Oxidative Stress - Science topic

effect of heavy metals and oxidative stress on human body which journal is preferred to publish this article with free of charge and with a few duration of time fast publishing?

What is the role of oxidative stress in toxin-induced carcinogenesis?

I am currently researching the impact of environmental toxins on children's health and would greatly appreciate insights from experts in the field. If you are an expert or researcher working on these issues, I would love to connect and discuss further. Please provide your WhatsApp number if you are interested in discussing recent issues related to kids' health.

So, I am working on a small protein (X) of Haloferax volcanii. It shows these results:

1. Mutant strain grows poorlycompared to wild type strain under low iron condition.

2. Growth of Mutant strain bettercompared to wild type under high iron condition.

With each subsequent passaging in low iron, growth of mutant strain keeps getting worse and worse.

3. Mutant strain showing less resistance to H2O2 stress.

4. It is surrounded by two iron related genes (dpsA, iron repressor).

1. Looking at its translation level (westernblot) in low,standard and high iron.

2. Via northern blot, look for expression of neighbouring genes under mentioned iron conditions.

Will be grateful for your precious suggestions.

Thanks

I bought a lipid peroxidation kit from Sigma and I want to get kits to measure nitrates, superoxide dismutase, catalase, and glutathione. Each one of those kits comes with a different lysis buffer. But to use all those different lysis buffers I would need a lot of samples. What I am wondering is, there is any solution that I could homogenize my samples with that should be compatible with all those tests?

in the Parkinson's model created with 6-OHDA, the application is performed unilaterally intrastriatically. after tretment, should the dopamine level be measured through the striatum on the side where the lesion occurs? or how should I decide which brain hemisphere to use for examining various parameters (oxidative stress and apoptosis)?

I would be glad if you help me.

Thank you very much in advance.

Hello everyone,

To examine oxidative stress, inflammation and apoptosis parameters in the brain tissue of a Parkinson's model rat, should i select specific regions in the brain or can i use total brain tissue homogenate?

I'm open to any kind of advice.

Thank you in advanve.

Do you have any suggestions, which SPE cartiges to use for markers of oxidation stress? I do a LC-MS analysis of quite various group of analytes, including bases (e.g. hydroxyguanosine), acids (e.g. ascorbic acid), aminoacids and peptides (e.g. tyrosine, glutathion), and also lipophilic substances (isoprostanes etc.). What first came to my mind was the HLB sorbent. But is there any other/better option? Or should I rather make two extraction protocols, for example one for the lipophilics and bases (maybe MCX?) and second for the acids and aminoacids?

I will be extracting those markers from serum or cell/tissue extracts, so I need to get rid of mainly proteins, phospholipides, anorganic ions.

Neurological disorders include a variety of conditions including Alzheimer’s, Motor Neuron and Parkinson’s disease, affecting longevity and quality of life and these have been associated with oxidative stress. Several of the chronic neurodegenerative pathologies of the central nervous system share some common features, such as oxidative stress, closely related to inflammation, synapse dysfunctions, protein misfolding, and defective autophagia. Sources of reactive oxygen species (ROS) that cause oxidative stress, relating oxidative damage with the pathogenesis of neurodegenerative disorders. Antioxidants can powerfully neutralise ROS and free radicals, decreasing oxidative damage. Antioxidant genes, like manganese superoxide dismutase (SOD-2) enzymes, can undergo epigenetic changes that reduce its expression, thus increasing oxidative stress in tissue or DNA can be altered by free radical damage. The epigenetic landscape of these genes can alter antioxidant function and can result in neurodegenerative disease. This imbalance of free radical production and antioxidant function increase the ROS that cause neuronal cell damage, often observed as an age-related event. Familial MND is associated with SOD-1 antioxidant gene polymorphism and function.

Increased antioxidant expression in mice is protective against ROS in neurons as is the exogenous supplementation of antioxidants. The associated manganese deficiency observed in Alzheimer’s suggests that this transition metal could be supplemented in deficient patients or SOD—2 therapy considered for age-related neurodegenerative disorders.

A new mimetic of SOD-2, Avasopasem manganese (GC4419 AVA), is described and suggested as putative treatment to reduce the oxidative stress that causes neurodegenerative diseases.

Hello everyone! I am new to this platform, I am looking for this book: "Bioquimica del estres Oxidativo" (Diego Camps, 2010)

I would like to know if anyone has it in digital format to share it with me. Waiting for a reply. Thank you very much!

High to resist oxidative stress and still high until the exam time or must be consumed in this resistance therefor we found it in low levels

How does oxidative stress contribute to the initiation and progression of various arrhythmias?

I want to study the expression of some proteins related to oxidative stress with western blot. I wonder what microglia cell line is the best for it.

I am working on HUVEC cells in order to Establish the Oxidative Stress Injury Model Induced by H2O2. I want to treat the cells with 5mM H2O2 from 30%h2o2 stock solution for 16 hours. How to prepare 5 mM hydrogen peroxide from 30% H2O2 stock solution?

