scholarly journals Cytotoxicity and Oxidative Stress Responses of Imidacloprid and Glyphosate in Human Prostate Epithelial WPM-Y.1 Cell Line

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Khaled Y. Abdel-Halim ◽  
Safaa R. Osman
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Stress Responses ◽  
Agricultural Sector ◽  
In Vitro Assays ◽  
Control Group ◽  
Electron Microscopic ◽  
Ic50 Values ◽  
And Oxidative Stress

Insecticide imidacloprid and herbicide glyphosate have a broad spectrum of applicable use in the agricultural sector of Egypt. Their ability to induce in vitro cytotoxic and oxidative stress on normal human cells (prostate epithelial WPM-Y.1 cell line) was evaluated with the methyl tetrazolium test (MTT) and histopathological investigation. Cell viability was evaluated with an MTT test for 24 h. The median inhibition concentration (IC50) values were 0.023 and 0.025 mM for imidacloprid and glyphosate, respectively. Sublethal concentrations: 1/10 and 1/50 of IC50 and IC50 levels significantly induced an increase in the lactate dehydrogenase (LDH) activity and malondialdehyde (MDA) level compared with the untreated cells. Rapid decrease in the glutathione (GSH) content and glutathione-S-transferase (GST) activity was induced. Significant increases were recorded in activities of catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), respectively, compared with the control group. Transmission electron microscopic (TEM) investigation showed significant defects in the cells following pesticide treatments for 24 h. Therefore, it is concluded that imidacloprid and glyphosate are very toxic in vitro assays and able to induce apoptotic effects as well as oxidative stress. So, these findings provide a scenario of multibiomarkers to achieve the imposed risks of pesticides at low doses.

scholarly journals Intra-Vitreal Administration of Microvesicles Derived from Human Adipose-Derived Multipotent Stromal Cells Improves Retinal Functionality in Dogs with Retinal Degeneration

2019 ◽  
Vol 8 (4) ◽  
pp. 510
Author(s):  
Anna Cislo-Pakuluk ◽  
Agnieszka Smieszek ◽  
Natalia Kucharczyk ◽  
Peter G.C. Bedford ◽  
Krzysztof Marycz
Keyword(s):  
Oxidative Stress ◽  
Retinal Degeneration ◽  
Stromal Cells ◽  
Clinical Studies ◽  
Stress Conditions ◽  
In Vitro Assays ◽  
Multipotent Stromal Cells ◽  
Mitochondrial Potential ◽  
And Oxidative Stress

This study was designed to determine the influence of microvesicles (MVs) derived from multipotent stromal cells isolated from human adipose tissue (hASCs) on retinal functionality in dogs with various types of retinal degeneration. The biological properties of hASC-MVs were first determined using an in vitro model of retinal Muller-like cells (CaMLCs). The in vitro assays included analysis of hASC-MVs influence on cell viability and metabolism. Brain-derived neurotrophic factor (BDNF) expression was also determined. Evaluation of the hASC-MVs was performed under normal and oxidative stress conditions. Preliminary clinical studies were performed on ten dogs with retinal degeneration. The clinical studies included behavioral tests, fundoscopy and electroretinography before and after hASC-MVs intra-vitreal injection. The in vitro study showed that CaMLCs treated with hASC-MVs were characterized by improved viability and mitochondrial potential, both under normal and oxidative stress conditions. Additionally, hASC-MVs under oxidative stress conditions reduced the number of senescence-associated markers, correlating with the increased expression of BDNF. The preliminary clinical study showed that the intra-vitreal administration of hASC-MVs significantly improved the dogs’ general behavior and tracking ability. Furthermore, fundoscopy demonstrated that the retinal blood vessels appeared to be less attenuated, and electroretinography using HMsERG demonstrated an increase in a- and b-wave amplitude after treatment. These results shed promising light on the application of cell-free therapies in veterinary medicine for retinal degenerative disorders treatment.

scholarly journals Identification of Toxicity Parameters Associated with Combustion Produced Soot Surface Chemistry and Particle Structure by in Vitro Assays

Biomedicines ◽  
2020 ◽  
Vol 8 (9) ◽  
pp. 345
Author(s):  
Heba Al Housseiny ◽  
Madhu Singh ◽  
Shaneeka Emile ◽  
Marvin Nicoleau ◽  
Randy L. Vander Wal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Surface Chemistry ◽  
Cell Viability ◽  
Health Effects ◽  
Stress Responses ◽  
Surface Composition ◽  
Particle Surface ◽  
In Vitro Assays ◽  
Epithelial Cell Line ◽  
And Oxidative Stress

