scholarly journals Vanadium Derivative Exposure Promotes Functional Alterations of VSMCs and Consequent Atherosclerosis via ROS/p38/NF-κB-Mediated IL-6 Production

2019 ◽  
Vol 20 (24) ◽  
pp. 6115 ◽  
Author(s):  
Chang-Ching Yeh ◽  
Jing-Yiing Wu ◽  
Guan-Lin Lee ◽  
Hsiu-Ting Wen ◽  
Pinpin Lin ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Intranasal Administration ◽  
Fossil Fuels ◽  
Ros Generation ◽  
Oxygen Species ◽  
Pathological Effect ◽  
Atherosclerotic Lesions ◽  
Anti Oxidant ◽  
Differentiation Marker ◽  
Urinary Vanadium

Vanadium is a transition metal widely distributed in the Earth’s crust, and is a major contaminant in fossil fuels. Its pathological effect and regulation in atherosclerosis remain unclear. We found that intranasal administration of the vanadium derivative NaVO3 significantly increased plasma and urinary vanadium levels and induced arterial lipid accumulation and atherosclerotic lesions in apolipoprotein E-deficient knockout mice (ApoE−/−) murine aorta compared to those in vehicle-exposed mice. This was accompanied by an increase in plasma reactive oxygen species (ROS) and interleukin 6 (IL-6) levels and a decrease in the vascular smooth muscle cell (VSMC) differentiation marker protein SM22α in the atherosclerotic lesions. Furthermore, exposure to NaVO3 or VOSO4 induced cytosolic ROS generation and IL-6 production in VSMCs and promoted VSMC synthetic differentiation, migration, and proliferation. The anti-oxidant N-acetylcysteine (NAC) not only suppresses IL-6 production and VSMC pathological responses including migration and proliferation but also prevents atherosclerosis in ApoE−/− mice. Inhibition experiments with NAC and pharmacological inhibitors demonstrated that NaVO3-induced IL-6 production is signaled by ROS-triggered p38-mediated NF-κB-dependent pathways. Neutralizing anti-IL-6 antibodies impaired NaVO3-mediated VSMC migration and proliferation. We concluded that NaVO3 exposure activates the ROS-triggering p38 signaling to selectively induce NF-κB-mediated IL-6 production. These signaling pathways induce VSMC synthetic differentiation, migration, and proliferation, leading to lipid accumulation and atherosclerosis.

scholarly journals Astaxanthin Prevents Human Papillomavirus L1 Protein Binding in Human Sperm Membranes

Marine Drugs ◽  
2018 ◽  
Vol 16 (11) ◽  
pp. 427 ◽  
Author(s):  
Gabriella Donà ◽  
Alessandra Andrisani ◽  
Elena Tibaldi ◽  
Anna Brunati ◽  
Chiara Sabbadin ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Human Sperm ◽  
Ros Generation ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Endogenous Reactive Oxygen Species ◽  
Anti Cancer ◽  
Anti Oxidant ◽  
L1 Protein ◽  
Gradient Separation

Astaxanthin (Asta), red pigment of the carotenoid family, is known for its anti-oxidant, anti-cancer, anti-diabetic, and anti-inflammatory properties. In this study, we evaluated the effects of Asta on isolated human sperm in the presence of human papillomavirus (HPV) 16 capsid protein, L1. Sperm, purified by gradient separation, were treated with HPV16-L1 in both a dose and time-dependent manner in the absence or presence of 30 min-Asta pre-incubation. Effects of HPV16-L1 alone after Asta pre-incubation were evaluated by rafts (CTB) and Lyn dislocation, Tyr-phosphorylation (Tyr-P) of the head, percentages of acrosome-reacted cells (ARC) and endogenous reactive oxygen species (ROS) generation. Sperm membranes were also analyzed for the HPV16-L1 content. Results show that HPV16-L1 drastically reduced membrane rearrangement with percentage of sperm showing head CTB and Lyn displacement decreasing from 72% to 15.8%, and from 63.1% to 13.9%, respectively. Accordingly, both Tyr-P of the head and ARC decreased from 68.4% to 10.2%, and from 65.7% to 14.6%, respectively. Asta pre-incubation prevented this drop and restored values of the percentage of ARC up to 40.8%. No alteration was found in either the ROS generation curve or sperm motility. In conclusion, Asta is able to preserve sperm by reducing the amount of HPV16-L1 bound onto membranes.

