The Impact of Oxidative Stress of Environmental Origin on the Onset of Placental Diseases

Oxidative stress (OS) plays a pivotal role in placental development; however, abnormal loads in oxidative stress molecules may overwhelm the placental defense mechanisms and cause pathological situations. The environment in which the mother evolves triggers an exposure of the placental tissue to chemical, physical, and biological agents of OS, with potential pathological consequences. Here we shortly review the physiological and developmental functions of OS in the placenta, and present a series of environmental pollutants inducing placental oxidative stress, for which some insights regarding the underlying mechanisms have been proposed, leading to a recapitulation of the noxious effects of OS of environmental origin upon the human placenta.

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Pathomechanisms of Oxidative Stress in Inflammatory Bowel Disease and Potential Antioxidant Therapies

Oxidative Medicine and Cellular Longevity ◽

10.1155/2017/4535194 ◽

2017 ◽

Vol 2017 ◽

pp. 1-18 ◽

Cited By ~ 96

Author(s):

Tian Tian ◽

Ziling Wang ◽

Jinhua Zhang

Keyword(s):

Oxidative Stress ◽

Inflammatory Bowel Disease ◽

Bowel Disease ◽

Defense Mechanisms ◽

Gastrointestinal Disease ◽

Mucosal Immune Response ◽

Stress Signaling ◽

Substantial Progress ◽

Inflammatory Bowel ◽

Underlying Mechanisms

Inflammatory bowel disease (IBD) is a chronic gastrointestinal disease whose incidence has risen worldwide in recent years. Accumulating evidence shows that oxidative stress plays an essential role in the pathogenesis and progression of IBD. This review highlights the generation of reactive oxygen species (ROS) and antioxidant defense mechanisms in the gastrointestinal (GI) tract, the involvement of oxidative stress signaling in the initiation and progression of IBD and its relationships with genetic susceptibility and the mucosal immune response. In addition, potential therapeutic strategies for IBD that target oxidative stress signaling are reviewed and discussed. Though substantial progress has been made in understanding the role of oxidative stress in IBD in humans and experimental animals, the underlying mechanisms are still not well defined. Thus, further studies are needed to validate how oxidative stress signaling is involved in and contributes to the development of IBD.

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Mineral Micronutrients in Asthma

Nutrients ◽

10.3390/nu13114001 ◽

2021 ◽

Vol 13 (11) ◽

pp. 4001

Author(s):

Dominika Zajac

Keyword(s):

Oxidative Stress ◽

Risk Factors ◽

Air Pollution ◽

Defense Mechanisms ◽

Redox Status ◽

Chronic Inflammatory Disease ◽

Modern World ◽

Medical Issues ◽

Persistent Inflammation ◽

The Impact

Asthma represents one of the most common medical issues in the modern world. It is a chronic inflammatory disease characterized by persistent inflammation of the airways and disturbances in redox status, leading to hyperresponsiveness of bronchi and airway obstruction. Apart from classical risk factors such as air pollution, family history, allergies, or obesity, disturbances of the levels of micronutrients lead to impairments in the defense mechanisms of the affected organism against oxidative stress and proinflammatory stimuli. In the present review, the impact of micronutrients on the prevalence, severity, and possible risk factors of asthma is discussed. Although the influence of classical micronutrients such as selenium, copper, or zinc are well known, the effects of those such as iodine or manganese are only rarely mentioned. As a consequence, the aim of this paper is to demonstrate how disturbances in the levels of micronutrients and their supplementation might affect the course of asthma.

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Reduced Oxidative Stress and Enhanced FGF21 Formation in Livers of Endurance-Exercised Rats with Diet-Induced NASH

Nutrients ◽

10.3390/nu11112709 ◽

2019 ◽

Vol 11 (11) ◽

pp. 2709 ◽

Cited By ~ 1

Author(s):

Janin Henkel ◽

Katja Buchheim-Dieckow ◽

José P. Castro ◽

Thomas Laeger ◽

Kristina Wardelmann ◽

...

Keyword(s):

