Oxidative Stress - Science topic
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
Questions related to Oxidative Stress
I would like to determine if there is leakage of mitochondrial DNA to the cytosol in cells (after oxidative stress) by qPCR by doing nDNA/mtDNA. According to the protocol in the reference, I have extracted cytosolic mtDNA and nDNA from cells.
But, the results of my experiment were not as expected.
Do I need to ensure that the concentration of DNA in each well is consistent？ If the nDNA of each sample is diluted to the same concentration, such as 1 μg/μl, should my mtDNA change by the corresponding multiple with nDNA?
I plan to measure total antioxidant status (TAS) and total oxidant status (TOS) in tissue lysates using kits purchased from Rel Assay. I have measured the protein concentration in all my lysates and plan to use the same concentration for all samples. The kits say they are suitable for use with tissue lysates but don't provide a specific working concentration range.
Therefore I plan to run several dilutions to check my samples are within working range of the assay (comparing with the standards provided). However, I am unsure of what concentration range I should apply. I was thinking a top concentration of 200ug/ml, then 150ug/ml, 100ug/ml, 50ug/ml, 25ug/ml. I have four different tissues for each individual and therefore plan to run the same dilutions for all the tissues too.
I would appreciate if anyone could inform me if they think my dilution range is too low or high, or if I need to change my strategy.
I want to quantify oxidative stress or one of its indirect marker on frozen tissue (at -80°C for more than 6 months), I want to know if it is still possible with our samples since they are frozen for a long time. Can anyone help me by providing this with reference articles?
The relevance of the Microbiota-Gut-Brain axis to Alzheimer’s and neurodegenerative diseases needs extensive analysis. The various articles indicate that there are various questions with relevance to microbiota-gut-brain axis that are relevant to the pathology, pathogenesis and treatment of neurodegnerative diseases.Several mechanistic studies are required to determine the underlying mechanisms for effective and safe probiotic treatment for AD and probiotic benefits remain to determined. The relevance of gut dysbiosis may induce inflammatory responses that may be the cause of the induction of the pathogenesis of AD and relevance of diet (unhealthy diets), probiotics and gut microbiota should be carefully assessed. The meta-analysis studies indicate that probiotics reduce inflammation and oxidative stress and enhances cognition in AD and MCI individuals. The effects of different types of probiotics on amyloid formation and deposition needs to be evaluated and probiotic mixture therapy may be unsafe. The safety of probiotic therapy for AD patients require investigation with relevance to neuron reprogramming and programmed cell death in AD. The risk of unsafe microbiota and probiotic use may lead to the inactivation of the anti-aging gene Sirtuin 1 and the generation of uncontrolled short chain fatty acid release that promote amyloid beta plaque formation.
The concerns with relevance to the induction of dyslipidemia and the role of safety of diet-microbiota-brain axis should be carefully assessed with relevance to the cholesterol-AD connections. The prebiotic, symbiotic and probiotic formulations should be carefully assessed for bacterial composition and living microorganisms such as gram negative and positive. The release of bacterial lipopolysaccharides (LPS) from gram negative bacteria needs to be controlled and the content of gram negative bacteria carefully assessed in these prebiotic, symbiotic and probiotic formulations. Unhealthy diets contain end products such as LPS and diets should be carefully assessed for LPS contents since LPS has been associated with the inactivation of Sirtuin 1. The gut microbiota based therapy is in progress and the relevance to the treatment of brain diseases such as AD is limited. The benefits, limitations and safety of gut microbiota and probiotics on Alzheimer’s disease needs to be placed under systematic review with relevance to dietary regulation and postbiotic supplementation that have the implications for amyloidosis and neurodegeneration. The role of probiotic therapies to create a health gut environment by balancing bacterial populations may require the activation of the anti-aging gene Sirtuin 1 to reverse the pathogenesis of Alzheimer’s disease. The literature indicates that yogurt is a prime source for probiotics and provide a healthy balance of live bacteria to provide health benefits to individuals in various countries of the world. However a recent article indicates that within 12 hours yoghurt can grow gram negative bacteria. The gram negative bacteria in yoghurt depending on daily or weekly intake can generate high levels of plasma LPS with relevance to prebiotic, synbiotic and probiotic quality products and ill health. Yoghurt products may need to be assessed for gram negative bacteria populations and LPS to determine the quality control of these products for international communities.