Hi, I want to evaluate oxidative stress in a neuroblastoma cell line, I know about SOD1, but I think it's not enough, so I was investigating and I found 4-hydroxynonenal, I have this in my lab 4-HNE B5605, but I don't find the concentration to use. Also I don't think it is the best marker for inmunofluorescence, It is more used in western blot . Do you know other types of marker that I can use for oxidative stress in a cell culture? I will appreciate your help.

I am working on HUVEC cells in order to make the Oxidative Stress Injury Model Induced by H2O2.I treated the cells with 0.3% H2O2(30%) for 16 hours, then IC50 was determined by MTT test, but in the validation stage of the model, the oxidative stress indicators were not as expected. what stock of hydrogen peroxide I should be used to induce oxidative stress?

Mr. Guillermo Zalba did not participate in the research of the article "Prevalence of Hypertension and Obesity: Profile of Mitochondrial Function and Markers of Inflammation and Oxidative Stress". I ask you please to remove it from your information

Best regards

Alejandra Guillermina Miranda-Díaz, MD, PhD

As an antioxidant role of zinc, conflicting reports are pouring. It is recognized that Zn has prominent role in reducing oxidative stress by scavenging and decreasing production of ROS. On the other hand, there are reports that Zn in hypoxia can activate NADPH oxidase by acting as phosphorylation modulator and thereby initiate ROS accumulation. I seek kind proper explanation from the researchers in this regard.

I'm trying to induce oxidative stress by using rotenone and SNP sodium nitroprusside in isolated mitochondria of rat brain. This is to study GSH assay from control (Mitochondria) group in comparison with { Mito + (SNP/Rotenone)}.

However, I'm not getting the promising results

could anyone suggest me why there is not decrease in GSH occurs significantly in (SNP or rotenone induced mitochondria comparision to control?

is there any matter of concentration?

or suggestions.

(doi : 10.14715/cmb/2014.60.2.6)

please fine protocol to perform GSH assay>

I am trying to stress HEK293T cells but they seem very resistent.

Does anyone tried oxidative stress?

Hi all!

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?

Thank you.

Dear community,

For my master's project, I want to design an experiment that will asses the efficiency of an antioxidant to stop/restore mitochondrial oxidative stress/redox balance in a PD mouse model, in both early and later stages of the disease. Redox balance will be assessed by using a roGFP lifetime measurements in vivo.

I was thinking to use MPTP model, due to it's effect on the mitochondria, simplicity and practicality. However I heard that this model can be difficult and dangerous to work with and might kill the mice faster than the experiment will end.

There is 6-ohda model, but I was reticent to use it because it has to be injected into the brain directly (which I believe might interfere with my fluorescence measurements) and the mechanisms behind it are not fully understood.

I would highly appreciate if anyone could share their experiences about working with these(or maybe other) models and give me an appreciation of their suitability in regard to my research question.

Thank you!

tissue infected with various parasitic disease

In order to save some energy, one decision our lab is examining would be to increase the temperature limit of the freezers at -70°C instead of -80°C. I guess 10°C difference in this very low temperatures may help to save substantial amount of energy supply. Therefore, we are wondering if samples can be stored at this temperature without causing any remaining molecular activities (oxidative stress and so on).

It is not super clear in the litterature why this threshold of -80°C has been selected, does it result from empirical measures or not?

If anyone has an idea on the reasons for the choice of -80°C, this could help us to take the best decision.

Thanks in advance

During examination of transmission electron microscopy images of skeletal muscle biopsies from patients suffering from different myopathies, sometimes I find somewhat unusual mitochondria with white spots. Initially, I assumed that is some sort of oxidative stress damage or even artifact, yet now I think I could be wrong; usually, in patients with frequent "white spotted" mitochondria, I find more pronounced pathological changes in mitochondria (such as paracrystalline inclusion or onion-like cristae) in other fibers, sooner or later.

That made me think, so I've tried to find similar images in other studies, but to no avail. I have no reasonable explanation as for now. Any ideas?

Are there publications on this?

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.

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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.

Many thanks,

Noni

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?

Seeking collaborators for the application of the Oxidative Stress Index (OSI) questionnaire in predicting the likelihood of disease onset and severity with increasing OSI.

Please contact Dr. Harold Zeliger at Zeliger Research, LLC.

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.

How Campylobacter and Helicobacter species isolated from patients stored @-80 survive oxidative stress if they faced temperature variations?

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 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?

Hi everyone;

is there any method, to differentiate this two products of oxidative stress in the same sample?

(apart from GC/MS)

thank you so much!

How to go about it statistically?

Hi All

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!

Sunjoo

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?

Serum TIBC and serum ferritin colorimetric assay protocol.

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 have tried with no success various UV-B stresses but I did not find an increase in beta galactosidase.

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:

for induction of oxidative stress

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?

Hi all,

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 working on Carum copticum extract and its seems it has itself induced oxidative stress at higher doses. 200mg/kg PO

Hello all,

What are some markers of oxidative stress in brain?

Thanks

the relationships between oxidation and inflammation

Susceptibility of Covid-19 patients to drug-induced OS

Hallo experts,

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

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?

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.

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.

Hello,

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.