Higher Level of Oxidative Stress Markers in Small for Gestational Age Newborns Delivered by Cesarean Section at Term

Dede, Hülya; Takmaz, Özgüç; Ozbasli, Esra; Dede, Suat; Güngör, Mete

doi:10.1080/15513815.2017.1303860

Cited by 15 publications

(13 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SOD and CAT are essential natural scavengers of superoxide radicals and hydrogen peroxide to prevent organisms from undergoing oxidative stress injury (36). MDA, the final product of lipid oxidation, is a common indicator of lipid peroxidation of the cellular membrane (37). The changes in these oxidative parameters in this study imply that H 2 O 2 successfully induced oxidative stress in nasal epithelial cells and that high PTEN expression further worsens the induced injury.…”

Section: Discussionmentioning

confidence: 66%

PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways

2017

View full text Add to dashboard Cite

Chronic rhinosinusitis (CRS) is a form of chronic inflammation of the nasal cavity and paranasal sinus with multi‑causal pathogenesis, including oxidative stress. Several lines of evidence have demonstrated that the phosphatase and tensin homolog gene (PTEN) can inhibit the activation of phosphoinositide 3‑kinase (PI3K) to affect phosphorylation of Akt. Importantly, the PI3K/PTEN/Akt signaling pathway is associated with various types of tumors, chronic inflammatory diseases, and autoimmune disease through its regulation of cell growth, apoptosis, proliferation, and metabolism. This in vitro study aimed to investigate the role of PTEN and the relationship between PTEN and the PI3K/Akt pathway in nasal epithelial cells under oxidative stress. H2O2 treatment was applied to induce a cell injury model of oxidative stress in rat nasal epithelial cells. Cells were divided into control, H2O2, H2O2+PTEN, and H2O2+siPTEN groups. Cell viability was measured using the CCK‑8 assay, and reactive oxygen species (ROS) levels and apoptosis rates were analyzed by flow cytometry (FCM). Oxidative parameters, including ROS, catalase (CAT), and malondialdehyde (MDA), were tested by enzyme‑linked immunosorbent assay (ELISA). The expression of apoptosis‑related genes and PI3K/Akt pathway was assayed by quantitative PCR (qPCR) and western blot. In H2O2‑injured cells, oxidative stress, due to increased ROS levels and apoptosis rates, was induced, and PTEN aggravated the injury. The levels of both p‑Akt and PTEN in H2O2‑injured cells were positively correlated and higher than in control cells. Unknown regulatory protein(s) may exist in the PI3K/PTEN/Akt pathway or the PTEN and PI3K/Akt pathways may be two independent signaling pathways that have cross interactions.

show abstract

Section: Discussionmentioning

confidence: 66%

PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways

2017

View full text Add to dashboard Cite

show abstract

“…Furthermore, OSM (MDA, SOD) were measured in SGA infants delivered by cesarean section (n = 21) or vaginally (n = 21). Results showed that SGA term newborns delivered by caesarean section had insufficient protective mechanisms against increased OSM at birth [133].…”

Section: Osm (8-isoprostane; Malondialdehyde [Mda]; Protein Carbonyl mentioning

confidence: 97%

Early predictors of perinatal brain damage: the role of neurobiomarkers

Bersani

Pluchinotta

Dotta

et al. 2019

Clinical Chemistry and Laboratory Medicine (CCLM)

View full text Add to dashboard Cite

The early detection of perinatal brain damage in preterm and term newborns (i.e. intraventricular hemorrhage, periventricular leukomalacia and perinatal asphyxia) still constitute an unsolved issue. To date, despite technological improvement in standard perinatal monitoring procedures, decreasing the incidence of perinatal mortality, the perinatal morbidity pattern has a flat trend. Against this background, the measurement of brain constituents could be particularly useful in the early detection of cases at risk for short-/long-term brain injury. On this scenario, the main European and US international health-care institutions promoted perinatal clinical and experimental neuroprotection research projects aimed at validating and including a panel of biomarkers in the clinical guidelines. Although this is a promising attempt, there are several limitations that do not allow biomarkers to be included in standard monitoring procedures. The main limitations are: (i) the heterogeneity of neurological complications in the perinatal period, (ii) the small cohort sizes, (iii) the lack of multicenter investigations, (iv) the different techniques for neurobiomarkers assessment, (iv) the lack of consensus for the validation of assays in biological fluids such as urine and saliva, and (v), the lack of reference curves according to measurement technique and biological fluid. In the present review we offer an up-to-date overview of the most promising developments in the use of biomarkers in the perinatal period such as calcium binding proteins (S100B protein), vasoactive agents (adrenomedullin), brain biomarkers (activin A, neuron specific enolase, glial fibrillary acidic protein, ubiquitin carboxyl-terminal hydrolase-L1) and oxidative stress markers.

show abstract

“…In humans, intrauterine growth restriction and a low birth weight is linked to increased oxidative stress, neuro-inflammation, perinatal mortality and lasting deficits in learning and memory in children and adolescents [242][243][244][245][246][247]. In addition, low vitC during pregnancy is linked to increased preterm births, pre-eclampsia and increased placental apoptosis; however, reports of a beneficial effect of antioxidant supplementation on these outcomes are currently conflicting [239,[248][249][250][251][252][253].…”

Section: Clinical Studiesmentioning

confidence: 99%

Vitamin C Deficiency in the Young Brain—Findings from Experimental Animal Models

Tveden‐Nyborg

2021

Nutrients

View full text Add to dashboard Cite

Severe and long-term vitamin C deficiency can lead to fatal scurvy, which is fortunately considered rare today. However, a moderate state of vitamin C (vitC) deficiency (hypovitaminosis C)—defined as a plasma concentration below 23 μM—is estimated to affect up to 10% of the population in the Western world, albeit clinical hallmarks in addition to scurvy have not been linked to vitC deficiency. The brain maintains a high vitC content and uniquely high levels during deficiency, supporting vitC’s importance in the brain. Actions include both antioxidant and co-factor functions, rendering vitamin C deficiency likely to affect several targets in the brain, and it could be particularly significant during development where a high cellular metabolism and an immature antioxidant system might increase sensitivity. However, investigations of a non-scorbutic state of vitC deficiency and effects on the developing young brain are scarce. This narrative review provides a comprehensive overview of the complex mechanisms that regulate vitC homeostasis in vivo and in the brain in particular. Functions of vitC in the brain and the potential consequences of deficiency during brain development are highlighted, based primarily on findings from experimental animal models. Perspectives for future investigations of vitC are outlined.

show abstract

Higher Level of Oxidative Stress Markers in Small for Gestational Age Newborns Delivered by Cesarean Section at Term

Abstract: Elevated MDA levels and decreased SOD activity in umbilical cord blood may show the possibility of insufficient protective mechanisms against increased oxidative stress in SGA neonates born by cesarean section.

Cited by 15 publications

References 35 publications

PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways

PTEN promotes apoptosis of H2O2‑injured rat nasal epithelial cells through PI3K/Akt and other pathways

Early predictors of perinatal brain damage: the role of neurobiomarkers

Vitamin C Deficiency in the Young Brain—Findings from Experimental Animal Models

Contact Info

Product

Resources

About