A. Marzban A, Rahmanian V, Marzban A, Ramezani Siakhulak F. The Role of Probiotics in Improving Alzheimer's Disease. JNFS. 2022; 7 (2) :136-138.
B. de Rijke TJ, Doting MHE, van Hemert S, De Deyn PP, van Munster BC, Harmsen HJM, Sommer IEC. A Systematic Review on the Effects of Different Types of Probiotics in Animal Alzheimer's Disease Studies. Front Psychiatry. 2022 Apr 27;13:879491.
C. Guo L, Xu J, Du Y, Wu W, Nie W, Zhang D, Luo Y, Lu H, Lei M, Xiao S, Liu J. Effects of gut microbiota and probiotics on Alzheimer's disease. Transl Neurosci. 2021 Dec 27;12(1):573-580.
D. Ji HF, Shen L. Probiotics as potential therapeutic options for Alzheimer's disease. Appl Microbiol Biotechnol. 2021 Oct;105(20):7721-7730.
E. D’Argenio V, Sarnataro D (2021) Probiotics, prebiotics and their role in Alzheimer’s disease. Neural Regen Res 16(9):1768-1769.
F. Bonfili L, Cuccioloni M, Gong C, Cecarini V, Spina M, Zheng Y, Angeletti M, Eleuteri AM. Gut microbiota modulation in Alzheimer's disease: Focus on lipid metabolism. Clin Nutr. 2022 Mar;41(3):698-708.
G. Naomi, R.; Embong, H.; Othman, F.; Ghazi, H.F.; Maruthey, N.; Bahari, H. Probiotics for Alzheimer’s Disease: A Systematic Review. Nutrients 2022, 14, 20.
H. Arora K, Green M, Prakash S. The Microbiome and Alzheimer's Disease: Potential and Limitations of Prebiotic, Synbiotic, and Probiotic Formulations. Front Bioeng Biotechnol. 2020 Dec 14;8:537847. doi: 10.3389/fbioe.2020.537847.
I. Peterson CT. Dysfunction of the Microbiota-Gut-Brain Axis in Neurodegenerative Disease: The Promise of Therapeutic Modulation With Prebiotics, Medicinal Herbs, Probiotics, and Synbiotics. J Evid Based Integr Med. 2020 Jan-Dec;25:2515690X20957225.
J. Kincaid HJ, Nagpal R, Yadav H. Diet-Microbiota-Brain Axis in Alzheimer's Disease. Ann Nutr Metab. 2021;77 Suppl 2:21-27. doi: 10.1159/000515700.
K. Alessio Vittorio Colombo Rebecca Katie Sadler Gemma Llovera Vikramjeet Singh Stefan Roth Steffanie Heindl Laura Sebastian Monasor Aswin Verhoeven Finn Peters Samira Parhizkar Frits Kamp Mercedes Gomez de Aguero Andrew J MacPherson Edith Winkler Jochen Herms Corinne Benakis Martin Dichgans Harald Steiner Martin Giera Christian Haass Sabina Tahirovic Arthur Liesz. (2021) Microbiota-derived short chain fatty acids modulate microglia and promote Aβ plaque deposition. eLife 10:e59826.
L. Anti-Aging Genes Improve Appetite Regulation and Reverse Cell Senescence and Apoptosis in Global Populations. Advances in Aging Research, 2016, 5, 9-26
M. Appetite Regulation and the Peripheral Sink Amyloid beta Clearance Pathway in Diabetes and Alzheimer’s Disease. Top 10 Commentaries in Alzheimer’s Disease (e-book). 2019;2:1-11. www.avidscience.com
N. Single Gene Inactivation with Implications to Diabetes and Multiple Organ Dysfunction Syndrome. J Clin Epigenet. Vol. 3 No. 3:24.
