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Toxicity - Science topic

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Pseudokirchneriella subcapitata for toxicity assay
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OK Tahar,
Here's another one that might be worth trying as it's even a bit closer to you. I work with a good lab that gets it s algae from here:
Museum National d’Histoire Naturelle - 12, rue Buffon, Case N°19 - 75005 PARIS
Good luck!
Paul
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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?
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May I suggest first that you replace your hexane extraction by cyclohexane as hexane is a known neurotoxicant so for your own health, best not to use it.
I would also recommend not using DMF (commonly used solvent) as this is about to be withdrawn too.
Typically, the logical one to have a go with is acetone.
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Maybe someone has information about the metabolism of N,N-dimethylthioformamide in the human body? Will it be more or less toxic than N,N-dimethylformamide?
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contact for free demo, info@viridischem.com
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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.
Regards
Silpa.
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Thanks Vijayakumar Samiyappan and
Carlos F. Marcos
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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.
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Xylene is considered an excellent lipid solvent despite the health hazard due to its insolubility in water which enables it to eliminate water from the tissue specimens (Suvana et al, 2018). According to Rajan and Malathi (2014), The Agency for toxic substances and disease registry (ATSDR) have proposed occupational and safety health guidelines regarding xylene which should be strictly adhered to by all personnel handling the clearing agent to minimize exposure and limit the toxic health effects of xylene.
References:
1. Rajan, Sharada & Malathi, Narasimhan. (2014). Health Hazards of Xylene: A Literature Review. Journal of clinical and diagnostic research : JCDR. 8. 271-274. 10.7860/JCDR/2014/7544.4079.
2. Suvarna, S. K., Layton, C ., and Bancroft, J.D. (2018). Bancroft's Theory and Practice of Histological Techniques (8th ed.). Philadelphia, PA: Churchill Livingstone Elsevier
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Hi fellowScientists,
I am going use DMSO as a positive control in a cytotoxicity assay involving CACO-2 cells. I am looking for medium to high toxicity levels. Would 2% and 5% be acceptable concentrations? Thanks!
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Thanks, I was hoping for an answer from someone with a direct experience, reports vary.
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In-silico analysis
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Thank you @Ali A. Al-Allaq
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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.
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The pollution of the environment by toxic pollutants constitutes a disaster for the terrestrial and aquatic flora and fauna, the harmful effects are irreversible which depends on the dose and also on the duration of exposure; the link of our published review on the toxicity of heavy metals for marine and freshwater fish: https://ejournals.epublishing.ekt.gr/index.php/jhvms/article/view/25407/23353
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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?
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Thank you for answering
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Chlorine is added to drinking water What is the highest concentration added so that it is not toxic?
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Kindly explain.
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J. C. Tarafdar Sir, obviously, silver cation is not a nanoparticle but silver cation is considered as Lewis acid which react with Lewis bases such phosphorus and Sulphur containing biomolecules. Similarly, when bacterial cell exposed to silver nanoparticles, silver ion release from it and exerts its effect on cell. Some times or most of the time silver nanoparticles act as silver bullet that directly fracture the cell. So, in this respect I asked the question.
Thank you sir for your insightful answer.
Definitely, it will be helpful in getting in depth knowledge.
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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?
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Amphotericin B contains polyene alkyl groups and hydroxyl groups. Forms a complex between two molecules due to hydrophobic interaction enhanced by hydrogen bonds. Hydrophobic interaction is not specific, but hydrogen bonds are specific. Toxicity is due to penetration into the cell and destruction of the membrane due to hydrophobic interaction. However, the complex does not release Amphotericin B molecules for hydrophobic interaction with the cell membrane. The interaction between the molecules of Amphotericin B is greater than between the cell membrane and the Amphotericin B molecule.
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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?
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Agree with Lewis S Coleman
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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?
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I am having an opposite problem with clodronate liposomes. It did not seem to really deplete any macrophages although 2 of my mice died 24 hours after the injection. Could there have been something wrong with my technique?
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Just want to know the right flow
Pre-formulation, formulation, characterization, Efficacy, toxicity and PK studies
or
Pre-formulation, formulation, characterization, toxicity, PK studies and Efficacy studies
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Depends upon how much data is already available for that compound, for example, if you have IND than after finding its primary effect, Toxicity studies are required before further evaluation, but if you have a known compound (for example; generic drugs) whose pharmacological activity and and toxicity is known and you are developing a new formulation without changing the chemical structure than efficacy studies are not required and only toxicity studies should be done followed by PK Studies.
