Does Normobaric Hyperoxia Cause Oxidative Stress in the Injured Brain? A Microdialysis Study Using 8-Iso-Prostaglandin F2α as a Biomarker

2017 ◽  
Vol 34 (19) ◽  
pp. 2731-2742 ◽  
Author(s):  
Marian Vidal-Jorge ◽  
Angela Sánchez-Guerrero ◽  
Gemma Mur-Bonet ◽  
Lidia Castro ◽  
Andreea Rădoi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prostaglandin F2α ◽  
Normobaric Hyperoxia ◽  
Injured Brain ◽  
Microdialysis Study

scholarly journals Maternal Urinary Metal and Metalloid Concentrations in Association with Oxidative Stress Biomarkers

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 114
Author(s):  
Pahriya Ashrap ◽  
Deborah J. Watkins ◽  
Ginger L. Milne ◽  
Kelly K. Ferguson ◽  
Rita Loch-Caruso ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prostaglandin F2α ◽  
Urine Samples ◽  
Oxidative Stress Marker ◽  
Essential Metals ◽  
Male Fetus ◽  
Metal Concentrations ◽  
Fetal Sex ◽  
Wide Range ◽  
And Oxidative Stress

Metal exposure has been associated with a wide range of adverse birth outcomes and oxidative stress is a leading hypothesis of the mechanism of action of metal toxicity. We assessed the relationship between maternal exposure to essential and non-essential metals and metalloids in pregnancy and oxidative stress markers, and sought to identify windows of vulnerability and effect modification by fetal sex. In our analysis of 215 women from the PROTECT birth cohort study, we measured 14 essential and non-essential metals in urine samples at three time points during pregnancy. The oxidative stress marker 8-iso-prostaglandin F2α (8-iso-PGF2α) and its metabolite 2,3-dinor-5,6-dihydro-15-15-F2t-IsoP, as well as prostaglandin F2α (PGF2α), were also measured in the same urine samples. Using linear mixed models, we examined the main effects of metals on markers of oxidative stress as well as the visit-specific and fetal sex-specific effects. After adjustment for covariates, we found that a few urinary metal concentrations, most notably cesium (Cs) and copper (Cu), were associated with higher 8-iso-PGF2α with effect estimates ranging from 7.3 to 14.9% for each interquartile range, increase in the metal concentration. The effect estimates were generally in the same direction at the three visits and a few were significant only among women carrying a male fetus. Our data show that higher urinary metal concentrations were associated with elevated biomarkers of oxidative stress. Our results also indicate a potential vulnerability of women carrying a male fetus.

scholarly journals 8-Isoprostanes and Asymmetric Dimethylarginine as Predictors of Mortality in Patients Following Coronary Bypass Surgery: A Long-Term Follow-Up Study

2022 ◽  
Vol 11 (1) ◽  
pp. 246
Author(s):  
Aleksandra Gołąb ◽  
Dariusz Plicner ◽  
Anna Rzucidło-Hymczak ◽  
Lidia Tomkiewicz-Pająk ◽  
Bogusław Gawęda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Mortality ◽  
Bypass Surgery ◽  
Asymmetric Dimethylarginine ◽  
Prostaglandin F2α ◽  
Cardiovascular Death ◽  
Long Term Follow Up ◽  
Nitric Oxide Bioavailability

Background: We previously demonstrated that enhanced oxidative stress and reduced nitric oxide bioavailability are associated with unfavorable outcomes early after coronary artery bypass grafting. It is not known whether these processes may impact long-term results. We sought to assess whether during long-term follow-up, markers of oxidative stress and nitric oxide bioavailability may predict cardiovascular mortality following bypass surgery. Methods: We studied 152 consecutive patients (118 men, age 65.2 ± 8.3 years) who underwent elective, primary, isolated on-pump bypass surgery. We measured plasma 8-iso-prostaglandin F2α and asymmetric dimethylarginine before surgery and twice after surgery (18–36 h and 5–7 days). We assessed all-cause and cardiovascular death in relation to these two biomarkers during a mean follow-up time of 11.7 years. Results: The overall mortality was 44.7% (4.7 per 100 patient-years) and cardiovascular mortality was 21.0% (2.2 per 100 patient-years). Baseline 8-iso-prostaglandin F2α was associated with cardiovascular mortality (HR 1 pg/mL 1.010, 95% CI 1.001–1.021, p = 0.036) with the optimal cut-off ≤ 364 pg/mL for higher survival rate (HR 0.460, 95% CI 0.224–0.942, p = 0.030). Asymmetric dimethylarginine > 1.01 μmol/L measured 18–36 h after surgery also predicted cardiovascular death (HR 2.467, 95% CI 1.140–5.340, p = 0.020). Additionally, elevated 8-iso-prostaglandin F2α measured at the same time point associated with all-cause mortality (HR 1 pg/mL 1.007, 95% CI 1.000–1.014, p = 0.048). Conclusions: Our findings indicate that in advanced coronary disease, increased oxidative stress, reflected by 8-iso-prostaglandin F2α before bypass surgery and enhanced asymmetric dimethylarginine accumulation just after the surgery are associated with cardiovascular death during long-term follow-up