O. Sirtuin 1, a Diagnostic Protein Marker and its Relevance to Chronic Disease and Therapeutic Drug Interventions”. EC Pharmacology and Toxicology 6.4 (2018): 209-215.
P. Nutritional diets accelerate amyloid beta metabolism and prevent the induction of chronic diseases and Alzheimer’s disease. Photon ebooks. 2015.
Q. Wassenaar TM, Zimmermann K. Lipopolysaccharides in Food, Food Supplements, and Probiotics: Should We be Worried? Eur J Microbiol Immunol (Bp). 2018 Aug 21;8(3):63-69.
R. The Future of Genomic Medicine Involves the Maintenance of Sirtuin 1 in Global Populations. Int J Mol Biol . 2017. 2(1): 00013.
S. Bacterial Lipopolysaccharides and Neuron Toxicity in Neurodegenerative Diseases. Neurology Research and Surgery. 2018; 1(1): 1-3.
T. C.J. Hervert, N.H. Martin, K.J. Boor, M. Wiedmann. Survival and detection of coliforms, Enterobacteriaceae, and gram-negative bacteria in Greek yogurt, Journal of Dairy Science, Volume 100, Issue 2, 2017, Pages 950-960.
U. Fisberg M, Machado R. History of yogurt and current patterns of consumption. Nutr Rev. 2015 Aug;73 Suppl 1:4-7.
I would like to measure H2O2 on tomato leaves. Just need a fast and quantitative complete protocol for the determination of H2O2.
I'm setting up some assays to assess the effect of different compounds over a cell line. I started using the CM-H2DCFDA from Thermo, as it seems to be more sensitive, but it's turning very expensive if I try to scale it to an HTS. So, I'm looking for alternatives that could give me the same readout in a large-scale screening.
I appreciate your comments.
I would like to know if there are any database or research study carried out mentioning about the proteins that doesn't have the cysteine aminoacid.
I knew few but would like to know more about them.
There is a antioxidant defense system in cell.
Have any signalling pathway or other things can influence ROS level in a extracelluar way?
As a Biomarkers, I have protein concentration, protein carbonyl content, and GST activity in tadpoles. From this data result, I prepared plots and now I want to explain the relation between them. Does anyone know how they are related to each other?
I would like to make an oxidative stress model for studying the antioxidant activity of a drug using C6 cells. Can I use the undifferentiated cells for the same.
Hi everyone, and thanks in advance for reading!
I want to determine oxidative stress human serum/plasma using protein damage; I´ve seen there are a lot of kits and methods, I want to try an ELISA for this, but as I read more and more papers, the methods described are many times vague and unclear.
Please, If someone is doing this in his Lab or have experience on this issue, can you please reach me a protocol for sample preparation and protein carbonylation detection?
It will be very useful as I see there are a lot of steps and I will save a lot of time (and money) on starting it up making my own mess...
Thank you all!
I need to carry out live cell imaging of the above gram-positive bacteria. However, when I transfer the cells from the liquid culture (cells are in exponential phase) to agar pad, the growth alts.
I do not have this issue with Gram-negatives. Any suggestion?
I am working of oxidative stress and found out one target protein form network pharmacology approach. We tried the molecular docking studies with some triazol derivatives. This gave us good result. Now we are planning to do wet work with this system but meanwhile i would like to so some simulation studies on the same. If any body is interested in collaboration pl mail me on
Dr. Manisha Modak
Dear all, I have been using blue light to induce oxidative stress in human cell line. I understand it's a phenomenon for the light irradiance to reduce after using of a period of time. However, other light panels that are not in use seemed to show a decrease as well. As for the cells, they were showing simialr response even though the irradiance has decreased. Could anyone please provide me with some advice on the possible reasons?
Thank you very much!
complement factor receptor (C3aR and C5aR) activation under oxidative stress conditions on ARPE-19 cells.