TLDR:
If Changes to Chemical Structure or IND than follow:- Primary Effect, Systemic Toxicity of IND , Pre-formulation, Formulation and its Characterization , Toxicity studies of Formulation, Efficacy, PK Studies
If no changes to the Chemical Structure (i.e. New Formulation/ Dosage Form Development):- Pre-formulation, Formulation and its Characterization, Toxicity study of the formulation, PK Studies
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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!
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The toxic response of the mentioned trace elements can be traced through various biological parameters (hematology, histopathology, biochemistry, ecological stress, etc) using mathematical formulas.
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Please, I need references talking about the unpalatability of some plants in arid areas (toxicity, rigidity, chemical composition "alcaloïds ...", flavor, astringency, laxativity, ...?
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- Rangelands of the arid and semi-arid zones in Uzbekistan
- Botanical Composition and Species Diversity of Arid and Desert Rangelands in Tataouine, Tunisia
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Silver nanoparticle nowa days used on many packaging and food leveling material.
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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.
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  • Basically, whatever transformations you apply to your variables is allowed if it results in data that meet the assumptions of the model you want to use.
  • But it may not be the most desirable approach.
  • I suspect that you have some misconceptions about the assumptions of anova. I assume you are conducting a two-way anova. In this case, the model is a general linear model, and the assumption is that the errors are normally distributed. We can check this by looking at the residuals from the analysis.
  • It's not very helpful to use a hypothesis test to test the assumptions of a model. It's better to look at plots of the residuals, or to understand the nature of the population that was sampled.
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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:
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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.
Thank you.
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Hi Lëonid,
Once happened to me and searching in literature I found some articles relating cAMP with this morphological change (PMIDs 2993305, 232579, 17557277, 20840080).
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Hello dear experts,
I have a challenge in disposing my MTT plates
Since the final MTT solution in the multi-well plates is quite toxic, I would like to know which way is the best for a harmless procedure of disposal
Thank you
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I would suggest you to consult the department of Tehran University of Medical Sciences who are concern with the disposal of biomedical wastes. The Tehran University of Medical Sciences must have a guidelines and procedure that you must have to follow in order to dispose biomedical research wastes and toxicants.
Do not throw it in the laboratory sink or nearby that otherwise may cause environmental pollution. Since the guidelines for the disposal of biomedical wastes/toxic materials are different in various countries, follow the university guidelines for disposal of biomedical research wastes.
Best
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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.
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I think the answer will lie in one (or more) of the following:
1- CD 95 levels
2- FLICE status
3- cytochrome c levels
4- p53 expression
5- APAF-1 levels
Probably you won't find one assay to check all the above at once, but there is a combination of them, such as: https://www.abcam.com/kits/apoptosis-assays#Apoptosis%20assays.
Hope that helps!
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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.
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I suggest you do a pilot study. Start with 1mg Cd /kg bd wt using a single rat followed by 2,3 ,4 and 5 (ip). If that fails change the route of administration, use the subcutaneous route.
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Hi,
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?
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Alternatively you could try other BL21 cells with pRIL for example. This may help to supplement tRNA abundance if your toxin exhibits some rare codons.
Compentent cells like:
BL21-CodonPlus RIL for example.
Good luck.
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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.
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If curcumin is made with Na OH solvent, it causes poisoning of the solution and death of rats
What is another solvent that does not cause the solution to be toxic?
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Bir çalışmada susan yağinda verilmiş.
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Suggest articles updated one which clearly tells about the toxicity or safety assessments of essential oils in food preservation
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Have a look to the following very useful RG link:
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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
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I think it depends upon what is the cause of the purported lacO toxicity. If it is due to repressor binding to so many lacO sites on the plasmid maybe using a strain not expressing any repressor would be good, or if the toxicity is due to the high number of lacO regions (ie all those repeats) in which case strains defective in various recombination pathways might help (SURE strains for example) or if your plasmid is expressing a protein that is somewhat toxic and the mutations are reducing protein expression, in which case making more repressor and growing with excess glucose might help.
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Hello everyone!
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!
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hello Martha mam, can u please share the reference for your statement.
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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 :)
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When doing DNA extractions we often use RNase to digest any RNA that is in the sample and DNase free water. When extracting RNA we do the opposite. It is effectively to prevent extractions for RNA specific assays being contaminated with DNA and in DNA assays contamination with RNA. Effectively you want to keep your yielded extracts as pure as possible.
Theoretically you could do both in the same area, you just need to keep everything clearly labelled and make sure you are using the right reagents. Most people would recommend you use filter-barrier tips with RNA extractions that you keep separate from you DNA extraction tips.