scholarly journals Induction of Oxidative Stress and Apoptosis in the Injured Brain: Potential Relevance to Brain Regeneration in Zebrafish.

2021 ◽  
Author(s):  
Surendra Kumar Anand ◽  
Manas Ranjan Sahu ◽  
Amal Chandra Mondal
Keyword(s):  
Oxidative Stress ◽  
Mrna Levels ◽  
Adult Zebrafish ◽  
Zebrafish Model ◽  
Stab Injury ◽  
Zebrafish Brain ◽  
Protein Levels ◽  
Injured Brain ◽  
Brain Regeneration ◽  
The Impact

Abstract In the recent years, zebrafish, owing to its tremendous adult neurogenic capacity, has emerged as a useful vertebrate model to study brain regeneration. Recent findings suggest a significant role of the BDNF/TrkB signaling as a mediator of brain regeneration following a stab injury in the adult zebrafish brain. Since BDNF has been implicated in a plethora of physiological processes, we hypothesized that these processes are affected in the injured zebrafish brain. In this small study, we examined the indicators of oxidative stress and of apoptosis using biochemical assays, RT-PCR and IHC to reflect upon the impact of stab injury on oxidative stress levels and apoptosis in the injured adult zebafish brain. Our results indicate induction of oxidative stress in the injured adult zebrafish brain. Also, apoptosis was induced in the injured brain as indicated by increased protein levels of cleaved caspase3 as well as enhanced mRNA levels of both pro-apoptotic and anti-apoptotic genes. This knowledge contributes to the overall understanding of adult neurogenesis in the zebrafish model and raises new questions pertaining to the compensatory physiological mechanisms in response to traumatic brain injury in the adult zebrafish brain.

scholarly journals Neuropharmacological Potential ofGastrodia elataBlume and Its Components

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Jung-Hee Jang ◽  
Yeonghoon Son ◽  
Seong Soo Kang ◽  
Chun-Sik Bae ◽  
Jong-Choon Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Function ◽  
Intracellular Signaling ◽  
Inflammatory Responses ◽  
Signaling Cascades ◽  
Sedative Medication ◽  
Synthetic Chemicals ◽  
Injured Brain ◽  
Injury Models ◽  
The Brain

Research has been conducted in various fields in an attempt to develop new therapeutic agents for incurable neurodegenerative diseases.Gastrodia elataBlume (GE), a traditional herbal medicine, has been used in neurological disorders as an anticonvulsant, analgesic, and sedative medication. Several neurodegenerative models are characterized by oxidative stress and inflammation in the brain, which lead to cell death via multiple extracellular and intracellular signaling pathways. The blockade of certain signaling cascades may represent a compensatory therapy for injured brain tissue. Antioxidative and anti-inflammatory compounds isolated from natural resources have been investigated, as have various synthetic chemicals. Specifically, GE rhizome extract and its components have been shown to protect neuronal cells and recover brain function in various preclinical brain injury models by inhibiting oxidative stress and inflammatory responses. The present review discusses the neuroprotective potential of GE and its components and the related mechanisms; we also provide possible preventive and therapeutic strategies for neurodegenerative disorders using herbal resources.