In a patient with hereditary desminopathy (mutation Thr341Pro DES in the heterozygous state) over the past three years, an increase in the blood uric acid level up to 440-480 µmol / l was established by 1.5 times (the norm is 428.4 µmol / l). With the progression of the disease, the level has risen and is above normal. It is known that uric acid is an antioxidant. Is it necessary to reduce the level of uric acid? The patient has no problems with the joints.
Dear all, I have been observing the activation of phosphorylated ERK1/2 in my healthy human retinal pigmented epithelium cells (ARPE-19) now and then during experiment. The healthy control group was treated similarly with the other treatment groups just that it was without oxidative stress induction. I have tried different harvesting methods (scrapping & trypsin) and also used a new vial of cell line but it didn't solve the problem. Could you please enlighten me about the possible reasons and how do I troubleshoot it?
Thank you very much!
So many researches have proved the effects of chronic inflammation or oxidative stress on human health, but no systematic discussion about the relationship between both. From what we can know now, the inflammatory process can induce oxidative stress, in return, the oxidative stress can also induce inflammation. Is it possible to decide who comes first? Or it is a new chicken-and-egg problem?
Well, we read a lot about how in vitro manipulation of oocytes can induce stress and therefore reduce their potential or as people call it "quality". I've been looking into the studies mostly, they focus on the oxidative stress and reactive oxygen species relation with calcium regulation. Other studies investigated the heating as a stress factor. Well, how they established that this oocyte is healthy and this one is stressed? On what basis? What kind of methods they used? Are the polscope data useful?
I am working on lung inflammatory disorder which is marked by oxidative stress. In order to measure mitochondrial ROS in bronchoalveolar lavage fluid (BALF) sample procured from mice, I am planning to utilize mitoSOX probe. I have a query if we can directly use mitoSOX on BALF cells and measure the fluorescent intensity through flow cytometry? OR
Do we need to use antibodies (along with mitoSOX) against specific markers of inflammatory cells involved in lung inflammatory disease?
Hi, I'm trying to study the impact of reactive oxygen species on whole blood with respect to how it may induce proteolysis on an intracellular protein in PBMC's in a simulated extracorporeal circulatory model. Instead of exposure of PMBC's to hydrogen peroxide, I need to mimic the actual inflammatory environment such as cardiopulmonary bypass and therefore need whole blood. Trialed H2O2 diluted down to 0.05% without much success. Any suggestions would be much appreciated.
There are a few manuscripts implying redox regulation of the actin cytoskeleton. This makes me wonder if actin B can be used as a good loading control when investigating protein expression during oxidative stress. If not, what would be a more suitable loading control?
s-glutathionylation is known to protect cysteines from irreversible oxidation and to keep the residue for reduction after oxidative stress is controlled.
I wonder, however, if the oxidative condition is persisting, even the glutathionylated cysteines can be further oxidized into an irreversible form particularly in the absence of enzymatic reactions.
Thanks for your answers in advance!
I am studying the influence of doses of plant extracts on rats, since the plant is toxic, the value of MDA (oxidative stress) increases with increasing doses. the problem is that for the maximum dose chosen the value of MDA decreased despite that at this dose an apoptosis occurred I have not found an explanation.
The tissue we are using is the cerebellum of black mice blc57, we are doing histopathology and oxidative stress assay, Should we use half the number of mice for each test or could we divide the cerebellum and do both tests for the whole number?
I have seen different results published online using CATALASE. I know that the outcome of the analysis depends on the type of tissue, and protocol used but I have seen gotten different results from my brain tissue sample using sample protocol.
oxidative stress, histopathology, leakage of enzymes, lipid profile, inflammation, apoptosis
Recently we treated retinal pigment epithelium (RPE) cells with hydrogen peroxide as oxidative stress, and the morphological changes do not look like apoptosis or necrosis. Does anyone give suggestions regarding oxidative stress-induced cell death? Many thanks.
