Total Hydroperoxide and Advanced Oxidation Protein Products in Preterm Hypoxic Babies

Buonocore, Giuseppe; Perrone, Serafina; Longini, Mariangela; Terzuoli, Lucia; Bracci, Rodolfo

doi:10.1203/00006450-200002000-00012

Cited by 157 publications

(118 citation statements)

References 27 publications

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“…Serum triglyceride and high-density lipoprotein (HDL)-cholesterol concentrations were assayed using commercial kits (Sekisui Medical Co., Tokyo, Japan). The serum concentration of derivatives of reactive oxygen metabolites (d-ROMs), a marker of oxidative stress, was measured using a previously described method [37]. The intra-and interassay coefficients of variation were all < 10%.…”

Section: Supplemental Materials and Methodsmentioning

confidence: 99%

The hepatic circadian clock is preserved in a lipid-induced mouse model of non-alcoholic steatohepatitis

Ando

Takamura

Nagata

et al. 2009

Biochemical and Biophysical Research Communications

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Recent studies have correlated metabolic diseases, such as metabolic syndrome and non-alcoholic fatty liver disease, with the circadian clock. However, whether such metabolic changes per se affect the circadian clock remains controversial. To address this, we investigated the daily mRNA expression profiles of clock genes in the liver of a dietary mouse model of non-alcoholic steatohepatitis (NASH) using a custom-made, high-precision DNA chip. C57BL/6J mice fed an atherogenic diet for five weeks developed hypercholesterolemia, oxidative stress, and NASH. DNA chip analyses revealed that the atherogenic diet had a great influence on the mRNA expression of a wide range of genes linked to mitochondrial energy production, redox regulation, and carbohydrate and lipid metabolism. However, the rhythmic mRNA expression of the clock genes in the liver remained intact. Most of the circadianly expressed genes also showed 24-h rhythmicity. These findings suggest that the biological clock is protected against such a metabolic derangement as NASH.

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Section: Supplemental Materials and Methodsmentioning

confidence: 99%

The hepatic circadian clock is preserved in a lipid-induced mouse model of non-alcoholic steatohepatitis

Ando

Takamura

Nagata

et al. 2009

Biochemical and Biophysical Research Communications

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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.…”

Section: Most Mammals Humans Exempted Possess the Enzyme Uricasementioning

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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“…Perinatal hypoxia is an important risk factor in the pathogenesis of IVH because it alters mechanisms that regulate cerebral blood flow and triggers a cascade of biochemical events that begins with a shift from oxidative to anaerobic metabolism and leads to oxidative brain damage resulting from excessive production of free radicals (4,5 ).…”

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confidence: 99%

Increased Plasma Concentrations of Activin A Predict Intraventricular Hemorrhage in Preterm Newborns

et al. 2006

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Background: Intraventricular hemorrhage (IVH) is a major cause of neurologic disabilities in preterm newborns. We evaluated the use of plasma activin A concentrations to predict the development of perinatal IVH. Methods: We measured nucleated erythrocyte (NRBC) counts, plasma activin A, hypoxanthine (Hyp), and xanthine (Xan) in arterial blood samples obtained from 53 preterm infants during the first hour after birth. Cerebral ultrasound was performed within 48 h of birth and repeated at 5-or 6-day intervals until the age of 4 weeks. Results: Grade I or II IVH was detected during the first 10 days of life in 11 of 53 patients (21%). Activin A, Hyp, and Xan concentrations and NRBC counts were higher in preterm newborns who subsequently developed IVH than in those who did not (P <0.0001, except P ‫؍‬ 0.019 for Xan). Neonatal activin A was correlated (P <0.0001) with Hyp (r ‫؍‬ 0.95), Xan (r ‫؍‬ 0.90), and NRBC count (r ‫؍‬ 0.90) in newborns without later IVH and in those who developed IVH (Hyp, r ‫؍‬ 0.89, P ‫؍‬ 0.0002; Xan, r ‫؍‬ 0.95, P <0.0001; NRBC count, r ‫؍‬ 0.90, P ‫؍‬ 0.0002). At a cutoff of 0.8 g/L activin A, the sensitivity and specificity were 100% [11 of 11; 95% confidence interval (CI), 71%-100%] and 93% (39 of 42; 95% CI, 81%-98%), and positive and negative predictive values were 79% (95% CI, 61%-100%) and 0% (95% CI, 0%-2%), respectively. The area under the ROC curve was 0.98. Conclusions: Activin A concentrations at birth are increased in preterm newborns who later develop IVH

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Total Hydroperoxide and Advanced Oxidation Protein Products in Preterm Hypoxic Babies

Cited by 157 publications

References 27 publications

The hepatic circadian clock is preserved in a lipid-induced mouse model of non-alcoholic steatohepatitis

The hepatic circadian clock is preserved in a lipid-induced mouse model of non-alcoholic steatohepatitis

Biochemical Measurement of Neonatal Hypoxia

Increased Plasma Concentrations of Activin A Predict Intraventricular Hemorrhage in Preterm Newborns

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