Effects of Normobaric Hyperoxia in a Rat Model of Focal Cerebral Ischemia—Reperfusion

2002 ◽  
Vol 22 (7) ◽  
pp. 861-868 ◽  
Author(s):  
Aneesh B. Singhal ◽  
Xiaoying Wang ◽  
Toshihisa Sumii ◽  
Tatsuro Mori ◽  
Eng H. Lo
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Protein Carbonyl ◽  
Blue Dye ◽  
Heme Oxygenase 1 ◽  
Normobaric Hyperoxia ◽  
Cerebral Ischemia Reperfusion ◽  
Carbonyl Formation

Recent studies suggest that normobaric hyperoxia can be beneficial, if administered during transient stroke. However, increased oxygenation theoretically may increase oxygen free-radical injury, particularly during reperfusion. In the present study, the authors assessed the benefit and risks of hyperoxia during focal cerebral ischemia and reperfusion. Rats were subjected to hyperoxia (Fio2 100%) or normoxia (Fio2 30%) during 2-hour filament occlusion and 1-hour reperfusion of the middle cerebral artery. At 24 hours, the hyperoxia group showed 70% (total) and 92% (cortical) reduction in infarct volumes as compared to the normoxia group. Levels of oxidative stress were evaluated using three indirect methods. First, since oxygen free radicals increase blood—brain barrier (BBB) damage, Evan's blue dye extravasation was quantified to assess BBB damage. Second, the expression of heme oxygenase-1 (HO-1), a heat shock protein inducible by oxidative stress, was assessed using Western blot techniques. Third, an immunoblot technique (“OxyBlot”) was used to assess levels of protein carbonyl formation as a marker of oxidative stress—induced protein denaturation. At 24 hours, Evan's blue dye extravasation per average lesion volume was similar between groups. There were no significant differences in HO-1 induction and protein carbonyl formation between groups, in the ipsilateral or contralateral hemispheres, at 6 hours and at 24 hours. These results indicate that hyperoxia treatment during focal cerebral ischemia—reperfusion is neuroprotective, and does not increase oxidative stress.

scholarly journals Phosphatidylethanolamine-Binding Protein 1 Ameliorates Ischemia-Induced Inflammation and Neuronal Damage in the Rabbit Spinal Cord

Cells ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 1370 ◽  
Author(s):  
Kim ◽  
Cho ◽  
Jung ◽  
Yoo ◽  
Oh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Neuronal Damage ◽  
Binding Protein ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Prostaglandin F2α ◽  
Proteomic Approach ◽  
Phosphatidylethanolamine Binding Protein

In a previous study, we utilized a proteomic approach and found a significant reduction in phosphatidylethanolamine-binding protein 1 (PEBP1) protein level in the spinal cord at 3 h after ischemia. In the present study, we investigated the role of PEBP1 against oxidative stress in NSC34 cells in vitro, and ischemic damage in the rabbit spinal cord in vivo. We generated a PEP-1-PEBP1 fusion protein to facilitate the penetration of blood-brain barrier and intracellular delivery of PEBP1 protein. Treatment with PEP-1-PEBP1 significantly decreased cell death and the induction of oxidative stress in NSC34 cells. Furthermore, administering PEP-1-PEBP1 did not show any significant side effects immediately before and after ischemia/reperfusion. Administration of PEP-PEBP1 improved the Tarlov’s neurological score at 24 and 72 h after ischemia, and significantly improved neuronal survival at 72 h after ischemia based on neuronal nuclei (NeuN) immunohistochemistry, Flouro-Jade B staining, and western blot study for cleaved caspase 3. PEP-1-PEBP1 administration decreased oxidative stress based on malondialdehyde level, advanced oxidation protein products, and 8-iso-prostaglandin F2α in the spinal cord. In addition, inflammation based on myeloperoxidase level, tumor necrosis factor-α level, and high mobility group box 1 level was decreased by PEP-1-PEBP1 treatment at 72 h after ischemia. Thus, PEP-1-PEBP1 treatment, which decreases oxidative stress, inflammatory cytokines, and neuronal death, may be an effective therapeutic strategy for spinal cord ischemia.

CYBA and GSTP1 variants associate with oxidative stress under hypobaric hypoxia as observed in high-altitude pulmonary oedema

2011 ◽  
Vol 122 (6) ◽  
pp. 299-311 ◽  
Author(s):  
Aastha Mishra ◽  
Zahara Ali ◽  
Arpana Vibhuti ◽  
Rahul Kumar ◽  
Perwez Alam ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Altitude ◽  
Pulmonary Oedema ◽  
Hypobaric Hypoxia ◽  
Glutathione Transferase ◽  
Prostaglandin F2α ◽  
Gene Interactions ◽  
Potential Candidate ◽  
Genotype Distribution ◽  
Risk Alleles

