A New Approach to Oxidative Stress and Inflammatory Signaling during Labour in Healthy Mothers and Neonates

The objective of the current study was to investigate for the first time and simultaneously the oxidative stress and inflammatory signaling induced during the delivery in healthy mothers and their neonates. 56 mothers with normal gestational course and spontaneous delivery were selected. Blood samples were taken from mother (before and after delivery) both from vein and artery of umbilical cord. Lower antioxidant enzymes activities were observed in neonates compared with their mothers and lower oxidative stress in umbilical cord artery with respect to vein. There was an overexpression of inflammatory cytokines in the mother, such as IL-6 and TNF-α, and, in addition, PGE2was also increased. Neonates showed lower levels of IL-6 and TNF-αand higher values of sTNF-RII and PGE2in comparison with their mothers. Parturition increases oxidative damage in the mother, although the indicators of oxidative damage were lower in umbilical cord artery with respect to umbilical vein. The overexpression of inflammatory cytokines reveals that fetus suffers its own inflammatory process during parturition.

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A Soccer Match’s Ability to Enhance Lymphocyte Capability to Produce ROS and Induce Oxidative Damage

International Journal of Sport Nutrition and Exercise Metabolism ◽

10.1123/ijsnem.19.3.243 ◽

2009 ◽

Vol 19 (3) ◽

pp. 243-258 ◽

Cited By ~ 18

Author(s):

Miguel David Ferrer ◽

Pedro Tauler ◽

Antoni Sureda ◽

Pedro Pujol ◽

Franchec Drobnic ◽

...

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Coenzyme Q ◽

Training Period ◽

Antioxidant Vitamin ◽

Antioxidant Enzyme Activities ◽

Double Blind ◽

Soccer Match ◽

Before And After ◽

Soccer Training

Soccer-associated oxidative stress has barely been studied. The aims of this study were to establish the effect of a soccer training match and the effect of a diet supplementation with a multivitamin complex and coenzyme Q during 3 months of soccer training on the pro-oxidant and antioxidant status of lymphocytes. In a randomized, double-blind trial, 19 male preprofessional soccer players were treated with either an antioxidant nutrient cocktail or placebo for 90 days. After this period the athletes played a soccer match lasting 60 min. All determinations were made under basal conditions before and after the training period and after the match. Basal lymphocyte hydrogen peroxide (H2O2) production did not change after the 3 months of training. Catalase activity decreased (about 50%) after the 3 months, whereas glutathione reductase increased its activity (150–200%) both with placebo and in the supplemented group. Basal ascorbate levels were maintained during the training period, whereas α-tocopherol and MDA decreased (about 40%) in both groups. The match increased H2O2 production (180%) in both groups when the lymphocytes were stimulated with phorbol myristate acetate, and it also increased MDA levels (150%). Antioxidant enzyme activities and antioxidant vitamin levels were maintained before and after the match. Regular soccer training modifies the lymphocyte strategy to eliminate ROS and increases protection against oxidative damage. A friendly soccer match raises lymphocyte capacity to produce ROS and oxidative damage, but it is not enough to induce a defensive response, thus leading to a situation of postexercise oxidative stress. Supplementation with low doses of antioxidant vitamins and coenzyme Q does not modify the endogenous antioxidant response to training.

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Panax Quinquefolius Saponin of Stem and Leaf Attenuates Intermittent High Glucose-Induced Oxidative Stress Injury in Cultured Human Umbilical Vein Endothelial Cells via PI3K/Akt/GSK-3βPathway

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2013/196283 ◽

2013 ◽

Vol 2013 ◽

pp. 1-7 ◽

Cited By ~ 5

Author(s):

Jingshang Wang ◽

Huijun Yin ◽

Ye Huang ◽

Chunyu Guo ◽

Chengdong Xia ◽

...

