scholarly journals Biomarkers of Oxidative Stress for Neonatal Lung Disease

2021 ◽  
Vol 9 ◽  
Author(s):  
Giuliana Ferrante ◽  
Giuseppe Carota ◽  
Giovanni Li Volti ◽  
Mario Giuffrè
Keyword(s):  
Oxidative Stress ◽  
Lung Disease ◽  
Arterial Oxygen Tension ◽  
Ease Of Use ◽  
Arterial Oxygen ◽  
Current Evidence ◽  
Antioxidant Systems ◽  
Postnatal Life ◽  
Neonatal Lung ◽  
Biomarkers Of Oxidative Stress

The transition from prenatal to postnatal life causes a significant increase in arterial oxygen tension and the activation of metabolic pathways enabling the newborn's adaptation to the extra-uterine environment. The balance between pro-oxidant and anti-oxidant systems is critical to preserve cellular functions. Indeed, oxidative stress (OS) occurs when the production of free radicals is not balanced by the activity of intracellular antioxidant systems, contributing to cellular and tissue damage. Perinatal OS may have serious health consequences during the postnatal period and later in life. Namely, OS has been recognized as the major cause of lung injury in newborns, especially those preterm born, due to their immature lung and antioxidant systems. The development of OS biomarkers has gained increasing research interest since they may provide useful insights about pathophysiological pathways underlying OS-mediated pulmonary diseases in newborns. Moreover, their implementation in clinical settings may help to early identify high risk-newborns and to provide targeted treatment. Ideally, a biomarker should demonstrate ease of use, biological validity and reproducibility, high sensitivity and specificity. However, none of the clinically validated biomarkers so far have been qualified for neonatal lung disease. Additionally, the complex technical procedures and the high cost of such determinations have hampered the use of OS biomarkers in clinical practice. This review aims to evaluate the current evidence on the application of biomarkers of oxidative stress for neonatal lung disease and exploring the most relevant issues affecting their implementation in practice, as well as the associated evidence gaps and research limitations.

Biomarkers of oxidative stress and tissue damage released by muscle and liver after a single bout of swimming exercise

2013 ◽  
Vol 38 (5) ◽  
pp. 507-511 ◽  
Author(s):  
Dionizio Ramos ◽  
Eduarda Gabrielle Martins ◽  
Diego Viana-Gomes ◽  
Gustavo Casimiro-Lopes ◽  
Verônica P. Salerno
Keyword(s):  
Oxidative Stress ◽  
Acute Exercise ◽  
Cellular Damage ◽  
Swimming Exercise ◽  
Antioxidant Systems ◽  
Inadequate Response ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Single Bout ◽  
Biomarkers Of Oxidative Stress

Both acute exercise and excessive training can cause oxidative stress. The resulting increase in free radicals and the inadequate response from antioxidant systems can lead to a framework of cellular damage. An association between affected tissue and the biomarkers of oxidative stress that appear in plasma has not been clearly established. The aim of this study was to evaluate the source of oxidative stress biomarkers found in the plasma of untrained rats after a single bout of swimming exercise at 2 different intensities: low intensity (SBLIE) or high intensity (SBHIE). Immediately after the exercise, aspartate transaminase (AST), alanine transaminase (ALT), γ-glutamyltransferase (GGT), and lactate dehydrogenase (LDH) were measured in plasma to characterize cell damage. Oxidative stress was assessed using protein carbonylation (PC), total antioxidant capacity (TAC), and thiobarbituric acid reactive substances (TBARS) quantified by malondialdehyde concentration. SBHIE raised levels of plasma AST (93%) and ALT (17%), and both exercise regimens produced an increase in GGT (7%) and LDH (∼55%). Plasma levels of PC and TBARS were greater in the SBHIE group; there were no changes in TAC. SBLIE caused only a modest increase in TBARS. In muscle, there were no changes in TAC, PC, or TBARS, regardless of exercise intensity, In the liver, TAC and TBARS increased significantly in both the SBLIE and SBHIE groups. This indicates that the oxidative stress biomarkers measured in the plasma immediately after a single bout of swimming exercise were generated primarily in the liver, not in muscle.

scholarly journals The Beneficial Effects of Oral Cotrimoxazole upon Likely Biomarkers of Oxidative Stress in Advanced Fibrotic Lung Disease

2017 ◽  
Vol 08 (03) ◽  
pp. 90-108 ◽  
Author(s):  
Veronica Varney ◽  
David Salisbury ◽  
Helen Parnell ◽  
Siva Ratnatheepan ◽  
Alex Nicholas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Disease ◽  
Beneficial Effects ◽  
Fibrotic Lung Disease ◽  
Biomarkers Of Oxidative Stress

scholarly journals Potential role of Toll-like receptors in programming of vascular dysfunction

2013 ◽  
Vol 125 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Jennifer A. Thompson ◽  
R. Clinton Webb
Keyword(s):  
Oxidative Stress ◽  
Gestational Age ◽  
Molecular Mechanisms ◽  
Vascular Dysfunction ◽  
Current Evidence ◽  
Postnatal Life ◽  
Ongoing Research ◽  
The Metabolic Syndrome ◽  
Prenatal Factors ◽  
Increased Risk