I am working on oral cancer cell line and i would like to observe the in vitro antioxidant activity in treated cancer cell line to evaluate the enzymatic activity like SOD, CAT, GST. I have read many papers and they have tried inducing oxidative stress in the cancer cells to observe this activity. I would like to know why we need to induce it when the cancer cells can also produce free radicals.
I am looking for the reagent which can scavenge superoxide in living cells. Most of ROS scavenger, like tempol, inhibit not only superoxide accumulation but also reactive nitrogen spices (RNS). But I am actually looking at the effect of RNS in oxidative stress but not superoxide. Dose anyone know the cell permeable superoxide scavenger?
I am searching for a lab to do In vitro study in neuronal cell lines like SH-SY5Y or N27 and the biochemical estimation by the following methods:
ELISA, Western blot
Oxidative stress markers (ROS, SOD, CAT and GPx)
Mitochondrial function (Mitochondrial Membrane Potential and Complex I activity)
Kindly suggest me a government lab.
Adding a drug causes cells to undergo oxidative stress as indicated by DCFDA fluorescence and an increase of ABCG2. However, I get inconsistent results of SOD1 after 24 hours of exposure. Also, if you want to get the expression, do you collect only the remaining live cells or also collect the floating/apoptotic cells?
I have been trying to estimate some biochemical parameters in urinary bladder but homogenization is problem with me as indicated by very low amount of protein in homogenate.
I'm a retired research chemist/physicist with Parkinson's disease and I've been working on upregulating Nrf2 with sulforaphane to fight oxidative stress.
The results I achieved on my PD and with a group of 8 people with PD have shown that sulforaphane strongly attenuated non-motor symptoms especially fatigue and lack of motivation, suggesting that the first target for Nrf2 seems to be mitochondria. I am not an expert in this subject and I would like to reach out to research groups and Parkinson's disease specialists to discuss how to take this idea further.
You can find the background here :
And a preprint I have written on RG here:
We are trying to design a clinical trial on type 2 diabetes patients. The main data that we want to assess include FBS, 2hpp, HbA1c, insulin, and HOMA-IR. Also, we will assess the lipid profile and stress oxidative indices (MDA and TAC). The problem is that we could not find any similar study to determine the sample size. In this situation is it possible to use the Cohen formula? If not what is the right way for determining the sample size?
I have been using hydrogen peroxide, Potassium ferricyanide and cumene hydroperoxide for my studies involving proteins with a redox switch. The proteins I typically worked and working are transcription factors and polymerases with redox switches like HXXXCXXC motif and Fe-S clusters. I purify the proteins under anaerobic and/or reducing conditions, oxidise them to observe the changes for example structural and activity related. Ferricyanide is a coloured compound and thus I can not use it for some methods, whereas hydrogen peroxide leads to the formation of air bubbles in the cuvette. Given these issues, It would be of a great help if any of you could suggest me any other chemicals that can be tested for the same purpose.
Thanks in Advance
I am looking for a new method for measuring oxidative stress in animal tissues ... a previously unrecognized method .... Thank you for your cooperation
I am planning to conduct a research on oxidative stress of the pregnant mothers. There I am planning to compare oxidative stress between mothers with PIH and mothers without PIH. I would like to know what would be the best research design to conduct this study. Is case control study design ok for this? Or is there a better way?
How can I best measure damage after oxidative stress in liver tissue harvested 24h after exposure stop?
Im thinking about TBARS Elisa kit, but maybe anyone have advice regarding a better endpoint to measure? 4-HNE maybe, or Protein Carbonyls?
If someone have kits to recommend – I will be very happy. (ELISA is preferable).
All the best, and hope everyone is safe
What media or salt solution (HBSS, EBSS, Tyrode) can be used for real-time intracelular h2o2 imaging? I am using a genetically-encoded biosensor based on roGFP and have to find the media that wouldn't have much buffering capacity as well as compounds acting like antioxidants, since it is important to see how the cells alone are coping with h2o2 adition.
Estimated duration of the experiment - 1-1.5 h.