Keyword(s):

Oxidative Stress ◽

Endothelial Cells ◽

Oxidative Damage ◽

Cell Viability ◽

High Glucose ◽

Umbilical Vein ◽

Panax Quinquefolius ◽

Stress Injury ◽

Intermittent High Glucose ◽

Umbilical Vein Endothelial Cells

Panax quinquefolius saponin of stem and leaf (PQS), the effective parts of American ginseng, is widely used in China as a folk medicine for diabetes and cardiovascular diseases treatment. In our previous studies, we have demonstrated that PQS could improve the endothelial function of type II diabetes mellitus (T2DM) rats with high glucose fluctuation. In the present study, we investigated the protective effects of PQS against intermittent high glucose-induced oxidative damage on human umbilical vein endothelial cells (HUVECs) and the role of phosphatidylinositol 3-kinase kinase (PI3K)/Akt/GSK-3βpathway involved. Our results suggested that exposure of HUVECs to a high glucose concentration for 8 days showed a great decrease in cell viability accompanied by marked MDA content increase and SOD activity decrease. Moreover, high glucose significantly reduced the phosphorylation of Akt and GSK-3β. More importantly, these effects were even more evident in intermittent high glucose condition. PQS treatment significantly attenuated intermittent high glucose-induced oxidative damage on HUVECs and meanwhile increased cell viability and phosphorylation of Akt and GSK-3βof HUVECs. Interestingly, all these reverse effects of PQS on intermittent high glucose-cultured HUVECs were inhibited by PI3K inhibitor LY294002. These findings suggest that PQS attenuates intermittent-high-glucose-induced oxidative stress injury in HUVECs by PI3K/Akt/GSK-3βpathway.

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Exposure of β H-crystallin to hydroxyl radicals enhances the transglutaminase-susceptibility of its existing amine-donor and amine-acceptor sites

Biochemical Journal ◽

10.1042/bj2950399 ◽

1993 ◽

Vol 295 (2) ◽

pp. 399-404 ◽

Cited By ~ 21

Author(s):

P J T A Groenen ◽

M Seccia ◽

R H P H Smulders ◽

E Gravela ◽

K H Cheeseman ◽

...

Keyword(s):

Oxidative Stress ◽

Hydroxyl Radicals ◽

Primary Amine ◽

Lens Crystallins ◽

Acceptor Substrate ◽

Transglutaminase Activity ◽

Donor Substrate ◽

Before And After ◽

First Time ◽

Oxidative Attack

beta H-crystallin was exposed to radiolytically generated hydroxyl radicals at defined radical concentrations, and its capacity to act as an amine-acceptor substrate and as an amine-donor substrate for transglutaminase were investigated. [14C]Methylamine was used as a probe for labelling amine-acceptor sites; a novel biotinylated hexapeptide was used to label amine-donor sites. The results demonstrate that both primary amine incorporation and hexapeptide incorporation by transglutaminase are considerably increased after oxidative attack on the crystallin. The identity of the labelled subunits was established, and it is shown that, in both cases, this increased incorporation is not due to the production of new substrates, but that the existing incorporation sites become more susceptible. Moreover, using the newly developed probe, we could identify, for the first time, the major crystallin subunits active as amine-donor substrates (both before and after treatment) to be beta B1-, beta A3- and beta A4-crystallin. These data support the proposal that oxidative stress and transglutaminase activity may be jointly involved in the changes found in lens crystallins with age and in the development of cataract.

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After In Vitro Digestion, Jackfruit Flake Affords Protection against Acrylamide-Induced Oxidative Damage

Molecules ◽

10.3390/molecules24183322 ◽

2019 ◽

Vol 24 (18) ◽

pp. 3322 ◽

Cited By ~ 1

Author(s):

Daofeng Qu ◽

Chu Liu ◽

Mengxue Jiang ◽

Lifang Feng ◽

Yuewen Chen ◽

...

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

High Performance ◽

In Vitro Digestion ◽

Protective Effects ◽

Physical Damage ◽

Before And After ◽

High Content Analysis ◽

High Level

Some studies have demonstrated that acrylamide (AA) was correlated with oxidative stress, resulting in physical damage. The jackfruit flake was an immature pulp that contained a high level of antioxidant activity. This study aimed to assess the defensive efficacy of jackfruit flake in AA-induced oxidative stress before and after simulated gastrointestinal digestion. Our results indicate that the total polyphenol content of Jackfruit flake digest (Digestive products of jackfruit flake after gastrointestinal, JFG) was diminished; however, JFG had raised the relative antioxidant capacity compared to Jackfruit flake extract (JFE). Additionally, the results of High Performance Liquid Chromatography-Mass Spectrometry (HPLC-MS) implied that a proportion of compounds were degraded/converted into other unknown and/or undetected metabolites. Further, by high content analysis (HCA) techniques, JFG markedly reduced cytotoxicity and excessive production of reactive oxygen species (ROS) in cells, thereby alleviating mitochondrial disorders. In this study, it may be converted active compounds after digestion that had preferable protective effects against AA-induced oxidative damage.

