New biomarkers of fetal‐neonatal hypoxic stress

Perrone, Serafina; Bracci, Rodolfo; Buonocore, Giuseppe

doi:10.1111/j.1651-2227.2002.tb02919.x

Cited by 37 publications

(26 citation statements)

References 38 publications

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“…Studies of neonatal cord blood indicate that increased activin protein levels may provide a reliable marker of perinatal hypoxia (Perrone et al, 2002;Bracci et al, 2006). In our hands, decreased oxygen capacity initiates activin mRNA increases in mice.…”

Section: Discussionmentioning

confidence: 60%

Activin is a Neuronal Survival Factor that is Rapidly Increased after Transient Cerebral Ischemia and Hypoxia in Mice

Mukerji

Katsman

Wilber

et al. 2006

J Cereb Blood Flow Metab

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One approach for developing targeted stroke therapies is to identify the neuronal protective and destructive signaling pathways and gene expression that follow ischemic insult. In some neural injury models, the transforming growth factor-beta family member activin can provide neuroprotective effects in vivo and promote neuronal survival. This study tests if activin supports cortical neurons after ischemic challenge in vitro and if signals after cerebral ischemia involve activin in vivo. In a defined cell culture model that uses hydrogen peroxide (H2O2)-free radical stress, activin addition maintained neuronal survival. H2O2 treatment increased activin mRNA twofold in surviving cortical neurons, and inhibition of activin with neutralizing antibodies caused neuronal death. These data identify activin gene changes as a rapid response to oxidative stress, and indicate that endogenous activin acts as a protective factor for cortical neurons in vitro. Similarly, after transient focal cerebral ischemia in adult mice, activin mRNA increased at 1 and 4 h ipsilateral to the infarct but returned to control values at 24 h after reperfusion. Intracellular activated smad signals were detected in neurons adjacent to the infarct. Activin was also increased after 2 h of 11% hypoxia. Activin mRNA increased at 1 h but not 4 or 24 h after hypoxia, similar to the time course of erythropoietin and vascular endothelial growth factor induction. These findings identify activin as an early-regulated gene response to transient ischemia and hypoxia, and its function in cortical neuron survival during oxidative challenge provides a basis to test activin as a potential therapeutic in stroke injury.

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Section: Discussionmentioning

confidence: 60%

Activin is a Neuronal Survival Factor that is Rapidly Increased after Transient Cerebral Ischemia and Hypoxia in Mice

Mukerji

Katsman

Wilber

et al. 2006

J Cereb Blood Flow Metab

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“…R eactive oxygen species are thought to be responsible for a variety of diseases of preterm infants, such as bronchopulmonary dysplasia, retinopathy of prematurity, hypoxic/ ischemic encephalopathy (1), and are considered to play a key role in some maternal pregnancy diseases and fetal development (2)(3)(4)(5). Free radical (FR) damage in the neonate may result from both accelerated FR production and low antioxidant levels (6,7).…”

mentioning

confidence: 99%

Plasma Esterified F2-Isoprostanes and Oxidative Stress in Newborns: Role of Nonprotein-Bound Iron

et al. 2008

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Nonprotein-bound iron (NPBI) and F 2 -isoprostanes, reliable markers of oxidative stress, are increased in plasma of newborns and inversely correlated to the gestational age. Because NPBI represents a pro-oxidant stimulus in plasma, we test the hypothesis that the entity of lipid peroxidation is related with NPBI concentrations. Plasma levels of free, esterified, and total F 2 -isoprostanes were investigated in relation to NPBI levels in 59 newborns and 16 healthy adults. The pro-oxidant role of iron was ascertained in vitro, by measuring all the forms of F 2 -isoprostanes after incubation with ammonium iron sulfate. Significant positive correlations were found between NPBI and total as well as esterified F 2 -isoprostanes in plasma of the newborns. The addition of ammonium iron sulfate induced a marked increase in all the forms of F 2 -isoprostanes after 2 hours of incubation. The higher NPBI concentration, the higher F 2 -isoprostanes levels. An increase NPBI dose dependent in total F 2 -isoprostanes formation was observed in dialyzed low density lipoprotein from adult plasma. The results clearly show that once NPBI is generated, whatever its source, it is capable of inducing oxidative stress. NPBI-induced oxidative stress may contribute to the morbidity in preterm infants that are particularly susceptible to free radical damage. (Pediatr Res 63: 287-291, 2008)

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“…Premature infants, in particular, are often exposed to supplemental oxygen concentrations as high as 95% (4,5); the result of which is the overproduction of reactive oxygen species (ROS). Numerous health conditions among preterm infants that are linked to oxidative stress include bronchopulmonary dysplasia, retinopathy of prematurity, intraventricular hemorrhage, necrotizing enterocolitis, and renal failure; all of which can lead to subsequent long-term complications in the physical and neurologic development of the child (5,6). The term "oxygen radical disease" was proposed to represent all the conditions affecting preterm infants that may contribute to neonatal morbidity (7).…”

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confidence: 99%

Tryptophan Released From Mother's Milk Has Antioxidant Properties

et al. 2009

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Bioactive factors in human milk (HM) are crucial to the health of newborns, especially preterm infants. These compounds assist in reducing the oxidative stress that may occur as a result of combined exposure to supplemental oxygen and immature physiologic defenses. To identify the components in HM that contribute to its greater resistance to oxidative stress compared with infant formulae, enzymatic hydrolysates of HM were prepared, ultrafiltered, separated, and analyzed for antioxidant potential. The antioxidant activity [M Trolox equivalent (TE/g)] of nondigested milk, whole digested milk, and derived ultrafiltrates were 80.4 Ϯ 13.3, 159.0 Ϯ 5.6, and 127.4 Ϯ 3.1, respectively. An HPLC fraction denoted as fraction 23 (5274 Ϯ 630 M TE/g) was obtained and its constituents identified as tryptophan (Trp), peptides HNPI, and PLAPQA. Scavenging activity was not observed for PLAPQA, whereas moderate activity was associated with HNPI (144 Ϯ 10.7 M TE/g) and very high activity to Trp (7986 Ϯ 468 M TE/g). Trp addition to HM and two infant formulas significantly increased formulae antioxidant properties. Trp appeared to be a powerful free radical scavenger naturally present in HM. Its antioxidant effects and potential application in the diets of infants, particularly preterm, must be examined further. (Pediatr Res 66: 614-618, 2009)

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New biomarkers of fetal‐neonatal hypoxic stress

Cited by 37 publications

References 38 publications

Activin is a Neuronal Survival Factor that is Rapidly Increased after Transient Cerebral Ischemia and Hypoxia in Mice

Activin is a Neuronal Survival Factor that is Rapidly Increased after Transient Cerebral Ischemia and Hypoxia in Mice

Plasma Esterified F2-Isoprostanes and Oxidative Stress in Newborns: Role of Nonprotein-Bound Iron

Tryptophan Released From Mother's Milk Has Antioxidant Properties

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