HAPE (high-altitude pulmonary oedema) is characterized by pulmonary hypertension, vasoconstriction and an imbalance in oxygen-sensing redox switches. Excess ROS (reactive oxygen species) contribute to endothelial damage under hypobaric hypoxia, hence the oxidative-stress-related genes CYBA (cytochrome b−245 α polypeptide) and GSTP1 (glutathione transferase Pi 1) are potential candidate genes for HAPE. In the present study, we investigated the polymorphisms −930A/G and H72Y (C/T) of CYBA and I105V (A/G) and A114V (C/T) of GSTP1, individually and in combination, in 150 HAPE-p (HAPE patients), 180 HAPE-r (HAPE-resistant lowland natives) and 180 HLs (healthy highland natives). 8-Iso-PGF2α (8-iso-prostaglandin F2α) levels were determined in plasma and were correlated with individual alleles, genotype, haplotype and gene–gene interactions. The relative expression of CYBA and GSTP1 were determined in peripheral blood leucocytes. The genotype distribution of −930A/G, H72Y (C/T) and I105V (A/G) differed significantly in HAPE-p compared with HAPE-r and HLs (P≤0.01). The haplotypes G-C of −930A/G and H72Y (C/T) in CYBA and G-C and G-T of I105V (A/G) and A114V (C/T) in GSTP1 were over-represented in HAPE-p; in contrast, haplotypes A-T of −930A/G and H72Y (C/T) in CYBA and A-C of I105V (A/G) and A114V (C/T) in GSTP1 were over-represented in HAPE-r and HLs. 8-Iso-PGF2α levels were significantly higher in HAPE-p and in HLs than in HAPE-r (P=2.2×10−16 and 1.2×10−14 respectively) and the expression of CYBA and GSTP1 varied differentially (P<0.05). Regression analysis showed that the risk alleles G, C, G and T of −930A/G, H72Y (C/T), I105V (A/G) and A114V (C/T) were associated with increased 8-iso-PGF2α levels (P<0.05). Interaction between the two genes revealed over-representation of most of the risk-allele-associated genotype combinations in HAPE-p and protective-allele-associated genotype combinations in HLs. In conclusion, the risk alleles of CYBA and GSTP1, their haplotypes and gene–gene interactions are associated with imbalanced oxidative stress and, thereby, with high-altitude adaptation and mal-adaptation.

Prostaglandin F2α metabolite and F2-isoprostane excretion rates in migraine

2001 ◽  
Vol 102 (1) ◽  
pp. 39-43 ◽  
Author(s):  
Johanna HELMERSSON ◽  
Peter MATTSSON ◽  
Samar BASU
Keyword(s):  
Oxidative Stress ◽  
Migraine Attack ◽  
Prostaglandin F2α ◽  
Urine Samples ◽  
Menopausal Women ◽  
The Mean ◽  
Post Menopausal ◽  
Excretion Rates ◽  
And Control ◽  
And Oxidative Stress

The pathophysiology theory of migraine postulates a local, neurogenic inflammation and the possible involvement of oxidative stress. We analysed the levels of 15-oxo-dihydro-prostaglandin F2α (a metabolite of prostaglandin F2α) and 8-iso-prostaglandin F2α (a major isoprostane), which are biomarkers for inflammation and oxidative stress respectively, in urine from 21 patients with migraine, with and without aura. Urine samples from migraine patients were collected during a migraine attack, and control samples were collected from the same subjects on a migraine-free morning. The mean basal levels of 15-oxo-dihydro-prostaglandin F2α and 8-iso-prostaglandin F2α in the morning control urine samples were 0.54±0.11 and 0.31±0.13nmol/mmol of creatinine respectively. The mean levels of 15-oxo-dihydro-prostaglandin F2α and 8-iso-prostaglandin F2α in the urine samples collected during the migraine attack in the 21 patients were 0.53±0.13 and 0.32±0.11nmol/mmol of creatinine respectively. Thus there were no differences in the 15-oxo-dihydro-prostaglandin F2α and 8-iso-prostaglandin F2α excretion rates during the migraine attack compared with on the migraine-free day. However, the basal 8-iso-prostaglandin F2α excretion levels on the migraine-free day were significantly lower in pre-menopausal women (0.24±0.08nmol/mmol of creatinine, n = 11) compared with post-menopausal women (0.39±0.14nmol/mmol of creatinine; n = 7; P = 0.009). In conclusion, in this study we found no support for the involvement of inflammation and oxidative stress in migraine pathophysiology. Our results indicate, however, a lower level of oxidative stress in pre-menopausal compared with post-menopausal women.

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