scholarly journals Imidacloprid - Induced Pathophysiological Damage in the Midgut of Locusta Migratoria (Orthoptera: Acrididae) in the Field

2021 ◽  
Author(s):  
Lamia M. El-Samad ◽  
Mohamed S. El-Gerbed ◽  
Hanaa S. Hussein ◽  
Justin Flaven-Pouchon ◽  
Abeer El Wakil ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Physiological Function ◽  
Locusta Migratoria ◽  
Reactive Oxygen ◽  
Oxygen Metabolism ◽  
Oxygen Species ◽  
Beneficial Insects ◽  
Markers Of Oxidative Stress ◽  
Activity Of Enzymes

Abstract Neonicotinoids are modern insecticides widely used in agriculture worldwide. Their impact on target (nervous system) and non-target (midgut) tissues has been well studied in beneficial insects including honeybees. However, their effects on pest insects on the field are comparably rarely described. Here, we have studied the effects of the neonicotinoid imidacloprid on the midgut of the pest insect Locusta migratoria caught in the field. We found that in the midgut of imidacloprid-exposed locusts the activity of enzymes involved in reactive oxygen metabolism was perturbed. By contrast, the activity of P450 enzymes that have been shown to be activated in a detoxification response and that were also reported to produce reactive oxygen species was elevated. Probably as a consequence, markers of oxidative stress including protein carbonylation and lipid peroxidation accumulated in midgut samples of these locusts. Histological analyses revealed that their midgut epithelium is disorganized and that the brush border of the epithelial cells is markedly reduced. Indeed, microvilli are significantly shorter, misshapen and possibly non-functional in imidacloprid-treated locusts. We hypothesize that imidacloprid induces oxidative stress in the locust midgut, thereby changing the shape of midgut epithelial cells and probably in turn compromising their physiological function. Presumably, these effects reduce the survival rate of imidacloprid-treated locusts and the damage they cause in the field.

scholarly journals Differential expression pattern of genes involved in oxygen metabolism in epithelial oviductal cells during primary in vitro culture

2019 ◽  
Vol 7 (2) ◽  
pp. 66-76
Author(s):  
Katarzyna Stefańska ◽  
Sandra Knap ◽  
Magdalena Kulus ◽  
Ievgenia Kocherova ◽  
Piotr Celichowski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
In Vitro Culture ◽  
Cellular Response ◽  
Reactive Oxygen ◽  
Oxygen Metabolism ◽  
Female Reproductive Tract ◽  
Oxygen Species

AbstractOxygen metabolism is crucial in establishing successful pregnancy, since excessive amount of reactive oxygen species (ROS) may exert deleterious effects on the developing embryo. There are several defense mechanisms against oxidative stress in the female reproductive tract, including production of antioxidant enzymes by oviductal epithelial cells (OECs). Undoubtedly, OECs play major part in female fertility and may also serve as an in vitro model of the oviduct. Therefore, the aim of this study was to investigate the expression of genes involved in oxygen metabolism. We have isolated OECs from oviducts of crossbred gilts (n=45) and maintained their in vitro culture for 30 days, collecting their RNA at days 1, 7, 15 and 30. The gene expression was determined with the use of Affymetrix® Porcine Gene 1.1 ST Array Strip. Our results revealed 166 differentially expressed genes belonging to four ontology groups: „cellular response to oxidative stress”, “cellular response to oxygen-containing compound”, “cellular response to oxygen levels” and “cellular response to reactive oxygen species”, most of which are also involved in other major processes in the organism. However, our findings provide a valuable insight into porcine reproductive biology and may be utilized in optimization of assisted reproduction techniques.Running title: Genes involved in oxygen metabolism in oviductal epithelial cells

scholarly journals Oxidative Stress Level in Onco-Surgical Treatment Dynamics at Patients with Malignant Colo-Rectal Tumors

2020 ◽  
Vol 71 (5) ◽  
pp. 450-461
Author(s):  
Maria Iuliana Gruia ◽  
Serban Marinescu ◽  
Dragos Predescu ◽  
George Jinescu ◽  
Bogdan Socea ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Colorectal Cancer ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Invasive Procedure ◽  
Surgical Excision ◽  
Oxygen Metabolism ◽  
Oxygen Species ◽  
Active Metabolites ◽  
Endogenous Antioxidant

