Questions related to Toxicity
Normally, I dissolve my extracts using DMSO for cell assay. However, for my methanol and hexane extract, it didn't dissolve completely. Is there any stable solvents (low toxicity) that I can use to dissolve the extracts for Cell assay?
I have some queries regarding COFs,
1.How can we ensure the cyclic structure of COFs after synthesis ? Is there any methods?
2.How can we ensure that the COFs are not toxic?
3. How can we decompose the COFs after their use?
4.How can we ensure the reversibility of covalent bonds?
Thanks in advance.
Xylene is the most common clearing agent used in histopathology, however, it is toxic. Numerous studies have been evaluating and finding safer alternatives to xylene, but it is still used.
Most pollution has become powerful tool human introduce by means of industry by discharging this substances into water and our environment that courses toxic which is poison and damage the animals and plants because it is harmful to them.
There are researches in which poultry waste is added to its feed
What is the highest concentration to be added in order not to be toxic?
Chlorine is added to drinking water What is the highest concentration added so that it is not toxic?
I read the literature. The aggregate state of the nano-complex drugs can be measured by UV-Vis. For example, amphotericin B and its nano-complex forms. The UV results are spectral with about four peaks (wavelengths around 300-350 nm). Then, the absorbance of the first peak (peak 1) is divided by the absorbance of the fourth peak (peak 4). The absorbance ratio from peak 1 to peak 4 indicates the state of the aggregated nano-complex. If the ratio is 1, it means a monomeric state, and if the ratio is > 2, it means a super-aggregation state. The monomer state is associated with high toxicity, and the super-aggregated state is associated with low toxicity.
Can anyone explain it to me?
What is the role (if any) of exchange transfusion in severe carbonmonoxide toxicity?
Does anyone have evidence, even if anecdotal of success/usefulness for exchange transfusion for this indication?
I have tried making sure it is at room temp by leaving it out for an hour. Spraying injection site with ethanol and injecting at a steady pace without letting it sit too long in the syringe between injections. Nevertheless, after 2-4 injections of 100ul administered 72 hours apart via I.P., some of the mice get toxicity. I get them from clodronateliposomes.org
Has anyone else faced this problem and found a solution?
Just want to know the right flow
Pre-formulation, formulation, characterization, Efficacy, toxicity and PK studies
Pre-formulation, formulation, characterization, toxicity, PK studies and Efficacy studies
I need the Toxic response factor for Mn, Fe, Al, Mo and Co for my research, as far as I know Hakanson, 1980 reported it just for 8 heavy metals!
Please, I need references talking about the unpalatability of some plants in arid areas (toxicity, rigidity, chemical composition "alcaloïds ...", flavor, astringency, laxativity, ...?
The data collected is on time to appearance of different developmental stages, of fish eggs in concentrations of toxicant. Five concentrations of toxicant and eight egg developmental stages were monitored (total of 40 cases). The data was ranked with the following results: the distribution of 15 variables were normally distributed (Shapiro-Wilk test) both before and after ranking using SPSS version 25 (37.5%). Twenty-one variables became normally distributed (52.5%), while two cases were not affected. I read somewhere that data normalized by ranking can be analyzed using parametric methods. Does this apply here? Thanks.
A new Dolos list article about Monsanto's fraudulent and pseudoscientific practices to defend glyphosate:
I also recommend an article recently published in an Elsevier journal about glyphosate toxicity:
Hello to all
I observed a strange phenomenon with CHO-K1 following the change of serum batch (it is surely the toxicity of this batch but I am very curious about the possible nature of this phenomenon. In practice, I will simply change serum. But the question remains open)
At the beginning of the culture, CHO-K1 grow normally. I observe a normal triangular morphology (round to cubic). The growth is fast as usual. But, once at confluence and not before, they start to take the shape of very elongated cells in parallel arrays evolving like fibroblasts.
I tried to dilute them as much as possible at the beginning of the culture. No change. They take a normal amount of time to grow to confluence, then they become fibroblasts-like.
Has anyone seen this kind of phenomenon? It is probably toxicity in the serum, but usually the toxicity is greater if you dilute the cells (" dilution death "). This is not the case this time. Any ideas would be helpful.
The toxicity is only being observed in anti CD54 antibody-treated cells and not with cells treated with anti IgG1 or anti CD86 treated antibodies.
Induction at gestation day 7 led to abortion and loss of pregnant mice. My suspicion is that my route of exposure intraperitoneal at 5mg/Kg was too high and this has been used previously by other studies in literature.