scholarly journals Exploitation of siderophore producing bacteria Acinetobacter soli (MTCC-5918) for lipids and reactive oxygen species in Chlorella variabilis (ATCC- PTA 12198) through co-cultivation

2020 ◽  
Author(s):  
Soundarya Rajapitamahuni ◽  
Pooja Bachani ◽  
Vamsi Bharadwaj ◽  
Sandhya Mishra
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Accumulation ◽  
Reactive Oxygen ◽  
Ash Content ◽  
Ros Generation ◽  
Oxygen Species ◽  
Chlorella Variabilis ◽  
Iron Deficient ◽  
Acinetobacter Soli

Abstract Background Increased iron uptake via siderophores triggers a series of physiological processes and generation of reactive oxygen species (ROS) which causes damage to proteins, lipids, carbohydrates, resulting into micro algal cell lysis. Moreover, there are reports mentioning oxidative stress is a mediator for increased lipid accumulation in microalgae. The main aim of this study is co-cultivation of the bacteria Acinetobacter soli (MTCC- 5918) and the microalgae Chlorella variabilis (ATCC-PTA 12198) under iron limiting conditions and the threshold value of iron that trigger oxidizing stress to microalgae. Further, the ROS generation in the microalgae C. variabilis was determined in terms of OH, SO2 and H2O2 concentration in the cells while co-cultivation. Results The co-cultured biomass contains (45.92 ± 0.74%) lipid content which was about 21% higher than that of the axenically grown microalgae. Carbohydrate content also increased to 40% than that of the control culture. Oxidative stress is a mediator for increased lipid accumulation in microalgae. As growth inhibition triggered due to the generation of high ROS toxicity during iron deficiency an increase in concentration of OH and H2O2 content was observed. In iron sufficient medium ash content of co-cultivated microalgae showed 32% and in iron deficient medium showed 14.23% which shows 44% decrease of ash content. Our novel approach significantly outperforms the involvement of different reactive oxygen species (ROS) in induction and in regulation of chelator release from cells at adequate Fe supply, which is also affecting the growth,lipids, carbohydrates, proteins, pigments, etc. Conclusions The findings of the present study highlights that oxidative stress is a mediator for increased lipid accumulation in microalgae that simultaneously becomes an alternative strategy for the improvement of biofuel potential in C. variabilis. The study portraysthe significance of co-cultivation of A. soli and C. variabilis induced oxidative stress (ROS generation) in microalgae caused due to higher uptake of iron via siderophore

scholarly journals CLA isomer t10,c12 induce oxidation and apoptosis in 3t3 adipocyte cells in a similar effect as omega-3 linolenic acid and DHA.

2017 ◽  
Vol 7 (2) ◽  
pp. 149 ◽  
Author(s):  
Jon Meadus ◽  
P. Vahmani ◽  
P. Duff ◽  
J.L. Zantinge ◽  
T.D. Turner ◽  
...  
Keyword(s):  
Linolenic Acid ◽  
Lipid Accumulation ◽  
Dairy Products ◽  
Caspase 3 ◽  
Lipid Hydroperoxide ◽  
Oxygen Species ◽  
Omega 3 ◽  
Anti Oxidant ◽  
Student’S T ◽  
One Way Anova