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Coenzyme Q10 Prevents Senescence and Dysfunction Caused by Oxidative Stress in Vascular Endothelial Cells

Oxidative Medicine and Cellular Longevity ◽

10.1155/2018/3181759 ◽

2018 ◽

Vol 2018 ◽

pp. 1-15 ◽

Cited By ~ 18

Author(s):

Jia Huo ◽

Zhe Xu ◽

Kazunori Hosoe ◽

Hiroshi Kubo ◽

Hiroki Miyahara ◽

...

Keyword(s):

Oxidative Stress ◽

Endothelial Cells ◽

Oxidative Damage ◽

Mitochondrial Function ◽

Coenzyme Q10 ◽

Vascular Endothelial Cells ◽

Umbilical Vein ◽

Tube Formation ◽

Reduced Form ◽

No Production

Oxidative damage in endothelial cells is proposed to play an important role in endothelial dysfunction and atherogenesis. We previously reported that the reduced form of coenzyme Q10 (CoQ10H2) effectively inhibits oxidative stress and decelerates senescence in senescence-accelerated mice. Here, we treated human umbilical vein endothelial cells (HUVECs) with H2O2 and investigated the protective effect of CoQ10H2 against senescence, oxidative damage, and reduction in cellular functions. We found that CoQ10H2 markedly reduced the number of senescence-associated β-galactosidase-positive cells and suppressed the expression of senescence-associated secretory phenotype-associated genes in H2O2-treated HUVECs. Furthermore, CoQ10H2 suppressed the generation of intracellular reactive oxygen species (ROS) but promoted NO production that was accompanied by increased eNOS expression. CoQ10H2 prevented apoptosis and reductions in mitochondrial function and reduced migration and tube formation activity of H2O2-treated cells. The present study indicated that CoQ10H2 protects endothelial cells against senescence by promoting mitochondrial function and thus could delay vascular aging.

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EGCG Attenuates Uric Acid-Induced Inflammatory and Oxidative Stress Responses by Medicating the NOTCH Pathway

Oxidative Medicine and Cellular Longevity ◽

10.1155/2015/214836 ◽

2015 ◽

Vol 2015 ◽

pp. 1-10 ◽

Cited By ~ 25

Author(s):

Hua Xie ◽

Jianqin Sun ◽

Yanqiu Chen ◽

Min Zong ◽

Shijie Li ◽

...

Keyword(s):

Oxidative Stress ◽

Uric Acid ◽

Inflammatory Cytokines ◽

Stress Responses ◽

Umbilical Vein ◽

Notch Pathway ◽

Notch 1 ◽

Western Blots ◽

And Oxidative Stress

Background. The aim of this study is to investigate whether (-)-epigallocatechin-3-gallate (EGCG) can prevent the UA-induced inflammatory effect of human umbilical vein endothelial cells (HUVEC) and the involved mechanisms in vitro.Methods. HUVEC were subjected to uric acid (UA) with or without EGCG treatment. RT-PCR and western blots were performed to determine the level of inflammation marker. The antioxidant activity was evaluated by measuring scavenged reactive oxygen species (ROS). Functional studies of the role of Notch-1 in HUVEC lines were performed using RNA interference analyses.Results. UA significantly increased the expressions of IL-6, ICAM-1, TNF-α, and MCP-1 and the production of ROS in HUVEC. Meanwhile, the expression of Notch-1 and its downstream effects significantly increased. Using siRNA, inhibition of Notch-1 signaling significantly impeded the expressions of inflammatory cytokines under UA treatment. Interestingly, EGCG suppressed the expressions of inflammatory cytokines and the generation of ROS. Western blot analysis of Notch-1 showed that EGCG significantly decreased the expressions of inflammatory cytokines through Notch-1 signaling pathways.Conclusions. In summary, our findings indicated that Notch-1 plays an important role in the UA-induced inflammatory response, and the downregulation of Notch-1 by EGCG could be an effective approach to decrease inflammation and oxidative stress induced by UA.