The developmental origins of the metabolic syndrome have been established through the consistent observation that small-for-gestational age and large-for-gestational age fetuses have an increased risk for hypertension and related metabolic disorders later in life. These phenotypes have been reproduced in various species subjected to a range of intrauterine insults and ongoing research is directed towards understanding the underlying molecular mechanisms. Current evidence suggests that the creation of a pro-inflammatory and pro-oxidant intrauterine milieu is a common thread among prenatal factors that have an impact upon fetal size. Furthermore, studies demonstrate that a shift in fetal redox status consequent to environmental cues persists after birth and drives the progression of vascular dysfunction and hypertension in postnatal life. TLR (Toll-like receptor) signalling has emerged as a key link between inflammation and oxidative stress and a pathogenic contributor to hypertension, insulin resistance and obesity, in both human patients and animal models of disease. Thus TLR activation and dysregulation of its signalling components represent potential molecular underpinnings of programmed hypertension and related disorders in those subjected to suboptimal intrauterine conditions, yet their contributions to developmental programming remain unexplored. We propose that danger signals mobilized by the placenta or fetal tissues during complicated pregnancy activate the fetal innate immune system through TLRs and thereby potentiate the generation of ROS (reactive oxygen species) and orchestrate fetal adaptive responses, including changes in gene expression, which later translate to vascular dysfunction. Furthermore, we suggest that, after birth, continual activation of TLR signalling propagates vascular oxidative stress and thereby accelerates the advancement of hypertension and heart failure.

Plasma Biomarkers of Oxidative Stress: Relationship to Lung Disease and Inhaled Nitric Oxide Therapy in Premature Infants

PEDIATRICS ◽  
2008 ◽  
Vol 121 (3) ◽  
pp. 555-561 ◽  
Author(s):  
P. L. Ballard ◽  
W. E. Truog ◽  
J. D. Merrill ◽  
A. Gow ◽  
M. Posencheg ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Lung Disease ◽  
Premature Infants ◽  
Inhaled Nitric Oxide ◽  
Plasma Biomarkers ◽  
Nitric Oxide Therapy ◽  
Biomarkers Of Oxidative Stress

scholarly journals EFFECT OF THE ANTIOXIDANT – HERBAL DERIVATE ON BIOMARKERS OF OXIDATIVE STRESS AND ANTIOXIDANT SYSTEMS ON THE MODEL OF GASTRIC ULCER

2017 ◽  
Vol 1 (3) ◽  
pp. 13-15
Author(s):  
O.I. Zalyubovska ◽  
T.I. Tiupka ◽  
A.O. Minaieva ◽  
V.V. Zlenko ◽  
M.I. Litvinenko ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastric Ulcer ◽  
Antioxidant Systems ◽  
Biomarkers Of Oxidative Stress

EFFECT OF THE ANTIOXIDANT – HERBAL DERIVATE ON BIOMARKERS OF OXIDATIVE STRESS AND ANTIOXIDANT SYSTEMS ON THE MODEL OF GASTRIC ULCER

scholarly journals Comparison of coenzyme Q10 or fish oil for prevention of intermittent hypoxia-induced oxidative injury in neonatal rat lungs

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Christina D’Agrosa ◽  
Charles L. Cai ◽  
Faisal Siddiqui ◽  
Karen Deslouches ◽  
Stephen Wadowski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lung Injury ◽  
Fish Oil ◽  
Coenzyme Q10 ◽  
Intermittent Hypoxia ◽  
Oxidative Injury ◽  
Adverse Outcomes ◽  
Neonatal Rat ◽  
Antioxidant Systems

Abstract Background Neonatal intermittent hypoxia (IH) results in oxidative distress in preterm infants with immature antioxidant systems, contributing to lung injury. Coenzyme Q10 (CoQ10) and fish oil protect against oxidative injury. We tested the hypothesis that CoQ10 is more effective than fish oil for prevention of IH-induced lung injury in neonatal rats. Methods Newborn rats were exposed to two clinically relevant IH paradigms at birth (P0): (1) 50% O2 with brief hypoxia (12% O2); or (2) room air (RA) with brief hypoxia (12% O2), until P14 during which they were supplemented with daily oral CoQ10, fish oil, or olive oil from P0 to P14. Pups were studied at P14 or placed in RA until P21 with no further treatment. Lungs were assessed for histopathology and morphometry; biomarkers of oxidative stress and lipid peroxidation; and antioxidants. Results Of the two neonatal IH paradigms 21%/12% O2 IH resulted in the most severe outcomes, evidenced by histopathology and morphometry. CoQ10 was effective for preserving lung architecture and reduction of IH-induced oxidative stress biomarkers. In contrast, fish oil resulted in significant adverse outcomes including oversimplified alveoli, hemorrhage, reduced secondary crest formation and thickened septae. This was associated with elevated oxidants and antioxidants activities. Conclusions Data suggest that higher FiO2 may be needed between IH episodes to curtail the damaging effects of IH, and to provide the lungs with necessary respite. The negative outcomes with fish oil supplementation suggest oxidative stress-induced lipid peroxidation.

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