Background: Commercial conjugated linoleic acid (CLA) dietary supplements of contain an equal mixture of the C18:2 isomers, cis-9,trans-11 and trans-10,cis-12. CLA-c9t11 occurs naturally in meat and dairy products as the dominant CLA at 75%, whereas the CLA-t10c12 occurs at <1%. CLA-c9t11 generally promotes lipid accumulation but CLA-t10c12 inhibits lipid accumulation and may promote inflammation.Methods: Purified CLA-c9t11 and CLA-t10c12 were added to 3T3 mature adipocyte cultures at 100uM concentrations and compared with 100uM C18:3(n-3) (α-linolenic acid) and 50uM docosahexaenoic acid (DHA) to study their effect on growth, gene transcription and general oxidation. The results of 4 separate trials were averaged and compared for significance using one way ANOVA and Student’s t-test.Results: C18:3(n-3), DHA and CLA-t10c12 were inhibitory to 3t3 adipose cell growth and caused significant lipid hydro peroxide activity. CLA-t10c12 and c9t11 increased AFABP, FAS and ACOX1 mRNA expression but DHA and C18:3(n-3) decreased the same mRNAs. CLA-c9t11 but not the t10c12 stimulated adipoQ expression even though; c9t11 had only a slightly greater affinity for PPARγ than CLA- t10c12. The expression of the xenobiotic metabolism genes, aldo-keto reductase 1c1  (akr1c1), superoxide dismutase (SOD) and inflammation chemokine secretions of  eotaxin (CCL11), Rantes (CCL5), MIG (CCL9) and MCP-1 were increased by DHA, C18:3(n-3) and CLA-t10c12. This correlated with apoptosis factors, caspase 3, Bcl-2 and BAXs which were partially reduced by co-treatment with lipophilic anti-oxidant α-tocopherol.Conclusions: Based on this evidence, CLA-t10c12 promoted more reactive oxygen species (ROS) than CLAc9t11, in a similar effect as C18:3(n-3) and DHA. In response, cascades of genes are activated to deal with the potentially damaging effects of ROS through detoxification, inflammation or apoptosis.Keywords: CLA-t10c12, CLA-c9t11, gene expression, adipocyte lipid hydroperoxide, DHA,3T3 adipocytes, apoptosis.

Mutant tp53 Causes a Gain of Function Increase in Sensitivity to Reactive Oxygen Species in Erythroid Precursors

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 2668-2668
Author(s):  
Troy C. Lund ◽  
Michelle L Carter ◽  
Ashley C. Kramer ◽  
Bruce R. Blazar ◽  
Julie A. Ross
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Oxygen Species ◽  
Wild Type ◽  
Gain Of Function ◽  
Qrt Pcr ◽  
Erythroid Precursors ◽  
Anti Oxidant

Abstract TP53 is mutated in approximated 10 – 15% of cases of leukemia and myelodysplastic syndrome. It is recently appreciated that oxidative stress plays a role in the dysplastic processes that drives these diseases. Animal modeling of oxidative stress has been a challenge as many of the central genes in the oxidative stress response pathway are necessary for life and knockout animals die as embryos due to overwhelming oxidative stress. The zebrafish model allows pro-oxidant exposure early in hematopoietic development, and gata1DsRed1 transgenic animals allow clear identification of erythroid precursors. We capitalized on these advantages to interrogate the effects of oxidative stress on erythroid precursors. The gata1DsRed1 erythroid precursors showed a dose-responsive increase in reactive oxygen species (ROS) generation after naphthol exposure. Pro-oxidant exposure significantly up-regulated several anti-oxidant genes including: hypoxia-inducible factor (hif1a), nuclear factor (erythroid derived)-like 2 (nrf2), ferritin heavy chain (fth1a), thioredoxin (txn), and heme oxygenase 1 (hmox1); (p < 0.05) shown by qRT-PCR. In silico promoter analysis of these genes revealed several tp53 binding sites within 4 kb upstream of the first exon in each gene. Pro-oxidant exposure was able to induce tp53 expression 3-fold over baseline by qRT-PCR. We next took advantage of the tp53 mutant line tp53M214K/M241K which has a mutation in the DNA binding region of tp53 rendering it non-functional. We found that tp53M214K/M124K fish were highly sensitive to pro-oxidant exposure with 80% of embryos showing severe to moderate anemia and cardiac edema after 72 hours of exposure to naphthol (versus 25% in wild-type control animals, n = 100/group; p < 0.001). There was a 3-fold decrease in the number of hemoglobin producing cells in naphthol treated tp53M214K/M124K animals as shown by o-dianisidine staining (versus control animals, n = 10/group; p < 0.01). A dose-response between the amount of pro-oxidant exposure and severity of anemia/edema also existed as determined by correlation of pro-oxidant concentration to an edema severity scale. We next measured the amount of ROS generated after naphthol exposure using CellROX detection assays and found that tp53M214K/M124K animals showed a 5 – 10-fold increase in ROS generated compared to wild-type (n = 30/group, p < 0.01). This increased ROS was maintained even in the heterozygous states of tp53M214K/wt suggesting a gain-of-function phenomenon. ROS generation could be completely reversed by treatment with the anti-oxidant n-acetylcysteine. When we completely abrogated mutant tp53 by morpholino knockdown, ROS generation and hemolysis were significantly decreased, providing further evidence that the ROS generation is a gain-of-function phenomenon of mutated tp53. Finally, uncoupling of mitochondrial respiration using oligomycin also decreased ROS generation by 50% (p < 0.01) implicating a dysregulatory process ongoing in mitochondria. In addition to the recently appreciated increased tumorigenicity caused by mutated tp53, our data suggest that cells harboring mutant tp53 also have increased ROS generation and increased sensitivity with pro-oxidant exposure. Understanding the mechanisms by which the anti-oxidant response is regulated will allow us to potentially find more effective druggable targets to treat the oxidative stress that accompanies the dysplastic process. Disclosures No relevant conflicts of interest to declare.