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Ubiquinol Improves Symptoms in Children with Autism

Oxidative Medicine and Cellular Longevity ◽

10.1155/2014/798957 ◽

2014 ◽

Vol 2014 ◽

pp. 1-6 ◽

Cited By ~ 26

Author(s):

Anna Gvozdjáková ◽

Jarmila Kucharská ◽

Daniela Ostatníková ◽

Katarína Babinská ◽

Dalibor Nakládal ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Neurodevelopmental Disorders ◽

Supportive Therapy ◽

Children With Autism ◽

Daily Dose ◽

Before And After ◽

Self Harm ◽

Dsm Iv ◽

First Time

Background. Autism is a spectrum of neurodevelopmental disorders with manifestation within 3 years after birth. Manifestations of autism include behavior problems (hyperactivity, toys destruction, self-harm, and agression) and sleep and eating disorders. Etiology of autism is poorly understood. Oxidative stress and antioxidants can participate in pathobiochemical mechanisms of autism.Methods. Twenty-four children, aged 3–6 years, with autism according to the DSM IV criteria and using CARS were included in the study. Concentrations ofCoQ10-TOTAL,γ- andα-tocopherol,β-carotene, and lipid peroxidation were determined in plasma before and after three months of supportive therapy with ubiquinol at a daily dose2×50 mg. Data on behavior of the children were collected from parents at the same time.Results. Ubiquinol supportive therapy improved symptoms in children with autism, as communication with parents (in12%), verbal communication (in21%), playing games of children (in42%), sleeping (in34%), and food rejection (in17%), withCoQ10-TOTALplasma level above2.5 μmol/L.Conclusions. Beneficial effect of ubiquinol in children with autism has been demonstrated for the first time. We assume that plasma concentration ofCoQ10-TOTALand lipid peroxidation could be used as relevant biomarkers of ubiquinol supportive therapy.

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Protective effects of peoniflorin against hydrogen peroxide-induced oxidative stress in human umbilical vein endothelial cells

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y11-034 ◽

2011 ◽

Vol 89 (6) ◽

pp. 445-453 ◽

Cited By ~ 34

Author(s):

Tao Chen ◽

Zai-pei Guo ◽

Xiao-yan Jiao ◽

Yu-hong Zhang ◽

Jing-yi Li ◽

...

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Endothelial Cells ◽

Oxidative Damage ◽

Umbilical Vein ◽

Flow Cytometric Analysis ◽

Vascular Diseases ◽

Protective Effects ◽

Human Umbilical Vein ◽

Umbilical Vein Endothelial Cells

Peoniflorin (PF), extracted from the root of Paeonia lactiflora Pall., has been reported to have anti-inflammation and antioxidant effects in several animal models. Herein, we investigated the protective effects of PF against hydrogen peroxide (H2O2)-induced oxidative damage in human umbilical vein endothelial cells (HUVECs). HUVECs were treated by H2O2 (240 µmol/L) with or without PF. PF significantly increased the percent cell viability of HUVECs injured by H2O2 using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. By flow cytometric analysis, PF markedly attenuated H2O2-induced apoptosis and intracellular reactive oxygen species production. In addition, PF also displayed a dose-dependent reduction of lactate dehydrogenase leakage, malondialdehyde formation, and caspase-3 proteolytic activities in H2O2-treated cells, which was accompanied with a restoration of the activities of endogenous antioxidants, including total superoxide dismutase and glutathione peroxidase. Finally, Western blot data revealed that H2O2 upregulated phosphorylation of extracellular signal-regulated kinase 1/2 in HUVECs, which was almost completely reversed by PF. Taken together, our data provide the first evidence that PF has a protective ability against oxidative damage in HUVECs. PF may be a candidate medicine for the treatment of vascular diseases associated with oxidative stress.