Cells: ipsc-derived neurons. Standart Neurobasal+B27 media was designed to protect neurons from any kind of oxidative damage and contains loads of antioxidants, so h2o2 don't get the chance to get inside the cell.
I am looking for a biological response of fish exposed to trinitrotoluene or its amino metabolites.
Maybe a more or less specific gene expression could help?
Oxidative stress is one good example but its not specific for nitroaromates.
My OD value had a huge variation between each trial, even blank one. The worst thing is blank two has higher OD than the corresponding sample no matter if it was diluted or not. The repeatability of the assay kit is not good. My protocol is as follows.
I also want to do some biochemical analyses and need to take some blood of the rats. To take the blood I need to use anesthetics. But I want to evaluate TNF-a and oxidative stress in the brain. Which anesthetic does no influence on this? I'm working on the model of VPA to induce austism.
Hello dear scientists:
When I treated the Pc12 cell line with H2O2, after 2h the cells seemed to be dead.
I didn't observe crystals, so I didn't add DMSO and left it with mtt in the incubator.
Today I checked it (after 24h) all the wells contained formazans. Also, oD was ok too. Is it a reliable result?
We are doing some biomarkers of oxidative stress research and need to construct calibration curves using BHA, BHT for comparison of antioxidative power in certain extracts, so I would like to know what quality (purity) the reagents (BHA and BHT) need to be.
Hello Can anyone suggest a good way of inducing oxidative stress in mice to exhibit proteinurea phenotype in the mice or a good method to induce oxidative stress in the mice to study kidney disease progression due to oxidative stress?
I'm looking for laboratories working with oxidative stress to test nitrocellulose redox permanganometry (NRP). NRP is a simple method for reductive capacity assessment based on the analysis of the MnO2 precipitate following redox reaction between KMnO4 and biological samples fixed onto the nitrocellulose. This method estimates how well the sample can give up its electrons to KMnO4, so it estimates the amount of chemical antioxidants. In other words this method can be used to measure total chemical antioxidant capacity of biological samples. Advantages of the method are: great precision and accuracy; the possibility to measure a lot of samples simultaneously; simplicity; cost (you only need a piece of nitrocellulose membrane and KMnO4). Moreover, the method can be used to obtain information on the spatial distribution of antioxidant capacity in tissue sections (both cryosections and FFPE can be used), providing unique information on the redox status of the tissue.
As the method is new, and we proposed it just recently, I'm looking for laboratories that are working with oxidative stress to test the method in their samples. We conducted thorough analyses and the method seems to be very robust. Nevertheless, I believe additional independent testing is always a good idea. Also, I believe comments of researchers closely working with oxidative stress would be beneficial for further development of this simple method.
The original paper can be found here:
A step by step protocol can be found here:
I have to measure oxidative stress and nitrite in tissue as well as plasma. For tissue we have the protocol in place but for plasma what is the procedure that should be followed for its preparation before proceeding for the assay?
I want to do study the oxidative stress induced by H2O2 in Keratinocytes cells. What is the volume and concentration of H202 added to the cells to study the H2O2 induced cell damage?
Protein carbonyls are important compounds to measure progression of oxidative stress in tissues.
Available articles online do not have details about how to do final estimation/calculation of the carbonyl content.
Which of the following genes is more important for diagnosing and examining apoptosis?
There is an increasing interest in the role of reactive oxygen species (ROS) and oxidative stress in the causation of male infertility. Can any one give us the exact mechanisms
So many reports mentioned the function of hemoglobin on ROS producction, but few reports could I found on "anti-ROS", does any researchers focus on this part. I think that is interesting to define the role of hemoglobin on redox reaction.
I want to induce oxidative stress by hydrogen peroxide in S. cerevisiae. The stress was measured by t-bar assay. But the cells are not taking stress.
Since 2017, in Redox Research Center, we are working on the use of hydrogen gas as a protective agent for preserving food products. Up to now, we have found an extraordinary effect of hydrogen gas on protecting the property of foods (see our publications in google scholar).