Oxidative Stress ◽

Endurance Exercise ◽

Weight Reduction ◽

Dietary Intervention ◽

Exercise Group ◽

Severe Form ◽

Alcoholic Fatty Liver ◽

Male Wistar Rats ◽

Underlying Mechanisms ◽

The Impact

Non-alcoholic fatty liver diseases (NAFLD) including the severe form with steatohepatitis (NASH) are highly prevalent ailments to which no approved pharmacological treatment exists. Dietary intervention aiming at 10% weight reduction is efficient but fails due to low compliance. Increase in physical activity is an alternative that improved NAFLD even in the absence of weight reduction. The underlying mechanisms are unclear and cannot be studied in humans. Here, a rat NAFLD model was developed that reproduces many facets of the diet-induced NAFLD in humans. The impact of endurance exercise was studied in this model. Male Wistar rats received control chow or a NASH-inducing diet rich in fat, cholesterol, and fructose. Both diet groups were subdivided into a sedentary and an endurance exercise group. Animals receiving the NASH-inducing diet gained more body weight, got glucose intolerant and developed a liver pathology with steatosis, hepatocyte hypertrophy, inflammation and fibrosis typical of NAFLD or NASH. Contrary to expectations, endurance exercise did not improve the NASH activity score and even enhanced hepatic inflammation. However, endurance exercise attenuated the hepatic cholesterol overload and the ensuing severe oxidative stress. In addition, exercise improved glucose tolerance possibly in part by induction of hepatic FGF21 production.

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Preserved placental oxygenation and development during severe systemic hypoxia

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00237.2005 ◽

2006 ◽

Vol 290 (3) ◽

pp. R844-R851 ◽

Cited By ~ 24

Author(s):

Leonhard Schäffer ◽

Johannes Vogel ◽

Christian Breymann ◽

Max Gassmann ◽

Hugo H. Marti

Keyword(s):

Hypoxia Inducible Factor ◽

Central Area ◽

Placental Tissue ◽

Tissue Hypoxia ◽

Placental Development ◽

Systemic Hypoxia ◽

Pregnant Mice ◽

Endothelial Nitric Oxide ◽

The Impact

Local tissue oxygenation profoundly influences placental development. To elucidate the impact of hypoxia on cellular and molecular adaptation in vivo, pregnant mice at embryonic days 7.5–11.5 were exposed to reduced environmental oxygen (6–7% O2) for various periods of time. Hypoxia-inducible factor (HIF)-1α mRNA was highly expressed in the placenta, whereas HIF-2α was predominantly found in the decidua, indicating that HIF-1 is a relevant oxygen-dependent factor involved in placental development. During severe hypoxia, HIF-1α protein was strongly induced in the periphery but, however, not in the labyrinth layer of the placenta. Accordingly, no indication for tissue hypoxia in this central area was detected with 2-(2-nitro-1 H-imidazol-1-yl)- N-(2,2,3,3,3-pentafluoropropyl)acetamide staining and VEGF expression as hypoxic markers. The absence of significant tissue hypoxia was reflected by preserved placental architecture and trophoblast differentiation. In the search for mechanisms preventing local hypoxia, we found upregulation of endothelial nitric oxide synthase (NOS) expression in the labyrinth layer. Inhibition of NOS activity by Nω-nitro-l-arginine methyl ester application resulted in ubiquitous placental tissue hypoxia. Our results show that placental oxygenation is preserved even during severe systemic hypoxia and imply that NOS-mediated mechanisms are involved to protect the placenta from maternal hypoxia.

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Ozone-Induced Oxidative Stress, Neutrophilic Airway Inflammation, and Glucocorticoid Resistance in Asthma

Frontiers in Immunology ◽

10.3389/fimmu.2021.631092 ◽

2021 ◽

Vol 12 ◽

Author(s):

Chioma Enweasor ◽

Cameron H. Flayer ◽

Angela Haczku

Keyword(s):

Oxidative Stress ◽

Airway Inflammation ◽

Γδ T Cells ◽

Air Pollutant ◽

Glucocorticoid Resistance ◽

Primary Data ◽

Alveolar Type ◽

Underlying Mechanisms ◽

The Impact

Despite recent advances in using biologicals that target Th2 pathways, glucocorticoids form the mainstay of asthma treatment. Asthma morbidity and mortality remain high due to the wide variability of treatment responsiveness and complex clinical phenotypes driven by distinct underlying mechanisms. Emerging evidence suggests that inhalation of the toxic air pollutant, ozone, worsens asthma by impairing glucocorticoid responsiveness. This review discusses the role of oxidative stress in glucocorticoid resistance in asthma. The underlying mechanisms point to a central role of oxidative stress pathways. The primary data source for this review consisted of peer-reviewed publications on the impact of ozone on airway inflammation and glucocorticoid responsiveness indexed in PubMed. Our main search strategy focused on cross-referencing “asthma and glucocorticoid resistance” against “ozone, oxidative stress, alarmins, innate lymphoid, NK and γδ T cells, dendritic cells and alveolar type II epithelial cells, glucocorticoid receptor and transcription factors”. Recent work was placed in the context from articles in the last 10 years and older seminal research papers and comprehensive reviews. We excluded papers that did not focus on respiratory injury in the setting of oxidative stress. The pathways discussed here have however wide clinical implications to pathologies associated with inflammation and oxidative stress and in which glucocorticoid treatment is essential.

