult-onset chronic non-communicable diseases (NCDs) can originate from early life through so-called the “developmental origins of health and disease” (DOHaD) or “developmental programming”. The DOHaD concept offers the “reprogramming” strategy to shift the treatment from adulthood to early life, before clinical disease is apparent. Melatonin, an endogenous indoleamine produced by the pineal gland, has pleiotropic bioactivities those are beneficial in a variety of human diseases. Emerging evidence support that melatonin is closely inter-related to other proposed mechanisms contributing to the developmental programming of a variety of chronic NCDs. Recent animal studies have begun to unravel the multifunctional roles of melatonin in many experimental models of developmental programming. Even though some progress has been made in research on melatonin as a reprogramming strategy to prevent DOHaD-related NCDs, future human studies should aim at filling the translational gap between animal models and clinical trials. Here, we review several key themes on the reprogramming effects of melatonin in DOHaD research. We have particularly focused on the following areas: mechanisms of developmental programming; the interrelationship between melatonin and mechanisms underlying developmental programming; pathophysiological roles of melatonin in pregnancy and fetal development; and insight provided by animal models to support melatonin as a reprogramming therapy. Rates of NCDs are increasing faster than anticipated all over the world. Hence, there is an urgent need to understand reprogramming mechanisms of melatonin and to translate experimental research into clinical practice for halting a growing list of DOHaD-related NCDs.

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“…Последние значительно оптимизируют формирование микрофлоры кишечника, активно участвующей в синтезе и метаболизме мелатонина [71,72]. В последние годы внимание исследователей привлечено к изучению в эксперименте эффекта применения мелатонина во время беременности и в постнатальном онтогенезе с целью репрограммирования развития патологий [73][74][75], что позволит определить объективные критерии риска и разработать методы профилактики патологических процессов.…”

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Role of the maternal melatonin circadian rhythm absence in early catch-up growth in children

Evsyukova

Ailamazyan

2020

Z.akus.zen.bolezn

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The review presents the results of experimental and clinical studies, according to which the absence of circadian melatonin production in pregnant women associated with the pathologies they have (obesity, diabetes mellitus, metabolic syndrome, pregnancy complicated by gestosis and chronic placental insufficiency, etc.) disrupts the genetic process of organizing the rhythmic activity of genes of the suprachiasmatic nuclei of the hypothalamus and melatonin production in the pineal gland of the fetus, leading to dysregulation of metabolic processes in the childs body after birth and programming pathology in following life. The significance of this factor in the pathophysiological mechanisms of catch-up growth during the first months of life determines a new approach to assessing the risk of obesity and necessitates learning the consequences of impaired development of the brain and other functional systems in fetuses that are born earlier than the 26th week of pregnancy and are thereby deprived of maternal melatonin, a key signaling molecule that directs and coordinates the genetic development process, during the most critical period of early ontogenesis.

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Protective effect of maternal prenatal melatonin administration on rat pups born to mothers submitted to constant light during gestation

Cited by 19 publications

References 37 publications

Prenatal Exposure to Continuous Constant Light Alters Endochondral Ossification of the Tibiae of Rat Pups

Prenatal Exposure to Continuous Constant Light Alters Endochondral Ossification of the Tibiae of Rat Pups

Developmental Programming of Adult Disease: Reprogramming by Melatonin?

Role of the maternal melatonin circadian rhythm absence in early catch-up growth in children

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