I am trying to express a gene which belong to classical TA (Toxin-Antitoxin) module. Specifically, I am trying to express the toxin gene using pBAD vector in BL21 cells. Despite trying out different arabinose concentration, I don't see the expression of gene on SDS gel ??
Is it because of its toxicity? Does anyone have any suggestions to circumvent this problem?
The production of ROS (Reactive Oxygen Species) is toxic to plant cells that deviate or interfere with the normal biochemical pathways. I had targeted quantifying different forms of ROS within specified tissue such as roots and leaves.
Suggest articles updated one which clearly tells about the toxicity or safety assessments of essential oils in food preservation
I am having trouble with a large plasmid that contains a ~10kb synthetic DNA insert that contains some short repetitive regions and a high number of LacO sites interspersed throughout.
When I re-isolated the plasmid from a glycerol stock, I noticed that the insert accumulated a lot of mutations, and most of these mutations are in the LacO sites. It seems like these LacO sites are to some extent toxic in this sequence context. The insert does not contain any long repeats, so homologous recombination is likely not an issue.
Has anyone experienced something similar with constructs like this with LacO sites? The plasmid has a pUC origin and we are using DH10b bacterial strain.
Thanks for your time and help
I would very much appreciate any help with the following. I have some experimental compounds which have never been tried in animal studies before, and have no close analogues. The only usable information about them are their LD50s (for mice), and I need to calculate appropriate doses for an experiment in rats (we are to evaluate efficacy, not toxicity). What would be the best approach to converting an LD50 to a presumably therapeutic dose for animals? Any advice would be super helpful.
Thanks in advance!
Why is it important to have one area for RNA extraction and another for DNA extraction.
is it because of the kind of reagents that are used for RNA purification that could be more volatile and toxic than the ones used for DNA purification?
I've seen that is common to use an extraction fume hood cabinet for RNA while for DNA is a laminar flow hood.
Is it completly necessary to separate this two technical areas?
Thank's for you'r valuable knowledge :)
Scientific community is aware of the present scenario of pollution level in aquatic ecosystems and changing climate.
Is the rate of description of new species of fishes correct/ justified? Where the minor changes in the environmental conditions and exposure to toxic conditions or pollution in developmental stages is bound to bring some changes, most probably negative and may bring changes in phenotypic characters. These changes may be seen in single specimen or a group. The long exposure may also bring in changes at genetic levels. These changes may be very small or measurable. Can this not be considered as deformity/ abnormality? Many times new species are described based on a single specimen and with smallest / minor change in character. Many times against the rule of nature breeding/ feritization may occur in two species; probability is more in closely related ones.
I feel a new species should not be described based on single specimen and with little change in character with closely related species, like very small change in number of gill raker or number of rays.
Upon checking individual ingredient toxicity for baby oil/body wash, found to be nontoxic. Later after formulation, the finished product was found to be toxic. We performed MTT assay to check cytotoxicity using L929 cells.Can some help in this regard.
I am doing experiment using two drugs to see their additive effect. On low dosages of A combined with B I noticed the additive effect on cell killing (using RTCA assay). However, on high dosages of A combined with B I did not see the additive effect because A is too toxic to kill the cells. I am planning to figure out the mechanism behind this additive effect, should I stick to low dosages of A to find out the mechanism behind or it is ok if I use higher doses?
I have this question because some phenotypes (apoptosis, senescence) might not be observed under low doses of A. So that some of my colleagues believe it is ok to use high doses to study the mechanism, saying that it is just the additive effect using high doses cannot be seen on RTCA, does not mean that the additive effect on mechanism cannot be seen. While I am worried that using high doses could be misleading because you might can see some phenotypes that was not the reason driven the additive effect using low doses (eg. the doses of the drug did not cause that phenotype or the effect of low doses and high doses are different/ biphasic). However, I did not see many publications really care about the drug dose when doing mechanism.
Could anyone share some insights? Thank you!
I am trying to determine whether these statements are true or not
- LPS toxicity is mediated by the toll-like receptor
- NO is mainly produced by Kupffer cells
- Liver necrosis is the main result of paracetamol toxicity
- cholestasis is the main result of LPS toxicity
- Glucuronyltransferases are involved in the GSH conjugation of NAPQI
- sulfurotransferases are involved in the GSH conjugation of NAPQI
- The liver is the main target of paracetamol because it has a high concentration of COX enzymes which are the target of paracetamol pharmacological activity
- the liver is the main target of paracetamol because sulfurotransferase expression is generally low
- GAPDH is used to normalize the concentration of gene of interest
- The number of cycles required to have a sufficiently detectable amount of fluorescence in the PCR is dependent on the original mRNA concentration
As we know, polymyxin B contains many components (e.g. polymyxin B1, B2, etc.), do we have any evidence to show that those major components have different antimicrobial activity, pharmacokinetic property and propensity for toxicity?