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The impact of the novel coronavirus infection COVID-19 on the mother-placenta-fetus system

Bulletin of Russian State Medical University ◽

10.24075/brsmu.2021.020 ◽

2021 ◽

Author(s):

NV Nizyaeva ◽

NA Lomova ◽

EL Dolgopolova ◽

UL Petrova ◽

TE Karapetyan ◽

...

Keyword(s):

Pregnant Women ◽

Clinical Manifestations ◽

Placental Tissue ◽

Inflammatory Factors ◽

The Novel ◽

Placental Development ◽

Index Group ◽

Elevated Expression ◽

Novel Coronavirus ◽

The Impact

Impaired placental development during early pregnancy associated with systemic damage to the vascular endothelium in patients with COVID-19 may result in a number of complications. The study was aimed to reveal histological and immunohistochemical (IHC) features of placental tissue in pregnant women with COVID-19 at different stages of gestation, and to examine the contribution of those to pathogenesis of the disease involving mother-placenta-fetus system. The following two groups of pregnant women were studied: index group of 66 patients with COVID-19, and comparison group of 40 women with no symptoms of viral infection. Macroscopic and microscopic examination, and the IHC analysis of placental samples were carried out. Clinical and anamnestic characteristics of patients with COVID-19 were analyzed taking into account disease severity, delivery route and perinatal outcome. ICH staining using primary antibody revealed elevated expression of proinflammatory factors (TNFα, IL8) and reduced level of anti-inflammatory factors (IL4) in placental structures of patients with moderate and severe СOVID-19 (р < 0.05). The villous tree rearrangement and the development of subclinical placental insufficiency, which could in some cases be decompensated during labor, resulting in clinical manifestations of acute fetal hypoxia were detected in the placental samples obtained from the index group patients. The obstetrical tactics for mothers with COVID-19 should be decided individually based on the risk factors; continuous cardiotocography should be used during labor. It may be appropriate to conduct IHC analysis of placenta in puerperant women with COVID-19 in order to fine-tune the tactics of neonatal management and to predict possible neonatal complications.

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Hydrogen Sulfide Protects against Chemical Hypoxia-Induced Injury via Attenuation of ROS-Mediated Ca2+Overload and Mitochondrial Dysfunction in Human Bronchial Epithelial Cells

BioMed Research International ◽

10.1155/2018/2070971 ◽

2018 ◽

Vol 2018 ◽

pp. 1-9 ◽

Cited By ~ 7

Author(s):

Cai-Xia Liu ◽

Yu-Rong Tan ◽

Yang Xiang ◽

Chi Liu ◽

Xiao-Ai Liu ◽

...

Keyword(s):

Oxidative Stress ◽

Hydrogen Sulfide ◽

Cell Injury ◽

Fluorescence Probe ◽

Environmental Pollutants ◽

Cell Counting ◽

Dependent Manner ◽

Mitochondria Membrane Potential ◽

Chemical Hypoxia ◽

The Impact

Oxidative stress induced by hypoxia/ischemia resulted in the excessive reactive oxygen species (ROS) and the relative inadequate antioxidants. As the initial barrier to environmental pollutants and allergic stimuli, airway epithelial cell is vulnerable to oxidative stress. In recent years, the antioxidant effect of hydrogen sulfide (H2S) has attracted much attention. Therefore, in this study, we explored the impact of H2S on CoCl2-induced cell injury in 16HBE14o- cells. The effect of CoCl2on the cell viability was detected by Cell Counting Kit (CCK-8) and the level of ROS in 16HBE14o- cells in response to varying doses (100–1000μmol/L) of CoCl2(a common chemical mimic of hypoxia) was measured by using fluorescent probe DCFH-DA. It was shown that, in 16HBE14o- cells, CoCl2acutely increased the ROS content in a dose-dependent manner, and the increased ROS was inhibited by the NaHS (as a donor of H2S). Moreover, the calcium ion fluorescence probe Fura-2/AM and fluorescence dye Rh123 were used to investigate the intracellular calcium concentration ([Ca2+]i) and mitochondria membrane potential (MMP) in 16HBE14o- cells, respectively. In addition, we examined apoptosis of 16HBE14o- cells with Hoechst 33342. The results showed that the CoCl2effectively elevated the Ca2+influx, declined the MMP, and aggravated apoptosis, which were abrogated by NaHS. These results demonstrate that H2S could attenuate CoCl2-induced hypoxia injury via reducing ROS to perform an agonistic role for the Ca2+influx and MMP dissipation.