Since 2007, many studies were performed for using hydrogen gas as a therapeutic agent in different illnesses. From these studies, many ones confirmed the antioxidant, anti-inflammatory and anti-apoptotic protective effects of hydrogen on cells and organs. Some studies reported the protective effect of hydrogen against irradiation lung damage (Terasaki et al., 2011), amelioration of hyperoxic lung injury (Kawamura et al., 2013), and reduction of the HBV DNA level in CHB patients (Xia et al., 2013)(refer to the links below). One of these studies reported that "patients receiving hydrogen treatment had improved tendencies in the liver function and HBV (hepatitis B virus) DNA level when compared with patients undergoing routine treatment" and they concluded that "Further study with long‐term treatment with hydrogen‐rich water is required to confirm the protective effect of hydrogen on the liver function and its suppressive effect on viral replication" and " hydrogen‐rich water may attenuate the oxidative stress and have the potential to improve the liver function and reduce the HBV DNA level in CHB patients." (Xia et al., 2013).
I invite the colleagues who work on the viral pathology, especially the COVID-19, to conduct assays on the possible application of hydrogen (in inhalation form, or intraperitoneal and oral administration of hydrogen‐rich water) as a potential and inexpensive treatment of COVID-19.
Please share this message with your colleagues to reach all the researchers and groups working on COVID-19 topics. Any potential use of this cheap treatment for COVID-19 treatment could help thousands of patients and all humanity to win the war against this fatal risk.
Best health for all
I'm working on a project to evaluate chemotherapy-induced cognitive impairment with cisplatin administration. I'm planning to use a biomarker, evaluated serially over time. My questions are:
1. What is the single best biomarker for this scenario (i.e. best in terms of sensitivity, specificity, and exclusively pointing to neuronal inflammation and oxidative stress)? I want it to be very specific, displaying aberrant results only when the neurons are injured. Many biomarkers such as interleukin or MDA increases in the event of systemic inflammation, which is almost inevitably happen under this research scenario (i.e. chemo almost always induces systemic inflammation).
2. Should it be derived from CSF or plasma?
Thank you in advance for anyone who can provide me with answers.
I'm using h2o2 as a positive control for h2dcfda assay for the detection of ROS. There's five fold less (20%) Ros than untreated control (100%) Thp1 cells. I'm treating cells for 24 Hours. Can I use some other controls which are less toxic and less expensive.
I am interested in researching intermittent fasting (IF) and caloric restriction (CR) in relation to hypothesized positive effects on oxidative stress in the nervous system, specifically in the aging, possibly pre-AD brain. I will be using a zebrafish model to study the topic. I am currently in the process of doing a general lit review on the topic, but will be thankful for any insight/difficulties with collecting similar research in the species. It'd be great to have a light shone on any articles I might miss (any species). Thank you for taking the time to read and answer!
I am organizing a Special Issue entitled “Oxidative stress, classification and quantitation” in the Antioxidants (IF 4.52; ISSN 2076-3921, http://www.mdpi.com/journal/antioxidants).
The Special Issue aims to expand our understanding and perspective on all aspects of redox status, its evaluation, homeostasis related adaptation and oxidative damage and repair
. I am particularly interested in your view on the apparent controversy regarding the use of the term Oxidative Stress and the more recently defined terms "Distress" and "Eustress".
In addition, the use of these terms relates to the possibility of quantitating OS. The problem is that the OS, as evaluated by the use of different biomarkers do not correlate with each other, namely, OS cannot be quantitated by a universal criterion and it depends on the biomarker used to evaluate it. Three complementary specific questions are:
(i) Should the term "Oxidative Stress" be re-defined to relate to more specific conditions than the original definition (Acute situations? Diseases? What else ? )
(ii) What term should we use to describe (if at all) imbalance between pro-oxidative and antioxidative components of a system ?.
(iii) Why should we quantitate “Oxidative Stress” (Is there any reason to try “to quantitate OS”?).
If you wish your answer to be publish in the special issue, please let me know
Looking forward to your replays