Air pollution has become the world’s single biggest environmental health risk of the past decade, causing millions of yearly deaths worldwide. One of the dominant air pollutants is fine particulate matter (PM2.5), which is a product of combustion. Exposure to PM2.5 has been associated with decreased lung function, impaired immunity, and exacerbations of lung disease. Accumulating evidence suggests that many of the adverse health effects of PM2.5 exposure are associated with lung inflammation and oxidative stress. While the physical structure and surface chemistry of PM2.5 are surrogate measures of particle oxidative potential, little is known about their contributions to negative health effects. In this study, we used functionalized carbon black particles as surrogates for atmospherically aged combustion-formed soot to assess the effects of PM2.5 surface chemistry in lung cells. We exposed the BEAS-2B lung epithelial cell line to different soot at a range of concentrations and assessed cell viability, inflammation, and oxidative stress. Our results indicate that exposure to soot with varying particle surface composition results in differential cell viability rates, the expression of pro-inflammatory and oxidative stress genes, and protein carbonylation. We conclude that particle surface chemistry, specifically oxygen content, in soot modulates lung cell inflammatory and oxidative stress responses.

Moderation of morphogenetic and oxidative stress responses in flax in vitro cultures by hydroxynonenal and desferrioxamine

2005 ◽  
Vol 162 (5) ◽  
pp. 537-547 ◽  
Author(s):  
Bohuš Obert ◽  
Erica E. Benson ◽  
Steve Millam ◽  
Anna Preťová ◽  
David H. Bremner
Keyword(s):  
Oxidative Stress ◽  
Stress Responses ◽  
In Vitro Cultures ◽  
Oxidative Stress Responses ◽  
And Oxidative Stress

scholarly journals Effects of Bronchoalveolar Lavage with Ambroxol Hydrochloride on Treating Pulmonary Infection in Patients with Cerebral Infarction and on Serum Proinflammatory Cytokines, MDA and SOD

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Fanhua Meng ◽  
Jing Cheng ◽  
Peng Sang ◽  
Jianhui Wang
Keyword(s):  
Oxidative Stress ◽  
Cerebral Infarction ◽  
Therapeutic Effect ◽  
Stress Responses ◽  
Pulmonary Infection ◽  
Control Group ◽  
Observation Group ◽  
Ambroxol Hydrochloride ◽  
Oxidative Stress Responses ◽  
And Oxidative Stress

Objective. This paper was aimed at investigating the effects of bronchoalveolar lavage (BAL) with ambroxol hydrochloride (AH) on treating pulmonary infection and on serum proinflammatory cytokines and oxidative stress responses in patients with cerebral infarction (CI). Methods. One hundred and two patients with cerebral infarction complicated with pulmonary infection (CIPI) who were treated in our hospital were enrolled as research objects, divided into an observation group (52 cases; AH combined with BAL) and a control group (50 cases; single AH) based on therapeutic schemes. They were compared in terms of the therapeutic effect and pre- and posttreatment serum inflammatory cytokines, pulmonary function, and serum indices of oxidative stress. Their adverse reactions during treatment were also recorded and compared. Results. The therapeutic effect in the observation group was remarkably better than that in the control group (P<0.05). After treatment, the serum inflammatory cytokines, pulmonary function, and serum indices of oxidative stress were remarkably improved in the two groups (P<0.05), but the improvement was remarkably better in the observation group (P<0.05). The differences were not significant in intratreatment adverse reactions between the two groups (P>0.05). Conclusion. For CIPI patients, BAL with AH has a better therapeutic effect and higher safety and can control the patients’ systemic inflammatory responses and oxidative stress responses, so it is worthy of further promotion in clinical practice.

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

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
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.

A Database of IC50 Values and Principal Component Analysis of Results from Six Basal Cytotoxicity Assays, for Use in the Modelling of the In Vivo and In Vitro Data of the EU ACuteTox Project

2008 ◽  
Vol 36 (5) ◽  
pp. 503-519 ◽  
Author(s):  
Richard Clothier ◽  
Paul Dierickx ◽  
Thaly Lakhanisky ◽  
Myriam Fabre ◽  
Monica Betanzos ◽  
...  
Keyword(s):  
Principal Component Analysis ◽  
Cell Line ◽  
Principal Component ◽  
Hepatic Cell ◽  
In Vitro Assays ◽  
Ic50 Values ◽  
Basal Cytotoxicity ◽  
The Eu

