Biochemical Markers of Neonatal Hypoxia

Plank, Megan S.; Boskovic, Danilo S.; Sowers, Lawrence C.; Angeles, Danilyn M.

doi:10.2217/17455111.2.4.485

Cited by 6 publications

(7 citation statements)

References 141 publications

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“…Neonates experiencing multiple oxygen desaturation events are at risk for hypoxia, which refers to an inadequate oxygen supply to the tissues. This leads to a reduced rate of oxidative phosphorylation by aerobic respiration and to reduced adenosine triphosphate (ATP) synthesis [ 23 ]. Because of the lack of oxygen as a final electron acceptor, the mitochondria are unable to maintain the proton gradient necessary to form ATP from adenosine diphosphate (ADP) and inorganic phosphate [ 24 ].…”

Section: Premature Infants Are In An Energy-deficit Statementioning

confidence: 99%

“…Under hypoxic conditions anaerobic metabolism is engaged, converting pyruvate to lactate and allowing the regeneration of nicotinamide-adenine dinucleotide (NAD + ), so glycolysis can continue to generate ATP. Nonetheless, the resulting ATP is expended quickly, resulting in a steady decrease of ATP stores [ 23 ].…”

Section: Premature Infants Are In An Energy-deficit Statementioning

confidence: 99%

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The Energy Costs of Prematurity and the Neonatal Intensive Care Unit (NICU) Experience

2018

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Premature neonates are in an energy deficient state due to (1) oxygen desaturation and hypoxia events, (2) painful and stressful stimuli, (3) illness, and (4) neurodevelopmental energy requirements. Failure to correct energy deficiency in premature infants may lead to adverse effects such as neurodevelopmental delay and negative long-term metabolic and cardiovascular outcomes. The effects of energy dysregulation and the challenges that clinicians in the Neonatal Intensive Care Unit (NICU) face in meeting the premature infant’s metabolic demands are discussed. Specifically, the focus is on the effects of pain and stress on energy homeostasis. Energy deficiency is a complex problem and requires a multi-faceted solution to promote optimum development of premature infants.

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Section: Premature Infants Are In An Energy-deficit Statementioning

confidence: 99%

Section: Premature Infants Are In An Energy-deficit Statementioning

confidence: 99%

The Energy Costs of Prematurity and the Neonatal Intensive Care Unit (NICU) Experience

2018

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“…Oxidative stress is a known contributor of developmental toxicity from hypoxia during pregnancy and malondialdehyde, a product of lipid peroxidation, is often used as a biomarker of hypoxia in newborns (Plank et al, 2008). Furthermore, it was found that GPx1 overexpression was protective against hypoxia in neonatal mouse brains, although SOD overexpression was not (Sheldon et al, 2008).…”

Section: Intersection Of Upr Apoptosis and Oxidative Stress In Dmentioning

confidence: 99%

Oxidative Stress, Unfolded Protein Response, and Apoptosis in Developmental Toxicity

Kupsco

Schlenk

2015

International Review of Cell and Molecular Biology

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Physiological development requires precise spatiotemporal regulation of cellular and molecular processes. Disruption of these key events can generate developmental toxicity in the form of teratogenesis or mortality. The mechanism behind many developmental toxicants remains unknown. While recent work has focused on the unfolded protein response (UPR), oxidative stress, and apoptosis in the pathogenesis of disease, few studies have addressed their relationship in developmental toxicity. Redox regulation, UPR, and apoptosis are essential for physiological development and can be disturbed by a variety of endogenous and exogenous toxicants to generate lethality and diverse malformations. This review examines the current knowledge of the role of oxidative stress, UPR, and apoptosis in physiological development as well as in developmental toxicity, focusing on studies and advances in vertebrates model systems.

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“…Animal blood may also be used while recognizing the potential for uricase-generated allantoin. Purine metabolites were linked to hypoxia as early as 1963 and the reliability of hypoxanthine, xanthine, and uric acid as biochemical indicators of neonatal hypoxia was validated by several investigators [10][11][12][13] . The HPLC method used for the quantification of purine compounds is fast, reliable, and reproducible.…”

mentioning

confidence: 99%

Biochemical Measurement of Neonatal Hypoxia

Plank

Calderon

Asmerom

et al. 2011

JoVE

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Neonatal hypoxia ischemia is characterized by inadequate blood perfusion of a tissue or a systemic lack of oxygen. This condition is thought to cause/exacerbate well documented neonatal disorders including neurological impairment 1-3 . Decreased adenosine triphosphate production occurs due to a lack of oxidative phosphorylation. To compensate for this energy deprived state molecules containing high energy phosphate bonds are degraded 2 . This leads to increased levels of adenosine which is subsequently degraded to inosine, hypoxanthine, xanthine, and finally to uric acid. The final two steps in this degradation process are performed by xanthine oxidoreductase. This enzyme exists in the form of xanthine dehydrogenase under normoxic conditions but is converted to xanthine oxidase (XO) under hypoxia-reperfusion circumstances 4, 5 . Unlike xanthine dehydrogenase, XO generates hydrogen peroxide as a byproduct of purine degradation 4, 6 . This hydrogen peroxide in combination with other reactive oxygen species (ROS) produced during hypoxia, oxidizes uric acid to form allantoin and reacts with lipid membranes to generate malondialdehyde (MDA) [7][8][9] . Most mammals, humans exempted, possess the enzyme uricase, which converts uric acid to allantoin. In humans, however, allantoin can only be formed by ROS-mediated oxidation of uric acid. Because of this, allantoin is considered to be a marker of oxidative stress in humans, but not in the mammals that have uricase.We describe methods employing high pressure liquid chromatography (HPLC) and gas chromatography mass spectrometry (GCMS) to measure biochemical markers of neonatal hypoxia ischemia. Human blood is used for most tests. Animal blood may also be used while recognizing the potential for uricase-generated allantoin. Purine metabolites were linked to hypoxia as early as 1963 and the reliability of hypoxanthine, xanthine, and uric acid as biochemical indicators of neonatal hypoxia was validated by several investigators [10][11][12][13] . The HPLC method used for the quantification of purine compounds is fast, reliable, and reproducible. The GC/MS method used for the quantification of allantoin, a relatively new marker of oxidative stress, was adapted from Gruber et al 7 . This method avoids certain artifacts and requires low volumes of sample. Methods used for synthesis of MMDA were described elsewhere 14,15 . GC/MS based quantification of MDA was adapted from Paroni et al. and Cighetti et al. 16,17 . Xanthine oxidase activity was measured by HPLC by quantifying the conversion of pterin to isoxanthopterin 18 . This approach proved to be sufficiently sensitive and reproducible.

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Biochemical Markers of Neonatal Hypoxia

Cited by 6 publications

References 141 publications

The Energy Costs of Prematurity and the Neonatal Intensive Care Unit (NICU) Experience

The Energy Costs of Prematurity and the Neonatal Intensive Care Unit (NICU) Experience

Oxidative Stress, Unfolded Protein Response, and Apoptosis in Developmental Toxicity

Biochemical Measurement of Neonatal Hypoxia

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