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Regulation of vascular growth and function in the human placenta

Reproduction ◽

10.1530/rep-09-0092 ◽

2009 ◽

Vol 138 (6) ◽

pp. 895-902 ◽

Cited By ~ 161

Author(s):

G J Burton ◽

D S Charnock-Jones ◽

E Jauniaux

Keyword(s):

Oxidative Stress ◽

Growth Factor ◽

Human Placenta ◽

Normal Pregnancy ◽

Maternal Circulation ◽

Placental Angiogenesis ◽

Terminal Villi ◽

And Function ◽

Endothelial Growth Factor ◽

The Impact

During the course of 9 months, the human placenta develops into a highly vascular organ. Vasculogenesis starts during the third week post-conception. Hemangioblastic cell cords differentiatein situfrom mesenchymal cells in the villous cores, most probably under the influence of vascular endothelial growth factor (VEGFA) secreted by the overlying trophoblast. The cords elongate through proliferation and cell recruitment, and connect with the vasculature of the developing fetus. A feto-placental circulation starts around 8 weeks of gestation. Elongation of the capillaries outstrips that of the containing villi, leading to looping of the vessels. The obtrusion of both capillary loops and new sprouts results in the formation of terminal villi. Branching and non-branching angiogenesis therefore play key roles in villous morphogenesis throughout pregnancy. Maternal circulating levels of VEGFA and placental growth factor vary across normal pregnancy, and in complicated pregnancies. Determining the impact of these changes on placental angiogenesis is difficult, as the relationship between levels of factors in the maternal circulation and their effects on fetal vessels within the placenta remains unclear. Furthermore, the trophoblast secretes large quantities of soluble receptors capable of binding both growth factors, influencing their bioavailability. Villous endothelial cells are prone to oxidative stress, which activates the apoptotic cascade. Oxidative stress associated with onset of the maternal circulation, and with incomplete conversion of the spiral arteries in pathological pregnancies, plays an important role in sculpting the villous tree. Suppression of placental angiogenesis results in impoverished development of the placenta, leading ultimately to fetal growth restriction.

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The impact of melatonin on antioxidant defense mechanisms in Alzheimer’s disease

Postępy Higieny i Medycyny Doświadczalnej ◽

10.5604/01.3001.0012.8252 ◽

2018 ◽

Vol 72 ◽

pp. 1114-1122

Author(s):

Daria Malicka ◽

Dominika Markowska ◽

Jarosław Nuszkiewicz ◽

Karolina Szewczyk-Golec

Keyword(s):

Oxidative Stress ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Defense Mechanisms ◽

Senile Plaques ◽

Biological Clock ◽

Cell Functions ◽

Increased Risk ◽

The Impact ◽

Phosphorylated Tau Protein

During aging, the increased risk of neurodegenerative disease development is observed. One of the most common and most serious disorders is Alzheimer’s disease manifested by the loss of nerve cell functions. In the course of the disease, extracellular senile plaques consisting of beta-amyloid and intracellular neurofibrillary tangles of hyper-phosphorylated tau protein are formed. As a result of aging, the repair potential of damaged nerve cells is reduced. Free radicals formed in excess generate augmented oxidative stress, which contributes to the damaging of biomolecules and the development of pathological changes. This mechanism is favored by a decrease in the efficiency of antioxidant enzymes and the deficiency of antioxidants, observed in aging organism. With age, the secretion of the pineal hormone melatonin, functioning as a biochemical biological clock, is significantly reduced. This compound has been proved to be a very effective antioxidant that plays a key role in protecting cells against excessive damage, especially in nervous tissue. Studies have shown that supplementation with exogenous melatonin can prevent oxidative stress-induced degeneration of neurons. Considering the action of melatonin and the pathogenesis of Alzheimer’s disease, the idea of using the hormone supplementation in the prevention and alleviation of the effects of the disease seems to be extremely interesting.

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COPPER AS AN ANSWER ON THE IMPACT OF OXYDESS STRESS ON THE EYES

Zeszyty Naukowe Uniwersytetu Zielonogórskiego / Inżynieria Środowiska ◽

10.5604/01.3001.0013.0259 ◽

2018 ◽

Vol 172 (52) ◽

pp. 23-28

Author(s):

Katarzyna Kempka ◽

Piotr Kamiński ◽

Grażyna Malukiewicz ◽

Maria Bogdzińska

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Environmental Conditions ◽

Defense Mechanisms ◽

Chemical Elements ◽

Reactive Oxygen ◽

Oxygen Species ◽

State Of Emergency ◽

The Impact ◽

And Oxidative Stress

The eyes are exposed to many factors, that contribute to the deterioration of their condition. These include environmental conditions and the influence of reactive oxygen species ROS and oxidative stress. Research shows, that one of the most important tasks of created in such way state of emergency is maintenance of relative balance between oxidants (contributing to the formation of ROS) and antioxidants (restraining their effect). Some chemical elements, especially copper, play a key role in blocking ROS and presents an overview of information on the impact of oxidative stress on the eyes and the defense mechanisms with the participation of copper.

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