I want to use the essential oil of the plant in diluted form for a topical application.. but I want to know what I can use as a thinner.
And which should not be toxic and dangerous on the skin
I'm working on biodegradation of a toxic substance with pure culture and I'm adapting my culture to the substance by using stepwise subculturing. A day after one of subcultures I suddenly realized that my culture had entered stationary phase and this was very strange because the conditions was as same as the last culture and the amount of the toxic substance was the same. The interesting thing was that I had a culture without the toxic substance and that one had entered stationary phase too, after observing the conditions I waited for another 24 hours but nothing changed, so I decided to dump the subculture and do a new one. Does anyone has the same experience to explain the reason of this happening for me ?
Were thinking of using gold nanoparticles for cells. The gold nanoparticles will be used to deliver proteins to cells.
Dear colleagues, I am attempting to differentiate K562 cells into RBCs. I am using the attached protocol and TMB staining to check differentiation. I have a lot of crystals after staining the cells, so I cannot count the stained cells. Is there anything wrong with the protocol? I would appreciate it if someone could suggest a solution to this issue.
Thanks in advance.
1. Prepare 0.5% acetic acid by diluting acetic acid 100%,1:200 (1mL acetic acid in 199ml H2O)
2. To prepare a 0.2% TMB, dissolve 2mg/ml TMB in 0.5% acetic acid
For 50ml: Dissolve 100mg in 50ml 0.5% acetic acid. This can be stored at 4C for up to 1 month.
3. Prepare just before use: Add 5ul of 30% hydrogen peroxide/1ml of 0.2% TMB.
For 10ml: Add 50ul of 30% hydrogen peroxide
Wash K562 cells once with PBS and resuspend in 250 ul of PBS. Add 1 volume (250ul) of 0.2% TMB working solution and incubate 10-30 minutes in the dark at room temperature (It’s toxic, so do not incubate longer than 30 min in total including picture taking). Count brown cells in light microscope.
I'm measuring cell toxicity in different cell lines against aggregated protein solutions. I'm performing various cell viability, toxicity, and ROS level assays. Except for these, what kind of parameters (or metabolites) can I detect to examine toxicity/alterations in cells?
every year in human toxicity field and environmental toxicity field, test species have been used to chemicla effect assessment. For examle d.rerio, d. magna, c. elegance and so on were used to a study. so far how many species have been used for chemical toxicity test ? regarding all species in the earth, what is the percentage of them? 1% or more? good question please
In the Reproductive toxicity test，Maternal general toxicity NOAEL:0.3 mg/m2.Embryofetal developmental toxicity NOAEL:0.45 mg/m2.Can I only choose embryo fetal toxicity NOAEL to calculate PDE？as follows。
I'm looking for databases for (eco)toxicology data of chemicals. Specifically; biodegradability, aquatic toxicity, and bioaccumulation. A strong interest is also for data of ionic liquids. Please recommend both public and commercial databases.
Hello, I work at a company where it is required to analyze variation on absorbance on daily testing (basically the correlation between volume, concentration and absorbance).
Someone in my team proposed to use acridine orange but I've been reading about it and I don't seem very convinced because it is suspected to be carcinogenic and toxic to water living organisms.
I am looking for a more eco-friendly alternative. The price is not a problem. This is considering that a lot of testing is going to be performed on a daily basis.
Conference Paper Optimizing deacetylation process for chitosan production fro...
From this research, I tried to make deacetylated chitosan from powdered shell.
The problem is I'm worried about things
1.Do you need to neutralize NaOH solution before pouring down to the drain? If yes, Is vinegar or acetic acid also a good choice to go? (I'm not into using HCl because it sounds risky and corrosive)
2.As the title said, the toxic gas from soaking the NaOH? how to handle it?
Bacteria has the ability to degrade the toxic textile azo dyes to less toxic products or intermediates .What are the expected non toxic degradation products of congo red and Acid violet 7 by bacteria ?
I have been preparing lentivirus particles (2nd gen) with both transgene of interest, and control lentivirus of GFP only by transfection of HEK293T with FuGENE HD reagent. pVSV-G envelope plasmid and psPAX2 packaging plasmid.
After 48 hours transfection, lentivirus supernatant is collected, centrifuged to remove debris and filtered through 0.45um filter. It is then concentrated either through ultracentrifugation or table top gradient sucrose centrifugation.
