Future applications of antioxidants in premature infants

Lee, Jennifer W.; Davis, Jonathan M.

doi:10.1097/mop.0b013e3283423e51

Cited by 138 publications

(97 citation statements)

References 44 publications

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“…This finding is in perfect accordance with the previous data published by other investigators (23)(24)(25)(26)(27), and could be explained by the inadequate supply of specific cofactors, essential for the proper functioning of these enzymes: copper, zinc and selenium, respectively; since placental maternal-to-fetal passage is very limited before (the latter part of) the third trimester (28). Production and activity of antioxidant enzymes increase markedly in the final days before birth, and even more so after birth (29). Therefore, premature birth could itself be considered an illness with a major oxidative component.…”

Section: Discussionsupporting

confidence: 78%

Cord Blood Superoxide Dismutase and Glutathione Peroxidase Activity in Premature Infants / Aktivnost Superoksid-Dismutaze I Glutation-Peroksidaze Kod Prevremeno Rodene Dece

Guržanova-Durnev¹,

Zisovska²,

Dosić-Markovska³

2013

Journal of Medical Biochemistry

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SummaryBackground: Birth involves strong oxidative stress for the infant, implying an increased production of free radicals. The aims of this study were to assess the antioxidant response to oxidative insult at birth, by estimating the superoxide dismutase (SOD) and glutathione peroxidase (GPX) activity in umbilical cord blood, and to evaluate their dependency on the degree of maturation of the newborns. Methods: In the present study, 60 preterm infants (study group) as well as a full-term healthy reference group (A=53) were included. Additionally, the preterms were divided in 3 groups according to their condition at the end of the 1st week of life: preterm control (B=25), on oxygen support (C=18), and ventilated group (D=17). Results: The obtained results indicate markedly lower antioxidant capacity of the preterm infants: they had significantly lower SOD and GPX activity than the full-term infants (p<0.001, for both). Investigated antioxidants also showed significant differences between the groups of preterms. SOD activity was higher in preterms with postnatal respiratory failure compared to preterm control (p<0.001). On the contrary, GPX activity was decreased in the oxygen supported group (10%) and even more in the ventilated group (28.5%) (p<0.001, for both). The newborns enzyme activities were also profoundly modulated by the gestational age and birth weight, specifically the GPX.

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Section: Discussionsupporting

confidence: 78%

Cord Blood Superoxide Dismutase and Glutathione Peroxidase Activity in Premature Infants / Aktivnost Superoksid-Dismutaze I Glutation-Peroksidaze Kod Prevremeno Rodene Dece

Guržanova-Durnev¹,

Zisovska²,

Dosić-Markovska³

2013

Journal of Medical Biochemistry

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“…Markers of oxidative stress are often overexpressed in the airways in several chronic lung disorders, and they are linked to ongoing airway inflammation and remodelling [12]. Oxidative stress has also been consistently associated with lung injury early in life, in infants who progress towards BPD [13], and there is increasing evidence to link early exposure to oxidative stress with potentially lifelong consequences [14]. Oxygen radicals have many complex effects on the body's homeostasis, being involved in normal organ development and contributing to several physiological functions [13].…”

mentioning

confidence: 99%

Evidence of unexpected oxidative stress in airways of adolescents born very pre-term

Filippone¹,

Bonetto²,

Corradi

et al. 2012

Eur Respir J

103

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Prematurity and its main respiratory complication, bronchopulmonary dysplasia (BPD), are potentially associated with lifelong respiratory morbidities and/or lung function abnormalities. The mechanisms behind these long-term respiratory problems are still unclear.We assessed airway oxidative stress in adolescents born very pre-term (f32 gestational weeks) by measuring 8-isoprostane concentration in exhaled breath condensate (EBC). In addition, the study protocol included spirometry and measurement of exhaled nitric oxide fraction (FeNO).The study groups included 34 ex-pre-term adolescents with BPD, 18 ex-pre-term adolescents without BPD and 34 healthy controls born at term.Regardless of a history of BPD, the ex-premature adolescents had higher EBC 8-isoprostane levels (median (interquartile range) BPD 9.5 (7.3-12.2) pg?mL -1 ; pre-term non-BPD 10 (8.1-16) pg?mL -1 ) than the controls (3.2 (1.9-6.5) pg?mL -1 ) (p,0.001). Forced expiratory volume in 1 s was lower in the BPD group (mean¡SD Z-score -2.1¡1.58) than in the pre-term non-BPD individuals (-1.13¡1.15), who showed in turn significantly lower values than the controls (0.18¡0.83; p,0.001). FeNO was similar in the three groups (p50.55).Our data show that, after premature birth, evidence of oxidative stress in the airways may be detected into adolescence, suggesting that long-term respiratory abnormalities after pre-term birth may be associated with an ongoing airway disease and not just a stabilised structural lung damage.