Colorectal cancer (CRC) is one of the most common human malignancies, affecting one of 20 persons in areas with high socio-economic standard. In Romania, the frequency of colorectal cancer is growing rapidly placing the country among countries with an average incidence of the disease. There are some etiologic factors involved and treatment of disease is carried out after proper staging. Biochemical mechanisms underlying malignant transformation in colorectal cancer are not all fully understood, therefore our work trying to enter in the path of oxygen metabolism at patients surgically treated. The aim of the study is to follow the production of active metabolites of oxygen, in the dynamics of the surgical procedure, and how the endogenous natural protection systems are activated, following the invasive procedure. Oxidative stress biochemistry assays, realized before and after surgical excision showed a direct relationship between the production of reactive oxygen species and the presence of tumor, without being able to distinguish exactly if malignant tissue is able to induce oxidative stress, or the latter occurs due to neoplastic changes. Based on the results we can say with certainty that the reactive oxygen species ROS primary attack occurs in the lipids, and then the proteins, following activation of endogenous antioxidant defence.

scholarly journals Effect of Indoxyl Sulfate on the Repair and Intactness of Intestinal Epithelial Cells: Role of Reactive Oxygen Species’ Release

2019 ◽  
Vol 20 (9) ◽  
pp. 2280 ◽  
Author(s):  
Simona Adesso ◽  
Marco Ruocco ◽  
Shara Francesca Rapa ◽  
Fabrizio Dal Piaz ◽  
Biagio Raffaele Di Iorio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Cell Monolayer ◽  
Reactive Oxygen ◽  
Indoxyl Sulfate ◽  
Uremic Toxin ◽  
Oxygen Species ◽  
Intestinal Epithelial

Chronic kidney disease (CKD) is characterized by an oxidative stress status, driving some CKD-associated complications, even at the gastrointestinal level. Indoxyl Sulfate (IS) is a protein-bound uremic toxin, poorly eliminated by dialysis. This toxin is able to affect the intestinal system, but its molecular mechanism/s in intestinal epithelial cells (IECs) remain poorly understood. This study’s aim was to evaluate the effect of IS (31.2–250 µM) on oxidative stress in IEC-6 cells and on the intactness of IECs monolayers. Our results indicated that IS enhanced oxidative cell damage by inducing reactive oxygen species (ROS) release, reducing the antioxidant response and affecting Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nuclear translocation as well its related antioxidant enzymes. In the wound healing assay model, IS reduced IEC-6 migration, slightly impaired actin cytoskeleton rearrangement; this effect was associated with connexin 43 alteration. Moreover, we reported the effect of CKD patients’ sera in IEC-6 cells. Our results indicated that patient sera induced ROS release in IEC-6 cells directly related to IS sera content and this effect was reduced by AST-120 serum treatment. Results highlighted the effect of IS in inducing oxidative stress in IECs and in impairing the intactness of the IECs cell monolayer, thus significantly contributing to CKD-associated intestinal alterations.

scholarly journals A difficult patient at a cosmetologist appointment: early lip changes in women smokers: causes, and methods of correction

2020 ◽  
Vol 23 (1) ◽  
pp. 57-64
Author(s):  
M. A. Shirshakova ◽  
Elena A. Morozova
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Oxidative Dna Damage ◽  
Antioxidant Properties ◽  
Reactive Oxygen ◽  
Chronic Obstructive ◽  
Oxygen Species ◽  
Difficult Patient ◽  
Chronic Obstructive Pulmonary Diseases ◽  
Markers Of Oxidative Stress

A smokers lips are more likely to change because of exposure to reactive oxygen species that contain oxygen in large quantities in tobacco smoke. Oxidative stress is a crucial factor in the development of smoking-related diseases, such as oral cancer, lung cancer, and chronic obstructive pulmonary diseases. The damaging effect occurs because of the imbalance between the generation of reactive oxygen species and their detoxification. Markers of oxidative stress include parameters of lipid peroxidation, the activity of glutathione and antioxidant enzymes, and oxidative DNA damage. The destruction of hyaluronic acid (HA), the only drug used to correct lip changes, in smokers is accelerated by its participation in reactions with active oxygen forms, and not just by pathemization because of enzymatic cleavage by hyaluronidase. Mannitol has strong antioxidant properties, which makes it an ideal auxiliary substance in the composition of fillers based on HA. The role of reactive oxygen species in the aging process and their effects on both endogenous HA and HA-based drugs developed for esthetic use are discussed. A review of drugs, based on mannitol with hyaluronic fillers, is provided. The inclusion of mannitol in hyaluronic fillers is an effective and safe way to improve both short-term and long-term esthetic effects of the HA injection.

scholarly journals Oxidative Stress and Endometriosis: A Systematic Review of the Literature

