Development of melatonin production in infants and the impact of prematurity.

Kennaway, David J.; Stamp, Georgina E.; Goble, Frans C.

doi:10.1210/jcem.75.2.1639937

Cited by 110 publications

(116 citation statements)

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“…In contrast, glutathione may be deficient in premature infants because of excessive oxidization by ROS coupled with reduced glutathione reductase reaction with the electron acceptor NADPH (72). Finally, melatonin acts as an antioxidant in the retina and brain (73), and its cyclic production is disrupted in premature infants (74), possibly increasing the risk of ROS-mediated damage.…”

Section: Antioxidant Defenses: Developmental Regulation and Vulnerabimentioning

confidence: 99%

Oxygen Toxicity and Reactive Oxygen Species: The Devil Is in the Details

2009

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ABSTRACT:Reactive oxygen species (ROS) serve as cell signaling molecules for normal biologic processes. However, the generation of ROS can also provoke damage to multiple cellular organelles and processes, which can ultimately disrupt normal physiology. An imbalance between the production of ROS and the antioxidant defenses that protect cells has been implicated in the pathogenesis of a variety of diseases, such as cancer, asthma, pulmonary hypertension, and retinopathy. The nature of the injury will ultimately depend on specific molecular interactions, cellular locations, and timing of the insult. This review will outline the origins of endogenous and exogenously generated ROS. The molecular, cellular, pathologic, and physiologic targets will then be discussed with a particular emphasis on aspects relevant to child development. Finally, antioxidant defenses that scavenge ROS and mitigate associated toxicities will be presented, with a discussion of potential therapeutic approaches for the prevention and/or treatment of human diseases using enzymatic and nonenzymatic antioxidants. . This review will focus on-1) origins of ROS: environment, cells, and cellular components; 2) molecular targets: classic and novel macromolecular targets and associated toxicity in infants and children; 3) antioxidant defenses: developmental regulation and vulnerabilities; and 4) antioxidant therapies: enzymatic and nonenzymatic approaches. Origins of ROSOxygen has a unique molecular structure and is abundant within cells. It readily accepts free electrons generated by normal oxidative metabolism within the cell, producing ROS, such as O 2 ·Ϫ and hydroxyl radical (HO · ), as well as the oxidant H 2 O 2 . Processes causing uncoupling of electron transport can enhance the production of ROS, with mitochondria being a major source (4). However, other cellular components, such as endoplasmic reticulum-bound enzymes, cytoplasmic enzyme systems, and the surface of the plasma membrane, also contribute (5,6). Activity of multiple enzyme systems, such as the cytochrome P 450 monoxygenase system, xanthine oxidoreductase, nitric oxide synthases, and several others involved in the inflammatory process (cyclooxygenase and lipoxygenase), can also increase the generation of ROS.

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Section: Antioxidant Defenses: Developmental Regulation and Vulnerabimentioning

confidence: 99%

Oxygen Toxicity and Reactive Oxygen Species: The Devil Is in the Details

2009

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“…Some evidence links pineal dysfunction and impaired development with increased prevalence of SIDS (6,7). A delayed melatonin production was found in infants who had experienced an apparent lifethreatening event (ALTE) (6).…”

mentioning

confidence: 99%

“…The ontogeny of melatonin production has been extensively studied (7)(8)(9)(10)(11). The urinary metabolite of melatonin, 6-sulfatoxymelatonin (6SMT), has been proven to be a very reliable index of melatonin production in humans including infants (11).…”