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Laminarin Pretreatment Provides Neuroprotection against Forebrain Ischemia/Reperfusion Injury by Reducing Oxidative Stress and Neuroinflammation in Aged Gerbils

Marine Drugs ◽

10.3390/md18040213 ◽

2020 ◽

Vol 18 (4) ◽

pp. 213 ◽

Cited By ~ 3

Author(s):

Joon Ha Park ◽

Ji Hyeon Ahn ◽

Tae-Kyeong Lee ◽

Cheol Woo Park ◽

Bora Kim ◽

...

Keyword(s):

Oxidative Stress ◽

Inflammatory Cytokines ◽

Pyramidal Neurons ◽

Ischemia Reperfusion Injury ◽

Neuroprotective Effect ◽

Ischemia Reperfusion ◽

Forebrain Ischemia ◽

Ca1 Pyramidal Neurons ◽

Before And After ◽

Anti Inflammatory

Laminarin is a polysaccharide isolated from brown algae that has various biological and pharmacological activities, such as antioxidant and anti-inflammatory properties. We recently reported that pretreated laminarin exerted neuroprotection against transient forebrain ischemia/reperfusion (IR) injury when we pretreated with 50 mg/kg of laminarin once a day for seven days in adult gerbils. However, there have been no studies regarding a neuroprotective effect of pretreated laminarin against IR injury in aged animals and its related mechanisms. Therefore, in this study, we intraperitoneally inject laminarin (50 mg/kg) once a day to aged gerbils for seven days before IR (5-min transient ischemia) surgery and examine the neuroprotective effect of laminarin treatment and the mechanisms in the gerbil hippocampus. IR injury in vehicle-treated gerbils causes loss (death) of pyramidal neurons in the hippocampal CA1 field at five days post-IR. Pretreatment with laminarin effectively protects the CA1 pyramidal neurons from IR injury. Regarding the laminarin-treated gerbils, production of superoxide anions, 4-hydroxy-2-nonenal expression and pro-inflammatory cytokines [interleukin(IL)-1β and tumor necrosis factor-α] expressions are significantly decreased in the CA1 pyramidal neurons after IR. Additionally, laminarin treatment significantly increases expressions of superoxide dismutase and anti-inflammatory cytokines (IL-4 and IL-13) in the CA1 pyramidal neurons before and after IR. Taken together, these findings indicate that laminarin can protect neurons from ischemic brain injury in an aged population by attenuating IR-induced oxidative stress and neuroinflammation.

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Prenatal exposure to testosterone impairs oxidative damage repair efficiency in the domestic chicken ( Gallus gallus )

Biology Letters ◽

10.1098/rsbl.2013.0684 ◽

2013 ◽

Vol 9 (5) ◽

pp. 20130684 ◽

Cited By ~ 22

Author(s):

L. A. Treidel ◽

B. N. Whitley ◽

Z M. Benowitz-Fredericks ◽

M. F. Haussmann

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Gallus Gallus ◽

Yolk Androgens ◽

Stress Markers ◽

Damage Repair ◽

Before And After ◽

Total Antioxidant ◽

Oxidative Challenge ◽

Acute Stressor

Elevated levels of maternal androgens in avian eggs affect numerous traits, including oxidative stress. However, current studies disagree as to whether prenatal androgen exposure enhances or ameliorates oxidative stress. Here, we tested how prenatal testosterone exposure affects oxidative stress in female domestic chickens ( Gallus gallus ) during the known oxidative challenge of an acute stressor. Prior to incubation, eggs were either injected with an oil vehicle or 5 ng testosterone. At either 17 or 18 days post-hatch, several oxidative stress markers were assessed from blood taken before and after a 20 min acute stressor, as well as following a 25 min recovery from the stressor. We found that, regardless of yolk treatment, during both stress and recovery all individuals were in a state of oxidative stress, with elevated levels of oxidative damage markers accompanied by a reduced total antioxidant capacity. In addition, testosterone-exposed individuals exhibited poorer DNA damage repair efficiencies in comparison with control individuals. Our work suggests that while yolk androgens do not alter oxidative stress directly, they may impair mechanisms of oxidative damage repair.

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