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Gennaro Scutiero ◽  
Piergiorgio Iannone ◽  
Giulia Bernardi ◽  
Gloria Bonaccorsi ◽  
Savino Spadaro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Systematic Review ◽  
Reactive Oxygen Species ◽  
Uterine Cavity ◽  
Reactive Oxygen ◽  
Oxygen Metabolism ◽  
Endometrial Tissue ◽  
Reproductive Age ◽  
Oxygen Species ◽  
Retrograde Menstruation

Endometriosis is one of the most common gynaecologic diseases in women of reproductive age. It is characterized by the presence of endometrial tissue outside the uterine cavity. The women affected suffer from pelvic pain and infertility. The complex etiology is still unclear and it is based on three main theories: retrograde menstruation, coelomic metaplasia, and induction theory. Genetics and epigenetics also play a role in the development of endometriosis. Recent studies have put the attention on the role of oxidative stress, defined as an imbalance between reactive oxygen species (ROS) and antioxidants, which may be implicated in the pathophysiology of endometriosis causing a general inflammatory response in the peritoneal cavity. Reactive oxygen species are intermediaries produced by normal oxygen metabolism and are inflammatory mediators known to modulate cell proliferation and to have deleterious effects. A systematic review was performed in order to clarify the different roles of oxidative stress and its role in the development of endometriosis. Several issues have been investigated: iron metabolism, oxidative stress markers (in the serum, peritoneal fluid, follicular fluid, peritoneal environment, ovarian cortex, and eutopic and ectopic endometrial tissue), genes involved in oxidative stress, endometriosis-associated infertility, and cancer development.

scholarly journals Inflammation and Oxidative Stress via Persistent Hyperglycemia in Progression of Diabetic Nephropathy in Type 2 Diabetes Mellitus

2013 ◽  
Vol 3 (1) ◽  
pp. 1-4 ◽  
Author(s):  
D Kafle ◽  
N Islam ◽  
B Aryal ◽  
P Adhikary ◽  
Neelina Singh
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Diabetic Nephropathy ◽  
Epithelial Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tubular Epithelial Cells ◽  
Oxidative Stress Biomarkers ◽  
Diabetic Kidney

Diabetic nephropathy is a major microvascular complication of diabetes, representing the leading cause of end stage renal disease in the world, and a major cause of morbidity and mortality in type 2 diabetic subjects. In the kidney, a number of pathways that generate reactive oxygen species (ROS) such as glycolysis, specific defects in the polyol pathway, uncoupling of nitric oxide synthase, xanthine oxidase, NAD (P) H oxidase, and advanced glycation have been identified as potentially major contributors to the pathogenesis of diabetic kidney disease. Changes in oxidative stress biomarkers, including super­oxide dismutase, catalase, glutathione reductase, glutathione peroxidase, glutathione levels, vitamins, lipid peroxidation, nitrite concentration, nonenzymatic glycosylated proteins have been associated with diabetic nephropathy due to oxidative stress induced hyperglycemia. Oxidative stress in diabetes is responsible for endothelial dysfunction releasing inflammatory markers cytokines from the damaged renal tissue. Hyperglycemia induces intracellular reactive oxygen species in mesan­gial and tubular epithelial cells which induces cytokines, IL-6 and TNF-α production in glomerular mesangial and tubular epithelial cells in diabetic kidney. Antioxidants inhibit high glucose induced transforming growth factors and extra cellular matrix expression in glomerular mesangial and tubular epithelial cells, which ameliorate features of diabetic nephropathy, suggesting that oxidative stress plays an important role in diabetic renal injury causing diabetic nephropathy. Journal of Chitwan Medical College 2013; 3(1): 1-4 DOI: http://dx.doi.org/10.3126/jcmc.v3i1.8456

scholarly journals Effects of Post‐Resuscitation Normoxic Therapy on Oxygen‐Sensitive Oxidative Stress in a Rat Model of Cardiac Arrest

2021 ◽  
Author(s):  
Yu Okuma ◽  
Lance B. Becker ◽  
Kei Hayashida ◽  
Tomoaki Aoki ◽  
Kota Saeki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiac Arrest ◽  
Weight Ratio ◽  
Reactive Oxygen ◽  
Oxygen Metabolism ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Multiple Organs ◽  
Oxygen Sensitive