At MOIs of approaching 1 cell death is significant in primary cells and apparent in HEK 293T cells vs control. I leave cells to transduce for 24hrs in 8-10ug.ml polybrene. The presence of polybrene does not appear to cause negative effects in either cells alone. I seed cells directly on top of lentivirus containing media, aiming for around 25-30% confluence at transduction.
I have taken several steps to ensure that the lentivirus prep itself is very clean, and rid of HEK media. What am I missing, or could do to solve this problem?
To deactivate an endoplasmic membrane enzyme, which is actually the last and key enzyme of a complex enzymatic reaction, I want to use the carboxyl group deletion.But I do not want to cause toxicity or inactivation of other cell components. In fact, I want to make this group water soluble. I know I can use carbodiimide, but is it enough to use it alone? What other points should I pay attention to?
My experiment requires to extract Tissue DNA from zebrafish intestine , this is my first time to learn Tissue DNA extraction. Recently I have learned about extracting DNA using magnetic beads, but i need more recommendations and and what is your experience about magnetic DNA extraction technique and how many samples can be extracted from single kit. Beside this , please can you suggest me any other methods that follow more simple steps.
The problem of the demand for fresh water is greatly exacerbated by the increasing consumption of water as a result of the increase in human population growth around the world on the one hand, and the persistence of the problem of climate change and global warming on the other hand. We do not want to talk about international problems and the possibility of wars due to the conflict over water in the riparian countries on the rivers, but we are talking about air pollution. Building more desalination plants leads to the release of larger quantities of toxic and greenhouse gases such as carbon dioxide, nitrogen dioxide, sulfur dioxide, etc. Are there solutions to control pollutants, or are there desalination plants that do not use fossil fuels?
Search for more details on anionic surfactant FFD-6 relatedness to antibiotics and its toxicity to aquatic ecosystems.
Kindly share your views.
While evaluating the cytotoxicity of a sample in cell line, what percentage of cell viability is considered inorder to conclude that the sample is toxic. Like if 80% of cell survives, is the sample toxic or not
I need to administer 10 mg/kg/day of simvastatin through an alzet mini osmotic pump for 42 days. Dissolving 100 mg of simvastatin has been a challenge. I have used multiple solvents ethanol 15%, 60%, 70%, 100%, as well as DMSO 50%, 100%. Ethanol 100% works.
The second challenge has been when filling the pump. The mean volume of the pump is 233.4 ul. So I have dissolved the simvastatin in ETOH 100% and then have taken the dose calculated for the mouse's weight (which is about 50% of a 1 ml tube) and added DMSO 100% to make up for the other 50% of 1 ml tube. So at the end, I have 50% ethanol plus 50% DMSO.
So I have 2 questions;
1. Does anybody know about the toxicity of this ETOH 50% plus DMSO 50% in mice?
2. Does anybody know if the pump will be ok with this combination?
Thank you very much in advance.
What are the best ways to measure toxicity and biodegradability of Diesel Oil-based emulsified acids with standardized ranges?
I have been working with Diesel Oil-based Emulsified Acids and need to measure their toxicity (LC50 test) and biodegradability but I am unable to find standardized ranges for Diesel based emulsion for both the tests.
I am trying to express T7 DNA polymerase in E. coli on low copy plasmid (pKD46, under pBAD promoter). I observed substantial slowing down of cell growth even without induction.
Then I looked into literature to find out that expression of T4, T5, Taq, Pfu DNA polymerases all confer toxicity to E. coli.
Provided T7 DNAP has the same 3D fold as E. coli Pol I, where does its toxicity come from?
do you know the minamata convention on mercury?
Article 4 of the Minamata Convention provides for the elimination of the import, export and manufacture of mercury thermometers and mercury sphygmomanometers used in health care by 2020, and the elimination of dental amalgam, 128 countries have signed the Convention.
is dental amalgam toxic enough to be vigilant in its elimination?
My drugs are insoluble in water and 5% alcohol, 5% DMSO as well. It fully dissolves in ethyl acetate however it is toxic for cells.
I would like to do a pilot study by feeding the mice with mouse diet which contains mushroom. Is there any ways to measure whether the mushroom-added diet cause toxicity to the mice or not while the animals are still alive?
I just started reading on Nano-QSAR model development. The very first step of building any QSAR model is the collection of data and its curation. I would be grateful to the research community if you could guide me on - what exact datasets and parameters are needed? & what are the sources of getting these datasets?