scholarly journals Reactive Oxygen Species in Host Plant Are Required for an Early Defense Response against Attack of Stagonospora nodorum Berk. Necrotrophic Effectors SnTox

Plants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1586
Author(s):  
Svetlana Veselova ◽  
Tatyana Nuzhnaya ◽  
Guzel Burkhanova ◽  
Sergey Rumyantsev ◽  
Igor Maksimov
Keyword(s):  
Reactive Oxygen Species ◽  
Early Stage ◽  
Reactive Oxygen ◽  
Triticum Aestivum L ◽  
Redox Status ◽  
Stagonospora Nodorum ◽  
Ros Generation ◽  
Ros Production ◽  
Oxygen Species ◽  
Necrotrophic Effectors

Reactive oxygen species (ROS) play a central role in plant immune responses. The most important virulence factors of the Stagonospora nodorum Berk. are multiple fungal necrotrophic effectors (NEs) (SnTox) that affect the redox-status and cause necrosis and/or chlorosis in wheat lines possessing dominant susceptibility genes (Snn). However, the effect of NEs on ROS generation at the early stages of infection has not been studied. We studied the early stage of infection of various wheat genotypes with S nodorum isolates -Sn4VD, SnB, and Sn9MN, carrying a different set of NE genes. Our results indicate that all three NEs of SnToxA, SnTox1, SnTox3 significantly contributed to cause disease, and the virulence of the isolates depended on their differential expression in plants (Triticum aestivum L.). The Tsn1–SnToxA, Snn1–SnTox1and Snn3–SnTox3 interactions played an important role in inhibition ROS production at the initial stage of infection. The Snn3–SnTox3 inhibited ROS production in wheat by affecting NADPH-oxidases, peroxidases, superoxide dismutase and catalase. The Tsn1–SnToxA inhibited ROS production in wheat by affecting peroxidases and catalase. The Snn1–SnTox1 inhibited the production of ROS in wheat by mainly affecting a peroxidase. Collectively, these results show that the inverse gene-for gene interactions between effector of pathogen and product of host sensitivity gene suppress the host’s own PAMP-triggered immunity pathway, resulting in NE-triggered susceptibility (NETS). These results are fundamentally changing our understanding of the development of this economical important wheat disease.

scholarly journals CBIO-07. CELL DEATH INDUCED BY AN OSCILLATING MAGNETIC FIELD IN PATIENT DERIVED GLIOBLASTOMA CELLS IS MEDIATED BY REACTIVE OXYGEN SPECIES

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii17-ii17
Author(s):  
Shashank Hambarde ◽  
Martyn Sharpe ◽  
David Baskin ◽  
Santosh Helekar
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cell Viability ◽  
Cortical Neurons ◽  
Reactive Oxygen ◽  
Great Promise ◽  
Antioxidant Vitamin ◽  
Ros Generation ◽  
Oxygen Species ◽  
Novel Therapy