Background Cardiac arrest (CA) can induce oxidative stress after resuscitation, which causes cellular and organ damage. We hypothesized that post‐resuscitation normoxic therapy would protect organs against oxidative stress and improve oxygen metabolism and survival. We tested the oxygen‐sensitive reactive oxygen species from mitochondria to determine the association with hyperoxia‐induced oxidative stress. Methods and Results Sprague–Dawley rats were subjected to 10‐minute asphyxia‐induced CA with a fraction of inspired O 2 of 0.3 or 1.0 (normoxia versus hyperoxia, respectively) after resuscitation. The survival rate at 48 hours was higher in the normoxia group than in the hyperoxia group (77% versus 28%, P <0.01), and normoxia gave a lower neurological deficit score (359±140 versus 452±85, P <0.05) and wet to dry weight ratio (4.6±0.4 versus 5.6±0.5, P <0.01). Oxidative stress was correlated with increased oxygen levels: normoxia resulted in a significant decrease in oxidative stress across multiple organs and lower oxygen consumption resulting in normalized respiratory quotient (0.81±0.05 versus 0.58±0.03, P <0.01). After CA, mitochondrial reactive oxygen species increased by ≈2‐fold under hyperoxia. Heme oxygenase expression was also oxygen‐sensitive, but it was paradoxically low in the lung after CA. In contrast, the HMGB‐1 (high mobility group box‐1) protein was not oxygen‐sensitive and was induced by CA. Conclusions Post‐resuscitation normoxic therapy attenuated the oxidative stress in multiple organs and improved post‐CA organ injury, oxygen metabolism, and survival. Additionally, post‐CA hyperoxia increased the mitochondrial reactive oxygen species and activated the antioxidation system.

Are reactive oxygen species important mediators of vascular dysfunction?

2019 ◽  
Vol 15 ◽  
Author(s):  
Gabriel T. do Vale ◽  
Carlos R. Tirapelli
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Vascular Dysfunction ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Metabolism ◽  
Ros Generation ◽  
Oxygen Species ◽  
Promising Alternative

Reactive oxygen species (ROS) are reactive derivatives of oxygen metabolism. The ROS generation can be mediated by distinctive enzymatic systems including NADPH oxidases. The components of this enzyme are expressed in endothelial and vascular smooth muscle cells, adventitial fibroblasts, and infiltrating monocytes/macrophages. Oxidative stress is a molecular dysregulation in ROS generation/elimination, which plays a key role in the development of vascular dysfunction in distinctive conditions including hypertension. It is characterized by vascular inflammation, a loss of NO bioavailability and endothelial dysfunction. Considering that oxidative stress is a key mediator of vascular dysfunction, antioxidant therapy with classic antioxidants seemed to be a promising alternative for the treatment of vascular diseases. In this sense, some commonly used drugs for the treatment of cardiovascular diseases such as angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor AT1 antagonists showed antioxidant effects that might have contributed, at least in part, to the beneficial effects of these drugs on the treatment of cardiovascular diseases. The effectiveness of these drugs shows that ROS are in fact important mediators of vascular dysfunction and that angiotensin II plays a critical role in such response.

scholarly journals BMAL1 Modulates Epidermal Healing in a Process Involving the Antioxidative Defense Mechanism

2020 ◽  
Vol 21 (3) ◽  
pp. 901
Author(s):  
Ericka J. D. Silveira ◽  
Carlos H. V. Nascimento Filho ◽  
Veronica Q. Yujra ◽  
Liana P. Webber ◽  
Rogerio M. Castilho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Epithelial Cells ◽  
Clock Genes ◽  
Reactive Oxygen ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Skin Healing

The circadian rhythm regulates the physiology and behavior of living organisms in a time-dependent manner. Clock genes have distinct roles including the control over gene expression mediated by the transcriptional activators CLOCK and BMAL1, and the suppression of gene expression mediated by the transcriptional repressors PER1/2 and CRY1/2. The balance between gene expression and repression is key to the maintenance of tissue homeostasis that is disrupted in the event of an injury. In the skin, a compromised epithelial barrier triggers a cascade of events that culminate in the mobilization of epithelial cells and stem cells. Recruited epithelial cells migrate towards the wound and reestablish the protective epithelial layer of the skin. Although we have recently demonstrated the involvement of BMAL and the PI3K signaling in wound healing, the role of the circadian clock genes in tissue repair remains poorly understood. Here, we sought to understand the role of BMAL1 on skin healing in response to injury. We found that genetic depletion of BMAL1 resulted in delayed healing of the skin as compared to wild-type control mice. Furthermore, we found that loss of Bmal1 was associated with the accumulation of Reactive Oxygen Species Modulator 1 (ROMO1), a protein responsible for inducing the production of intracellular reactive oxygen species (ROS). The slow healing was associated with ROS and superoxide dismutase (SOD) production, and pharmacological inhibition of the oxidative stress signaling (ROS/SOD) led to cellular proliferation, upregulation of Sirtuin 1 (SIRT1), and rescued the skin healing phenotype of Bmal1−/− mice. Overall, our study points to BMAL1 as a key player in tissue regeneration and as a critical regulator of ROMO1 and oxidative stress in the skin.

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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