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“…In addition to these agents, antioxidants are believed to represent a promising treatment option, not only for preterm birth (7,14,24) but also for neonatal disorders, bronchopulmonary dysplasia, retinopathy of prematurity, necrotizing enterocolitis, and periventricular leukomalacia (25). We showed that TRX is one of the potential agents for intrauterine infection/inflammation by its antioxidant and anti-inflammatory properties.…”

Section: Discussionmentioning

confidence: 93%

Human thioredoxin-1 attenuates the rate of lipopolysaccharide-induced preterm delivery in mice in association with its anti-inflammatory effect

et al. 2016

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Background:Maternal intrauterine infection/inflammation represents the major etiology of preterm delivery and the leading cause of neonatal mortality and morbidity. The aim of this study was to investigate the anti-inflammatory properties of thioredoxin-1 in vivo and its potential ability to attenuate the rate of inflammation-induced preterm delivery. Methods: Two intraperitoneal injections of lipopolysaccharide from Escherichia coli were administered in pregnant mice on gestational day 15, with a 3-h interval between the injections. From either 1 h before or 1 h after the first lipopolysaccharide injection, mice received three intravenous injections of either recombinant human thioredoxin-1, ovalbumin, or vehicle, with a 3-h interval between injections. results: Intraperitoneal injection of lipopolysaccharide induced a rise of tumor necrosis factor-α, interferon-γ, monocyte chemotactic protein 1, and interleukin-6 in maternal serum levels and provoked preterm delivery. Recombinant human thoredoxin-1 prevented the rise in these proinflammatory cytokine levels. After the inflammatory challenge, placentas exhibited severe maternal vascular dilatation and congestion and a marked decidual neutrophil activation. These placental pathological findings were ameliorated by recombinant human thioredoxin-1, and the rate of inflammation-induced preterm delivery was attenuated. conclusion: Thioredoxin-1 may thus represent a novel effective treatment to delay inflammation-induced preterm delivery.t he estimated number of preterm births (defined as birth before gestational week 37) worldwide was 15 million in 2010 (11.1%) (1). Preterm birth is the most frequent cause of infant mortality and leads to one million deaths per year. Premature infants face increased risk of neonatal complications, such as intraventricular hemorrhage, bronchopulmonary dysplasia, retinopathy, and necrotizing enterocolitis as well as increased risk of adult-onset obesity, diabetes, and hypertension (2,3).Intrauterine infection or inflammation caused by various bacteria, including Escherichia coli, Gardnerella vaginalis, anaerobic bacteria, and genital mycoplasmas, can lead to preterm birth (4,5). Animal models of bacterial componentinduced preterm birth have been established (6,7).Thioredoxin-1 (TRX), originally cloned as a soluble factor called adult T-cell leukemia-derived factor (8), is one of the most important molecules controlling the redox regulation system and contains a redox-active disulfide/dithiol within the conserved active site sequence Cys 32 -Gly-Pro-Cys 35 (ref. (9)). TRX has a pivotal role in scavenging reactive oxygen species (ROS) with peroxiredoxins, and thus, it prevents apoptosis of various cells (10). Moreover, circulating TRX inhibits neutrophil infiltration into the sites of inflammation by blocking the adhesion of lipopolysaccharide (LPS)-stimulated neutrophils on endothelial cells (11). Overexpression of human TRX in transgenic mice induced resistance to harmful conditions, including thioacetamide-or LPS-induced acute hepati...

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Future applications of antioxidants in premature infants

Cited by 138 publications

References 44 publications

Cord Blood Superoxide Dismutase and Glutathione Peroxidase Activity in Premature Infants / Aktivnost Superoksid-Dismutaze I Glutation-Peroksidaze Kod Prevremeno Rodene Dece

Cord Blood Superoxide Dismutase and Glutathione Peroxidase Activity in Premature Infants / Aktivnost Superoksid-Dismutaze I Glutation-Peroksidaze Kod Prevremeno Rodene Dece

Evidence of unexpected oxidative stress in airways of adolescents born very pre-term

Human thioredoxin-1 attenuates the rate of lipopolysaccharide-induced preterm delivery in mice in association with its anti-inflammatory effect

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