Dear readers, I am a master degree student currently working on phototoxicity assessment using Balb/c 3T3 cell line. However, I have encountered some technical issue during the running of this assay, for both UV- and UV+ exposed well plates. The cells (passage number 20, cultured in DMEM + 10%Calf serum +1% Pen-Strep 5% CO2, 37°C ) get rounded and detach after the first and in particular after the second washing step required by the test guideline at day 2 after the 1h and 50 min incubation with the test substance (1h in incubator and 50min in dark or under UV-light exposure). I would underline that, in my case, the test substance consist of only 1% DMSO in HBSS (Mg+Ca+) because the issue of detachment occurs even with this vehicle (we have tried also with just HBSS but we obtained the same issue).
Do you have any clue on how to troubleshoot this problem? Thank you in advance.
- 96-well plate NUNC 96-well plate (#167 008) (I have tried also with poly-lysinated or collagenated plates, both were unsuccessful)
- Buffer for washing: warmed HBSS (Mg+ Ca+)
- 8-pin manifold to remove buffer (we have tried also to invert the plate over a absorbent paper, but was unsuccessful)
- Serum used: Calf serum (we have tried also with FBS or with combination of Calf+FBS, both were unsuccessful).
My project looks at the joint toxicity in yeast cells (Saccharomyces cerevisiae), I am using lipid derived electrophiles (LDEs) such as acrolein (ACR), crotonaldehyde (CRO), methyl vinyl ketone (MVK), and hexenal (HEX). I treated 1 million yeast cells in 24 well plates with the LDEs individually, as well as combining them in concentrations that didn't cause significant toxicity when treated alone, but produces a significant toxicity when mixed.
I used the following concentrations:
ACR- 0.05 mM
CRO- 0.3 mM
MVK- 0.02 mM
HEX- 0.6 mM
In triplicates, I treated 50 microliters of LDEs in a well containing 900 microliters of YPD media and 50 microliters of live culture.
For the mixture I added 50 microliters of each of these four LDEs in a well containing 750 microliters YPD and 50 microliters live culture.
I then incubated the plate in a spectrophotometer at 30 C for 18 hours with a 5 second shake ever 30 minutes.
After processing the results, the curves were as expected, however during the stationary phase towards the end, the wells that were treated with the toxicants showed an increased absorbance compared to the control, even the mixture that showed the most toxicity had the highest absorbance compared to other curves, which I find counterintuitive.
I have attached the graph.
So can anyone help me with what is happening here?
Hello, everybody. My PhD research is about eutrophication
processes in a hypersaline lagoon which has registered episodes
of fish mortality. My study includes a phytoplankton species
inventory. I would like a guide of toxic and/or potential harmful
phytoplankton. Thanks to all.
Phenol toxicity is reported in cats, especially related to disinfectants and essential oils but a toxic dose is not usually indicated. Can its use be toxic to feline patients that need repeated administrations of a medication containing phenol as a preservative?
Hello, everybody! In your opinion, in an environmental risk assessment, if exists, which is the most critical criterion: bioaccumulation potential, acute aquatic toxicity, or biodegradation? For example: which compound offers more risk to the environment and why?:
Compound 1: very high acute toxicity, low bioaccumulation, high biodegradability;
Compound 2: very high bioaccumulation, low acute toxicity; high biodegradability;
Compound 3: very low biodegradability; low acute toxicity; low bioaccumulation.
Thank you in advance!
I performed a toxicity experiment based on the protocol by Chiu et al 2017 (DOI:10.1038/s41598-017-08983-y, except that water was used as control) to test the toxic effect of a few chemicals on a coleopteran beetle. This experiment was design to select the most toxic chemical of out the many to be used in the bioassay for DGE study. Can I use the same doses (LC50) to feed the insect via semi-artificial diet and/or droplet feeding with water or any other solvent like acetone? If yes, please guide me the conversion calculation.
- Supposedly, the LC50 for a chemical of density 0.791g/ml is 433.342 μL/L. How can use it for-
- (a) If i want to achieve the same amount of chemical in a semi-artificial diet of volume 66.31ml?
- (b) droplet feeding with water in the ratio of 1:1, and 1:2 (water:chemical)?
Actually I found in previous research papers that both Cr forms i.e. trivalent and hexavalent are interconvertible. So I want to know the exact amount of both the forms of Cr in soil sample in which I have supplied only hexavalent Cr. It will help me to understand the mechanism behind toxic behavior of both the forms.
For ripening fruits like mango, calcium carbide application is well known having low market price, though it has controversy. i would like to know if anyone use on mango for ripening , how many days carbide toxicity exist.
Does gender really matters, when it comes to the toxic effects of arsenic exposure in human beings.
Not only arsenic exposure. What about gender influence on other types of metal poisoning?
I have read in some research articles wherein it has been mentioned like males are more susceptible as far as toxic effects of arsenic are concerned.