The main aim of the ACuteTox project (part of the EU 6th Framework programme) is to demonstrate that animal tests for acute systemic toxicity can be replaced by alternative in vitro assays. In this project, data for 97 reference chemicals were collected in the AcuBase database, designed to handle deposited in vitro and in vivo (human and animal) data. To demonstrate the applicability of in vitro basal cytotoxicity tests and in vitro– in vivo modelling, it was deemed necessary to obtain data that were generated via defined standard operating procedures. The molar basal cytotoxicity IC50 values (the 50% inhibitory concentrations for the endpoint measured) for a mouse fibroblast cell line (3T3), a human hepatic cell line (HepG2), a rat hepatic cell line (Fa32), and a human neutrophil cell line (HL-60), were compared, and gave an R2 correlation of 0.83. To identify chemicals that showed differential cytotoxicity to the various cell types involved, principal component analysis (PCA) was undertaken independently, once all the results had been returned. This showed that colchicine, cycloheximide, digoxin, 5-fluorouracil and hexachlorobenzene gave the lowest correlations with the first score vector of the PCA. The results presented are to be used to identify outliers that need to be further studied via the use of tissue-specific in vitro assays.

scholarly journals OsnR is an autoregulatory negative transcription factor controlling redox-dependent stress responses in Corynebacterium glutamicum

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Haeri Jeong ◽  
Younhee Kim ◽  
Heung-Shick Lee
Keyword(s):  
Oxidative Stress ◽  
Corynebacterium Glutamicum ◽  
Stress Responses ◽  
Promoter Region ◽  
Underlying Mechanism ◽  
In Vitro Assays ◽  
Expression Of Genes

Abstract Background Corynebacterium glutamicum is used in the industrial production of amino acids and nucleotides. During the course of fermentation, C. glutamicum cells face various stresses and employ multiple regulatory genes to cope with the oxidative stress. The osnR gene plays a negative regulatory role in redox-dependent oxidative-stress responses, but the underlying mechanism is not known yet. Results Overexpression of the osnR gene in C. glutamicum affected the expression of genes involved in the mycothiol metabolism. ChIP-seq analysis revealed that OsnR binds to the promoter region of multiple genes, including osnR and cg0026, which seems to function in the membrane-associated redox metabolism. Studies on the role of the osnR gene involving in vitro assays employing purified OsnR proteins and in vivo physiological analyses have identified that OsnR inhibits the transcription of its own gene. Further, oxidant diamide stimulates OsnR-binding to the promoter region of the osnR gene. The genes affected by the overexpression of osnR have been found to be under the control of σH. In the osnR-overexpressing strain, the transcription of sigH is significantly decreased and the stimulation of sigH transcription by external stress is lost, suggesting that osnR and sigH form an intimate regulatory network. Conclusions Our study suggests that OsnR not only functions as a transcriptional repressor of its own gene and of those involved in redox-dependent stress responses but also participates in the global transcriptional regulation by controlling the transcription of other master regulators, such as sigH.

scholarly journals LAMTOR5-AS1 regulates chemotherapy-induced oxidative stress by controlling the expression level and transcriptional activity of NRF2 in osteosarcoma cells

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Youguang Pu ◽  
Yiao Tan ◽  
Chunbao Zang ◽  
Fangfang Zhao ◽  
Cifeng Cai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Line ◽  
Transcriptional Activity ◽  
High Throughput Sequencing ◽  
Feedback Regulation ◽  
In Vitro Assays ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Sequencing Analysis

AbstractLong-noncoding RNAs (lncRNAs) play roles in regulating cellular functions. High-throughput sequencing analysis identified a new lncRNA, termed LAMTOR5-AS1, the expression of which was much higher in the chemosensitive osteosarcoma (OS) cell line G-292 than in the chemoresistant cell line SJSA-1. Further investigations revealed that LAMTOR5-AS1 significantly inhibits the proliferation and multidrug resistance of OS cells. In vitro assays demonstrated that LAMTOR5-AS1 mediates the interaction between nuclear factor erythroid 2-related factor 2 (NFE2L2, NRF2) and kelch-like ECH-associated protein 1 (KEAP1), which regulate the oxidative stress. Further mechanistic studies revealed that LAMTOR5-AS1 inhibited the ubiquitination degradation pathway of NRF2, resulting in a higher level of NRF2 but a loss of NRF2 transcriptional activity. High level of NRF2 in return upregulated the downstream gene heme oxygenase 1 (HO-1). Moreover, NRF2 controls its own activity by promoting LAMTOR5-AS1 expression, whereas the feedback regulation is weakened in drug-resistant cells due to high antioxidant activity. Overall, we propose that LAMTOR5-AS1 globally regulates chemotherapy-induced cellular oxidative stress by controlling the expression and activity of NRF2.

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