Abstract Noninvasive cancer therapy with minimal side effects would be ideal for improving patient outcome in the clinic. We have developed a novel therapy using strong rotating magnets mounted on a helmet. They generate oscillating magnetic fields (OMF) that penetrate through the skull and cover the entire brain. We have demonstrated that OMF can effectively kill patient derived glioblastoma (GBM) cells in cell culture without having cytotoxic effects on cortical neurons and normal human astrocytes (NHA). Exposure of GBM cells to OMF reduced the cell viability by 33% in comparison to sham-treated cells (p&lt; 0.001), while not affecting NHA cell viability. Time lapse video-microscopy for 16 h after OMF exposure showed a marked elevation of mitochondrial reactive oxygen species (ROS), and rapid apoptosis of GBM cells due to activation of caspase 3. Addition of a potent antioxidant vitamin E analog Trolox effectively blocked OMF-induced GBM cell death. Furthermore, OMF significantly potentiated the cytotoxic effect of the pro-oxidant Benzylamine. The results of our studies demonstrate that OMF-induced cell death is mediated by ROS generation. These results demonstrate a potent oncolytic effect on GBM cells that is novel and unrelated to any previously described therapy, including a very different mechanism of action and different technology compared to Optune therapy. The effect is very powerful, and unlike Optune, can be seen within hours after initiation of treatment. We believe that this technology holds great promise for new, effective and nontoxic treatment of glioblastoma.

scholarly journals Multifunctional Role of Chitosan Edible Coatings on Antioxidant Systems in Fruit Crops: A Review

2021 ◽  
Vol 22 (5) ◽  
pp. 2633
Author(s):  
Giuseppina Adiletta ◽  
Marisa Di Matteo ◽  
Milena Petriccione
Keyword(s):  
State Of The Art ◽  
Antioxidant Systems ◽  
Edible Coatings ◽  
Ros Production ◽  
Oxygen Species ◽  
Fruit Crops ◽  
Oxidative Damages ◽  
Film Forming ◽  
Anti Oxidant

Chitosan-based edible coatings represent an eco-friendly and biologically safe preservative tool to reduce qualitative decay of fresh and ready-to-eat fruits during post-harvest life due to their lack of toxicity, biodegradability, film-forming properties, and antimicrobial actions. Chitosan-based coatings modulate or control oxidative stress maintaining in different manner the appropriate balance of reactive oxygen species (ROS) in fruit cells, by the interplay of pathways and enzymes involved in ROS production and the scavenging mechanisms which essentially constitute the basic ROS cycle. This review is carried out with the aim to provide comprehensive and updated over-view of the state of the art related to the effects of chitosan-based edible coatings on anti-oxidant systems, enzymatic and non-enzymatic, evaluating the induced oxidative damages during storage in whole and ready-to-eat fruits. All these aspects are broadly reviewed in this review, with particular emphasis on the literature published during the last five years.

scholarly journals Fighting Oxidative Stress with Sulfur: Hydrogen Sulfide in the Renal and Cardiovascular Systems

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 373
Author(s):  
Joshua J. Scammahorn ◽  
Isabel T. N. Nguyen ◽  
Eelke M. Bos ◽  
Harry Van Goor ◽  
Jaap A. Joles
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Redox Status ◽  
The Body ◽  
Therapeutic Interventions ◽  
Oxygen Species ◽  
Enzymatic Production ◽  
Age Related ◽  
Anti Oxidant ◽  
Enzymatic Pathways

Hydrogen sulfide (H2S) is an essential gaseous signaling molecule. Research on its role in physiological and pathophysiological processes has greatly expanded. Endogenous enzymatic production through the transsulfuration and cysteine catabolism pathways can occur in the kidneys and blood vessels. Furthermore, non-enzymatic pathways are present throughout the body. In the renal and cardiovascular system, H2S plays an important role in maintaining the redox status at safe levels by promoting scavenging of reactive oxygen species (ROS). H2S also modifies cysteine residues on key signaling molecules such as keap1/Nrf2, NFκB, and HIF-1α, thereby promoting anti-oxidant mechanisms. Depletion of H2S is implicated in many age-related and cardiorenal diseases, all having oxidative stress as a major contributor. Current research suggests potential for H2S-based therapies, however, therapeutic interventions have been limited to studies in animal models. Beyond H2S use as direct treatment, it could improve procedures such as transplantation, stem cell therapy, and the safety and efficacy of drugs including NSAIDs and ACE inhibitors. All in all, H2S is a prime subject for further research with potential for clinical use.

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