mentioning

confidence: 99%

Melatonin Production in Healthy Infants: Evidence for Seasonal Variations

Sivan¹,

Laudon

Tauman³

et al. 2001

Pediatr Res

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The objective of this study was to determine the normal range of nocturnal urinary excretion of the major melatonin metabolite, 6-sulfatoxymelatonin (6SMT) in a large sample of healthy fullterm infants (8 and 16 wk old) and assess whether the endogenous production of melatonin changes with season. 6SMT was assessed in urine samples extracted from disposable diapers removed from full-term, 8-(n ϭ 317) and 16-wk-old (n ϭ 93) infants over the nocturnal period (19:00 -08:00 h). In addition, 6SMT was assessed in 8-wk-old (n ϭ 35) healthy infants over the entire 24-h period. 6SMT was determined by an ELISA assay. 6SMT excretion at 8 wk of age exhibited diurnal variations with (mean Ϯ SD) 61 Ϯ 18% of the daily production excreted during the nocturnal period regardless of season. The nocturnal 6SMT values in the entire cohort (at 8 as well as 16 wk of age) were found to significantly depart from normal distribution (Kolmogorov-Smirnov test). A normal distribution was obtained using a natural base logarithmic (ln) transformation of the data. The normal range (2.5-97.5 percentile of the ln 6SMT excretion per night) was thus defined as 4.66 -8.64 (106 -5646 ng/night) for 8-wk-old and 5.19 -9.67 (180 -15,820 ng/night) for 16-wk-old infants. A significant effect of the month of birth on 6SMT production at the age of 8 wk was found (ANOVA, p Ͻ 0.002) with maximal levels produced by infants born in June (summer solstice) and minimal excretion in infants born in December (winter solstice). Short-photoperiod-born infants excreted on average about threefold less 6SMT compared with long-photoperiod-born infants (t test, p ϭ 0.01). The seasonal variations were no longer present at 16 wk of age. No effect of breast-feeding at the time of sampling on seasonality of 6SMT was found. Normal ranges for the nocturnal urinary excretion of 6SMT in full-term infants at 8 and 16 wk of age are defined. This enables the evaluation of nocturnal 6SMT excretion as a prognostic and diagnostic factor for child development. The strong effect of season on the normal excretion of nocturnal 6SMT at 8 but not 16 wk of age suggests prenatal influence of the photoperiod on the ontogeny of melatonin. The changes in photoperiod are major environmental cues for initiating seasonal acclimatization of thermoregulatory mechanisms and reproduction. In all mammals studied to date, including humans, the nocturnal production of melatonin by the pineal gland reflects the photoperiod (1, 2) and plays a key role in seasonal acclimation. Humans are not considered photoperiod sensitive, although some disorders such as seasonal affective disorders (3) and cluster headache (4) have been associated with a particular season.Sudden infant death syndrome (SIDS) was shown to occur more frequently during the winter months, during the night, and during the first months of life (5). Some evidence links pineal dysfunction and impaired development with increased prevalence of SIDS (6, 7). A delayed melatonin production was found in infants who had experienced an apparent lifethreate...

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“…21 The daily rhythm of melatonin secretion is not present at birth, but develops in the 1st months of life, [22][23][24][25] is strongest at around 4-7 years of age and then steadily decreases in amplitude across the lifespan. [26][27][28] In adolescence, the onset and offset of melatonin secretion have been shown to be delayed with increasing age and throughout pubertal development.…”

Section: Factors Modulating Developmental Changes In the Sleep-wake Cmentioning

confidence: 99%

Variations in the sleep–wake cycle from childhood to adulthood: chronobiological perspectives

Carpenter¹,

Robillard²,

Hickie³

2015

CPT

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Changes in the sleep-wake cycle across development from childhood to adulthood, typically involve a steady shortening of the sleep period and a delay of sleep phase, with a period of more rapid change across adolescence. Accompanying these changes is the maturation of neuroendocrine rhythms such as melatonin, cortisol, and pubertal hormones. These endogenous rhythms are closely associated with behavioral changes in rest and activity rhythms, although environmental factors such as light exposure and academic and social demands likely play an interactive role. Other behavioral aspects, such as physical activity and eating behaviors, are also associated with changes in sleep-wake rhythms, and may be mediational factors in the development of physical illnesses. The sleep-wake cycle and related factors are implicated in the development of mental illnesses. There are several potential avenues of future research that may be valuable in terms of improving interventions and treatments for both mental and physical illnesses.

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Development of melatonin production in infants and the impact of prematurity.

Cited by 110 publications

References 9 publications

Oxygen Toxicity and Reactive Oxygen Species: The Devil Is in the Details

Oxygen Toxicity and Reactive Oxygen Species: The Devil Is in the Details

Melatonin Production in Healthy Infants: Evidence for Seasonal Variations

Variations in the sleep–wake cycle from childhood to adulthood: chronobiological perspectives

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Development of melatonin production in infants and the impact of prematurity.

Cited by 110 publications

References 9 publications

Oxygen Toxicity and Reactive Oxygen Species: The Devil Is in the Details

Oxygen Toxicity and Reactive Oxygen Species: The Devil Is in the Details

Melatonin Production in Healthy Infants: Evidence for Seasonal Variations

Variations in the sleep&ndash;wake cycle from childhood to adulthood: chronobiological perspectives

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Variations in the sleep–wake cycle from childhood to adulthood: chronobiological perspectives