A main concern may also be the temperature... DNA is reasonably stable at room temperature while RNA degrades more easily.
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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.
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non toxic alternative for formalin
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I would suggest you plastination see this article
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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.
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MTT assay using L929 cells@10 K is used., allowed to attach for 24 hrs. Sample preparation. 0.1 % weighed or pipetted and dissolved in DMEM medium with FBS and sonicated for 20 hz for 5 min. Then 100 ul loaded and treated for 24 hrs, then media is removed, washed twice using PBS. MTT reagent was added and then incubated for 3 hrs and so on.
Is this procedure is correct, mainly sample preparation?
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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!
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Dear Dr Wendi
I have read a very interesting article entitled : Differential activation of receptors and signal pathways upon stimulation by different doses of sphingosine-1-phosphate in endothelial cells.
This paper exactly responds to your valuable question, probably and hopefully!
Good Luck
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Which characteristics (Surface charge and Size) of Silver nanoparticle exerts more toxicity for microbial cell???
Kindly comment your view or experience.
Thank you
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موضوع متميز وانا اتابع الاجابات رغم انه ليس من اختصاصي لكني مهتمه بهذه المواضيع
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I am trying to determine whether these statements are true or not
  1. LPS toxicity is mediated by the toll-like receptor
  2. NO is mainly produced by Kupffer cells
  3. Liver necrosis is the main result of paracetamol toxicity
  4. cholestasis is the main result of LPS toxicity
  5. Glucuronyltransferases are involved in the GSH conjugation of NAPQI
  6. sulfurotransferases are involved in the GSH conjugation of NAPQI
  7. 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
  8. the liver is the main target of paracetamol because sulfurotransferase expression is generally low
  9. GAPDH is used to normalize the concentration of gene of interest
  10. The number of cycles required to have a sufficiently detectable amount of fluorescence in the PCR is dependent on the original mRNA concentration
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Negin Rahimi Liver damage results not from paracetamol itself, but from one of its metabolites, N-acetyl-p-benzoquinone imine (NAPQI). NAPQI decreases the liver's glutathione and directly damages cells in the liver. Diagnosis is based on the blood level of paracetamol at specific times after the medication was taken.
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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?
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This paper could address the issue:
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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
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Hello everyone
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 ?
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Most times, nutrients and minerals required for growth are optimally enriched in Environment where organisms are collected from. The culture medium used in the laboratory may deplete the growth of the organism due to insufficient growth nutrients and environmental factors i.e the organism might be aerobic and culturing them anaerobically may deplete their growth..
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If a chemical is soluble in 30 mg in 1 ml100% ethanol or 100% DMSO, how can i dilute it without affecting the solubility and to avoid toxicity on living organisms?
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Dear Sara shohdy Thabit dilution of such solutions is generally not a problem. If 30 mg of your compound is soluble in 1 ml of 100% ethanol or 100% DMSO it will also be soluble in 10 ml or 1 liter of the same solvents. On the other side, concentration of the solutions could cause problems if the maximum concentration is reached and the compound starts precipitating. The toxicity on living organisms depends more on the nature of the compound and the amount, but not on the concentration of the solution.
Good luck with your work!
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Both are inorganic species of selenium. However, the previous study had shown that selenite more toxic compared to selenate. What's affected the difference in the toxicity threshold in aquatic environment?
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Please anyone explain inorganic form is highly toxic than organic form ?
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Arsenites (As3+ or trivalent, arsenic trioxide) are 5–10 times more toxic than arsenates (As5+ or pentavalent) due to their higher solubility. See the useful link: https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/arsenites
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Why nature-based products are considered biocompatible for drug delivery although many natural products can be toxic or dangerous
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They are products of biosystems and compatible with majority of biochemical reaction, pathways and products of primary, and secondary metabolites. The receptor affinity is of prime importance for a natural product to bind and produce effects, the choice of the receptor or exactly the natural products pharmacophore fitting the receptor type will produce the effects the receptor is responsible for. Not all natural products bind to many receptors, rather specific in nature. Multivalent binding and specific receptors produce their effects, at times harmful as their intrinsic property.
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Were thinking of using gold nanoparticles for cells. The gold nanoparticles will be used to deliver proteins to cells.
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The toxicity can be mainly to what is in the surface of either nanoparticle. Hence, gold nanorods are way more toxic.
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Dear All
Since 2-ME is highly toxic and volatile, with an extremely pungent and unpleasant aroma, I would be happy if you let me know a suitable alternative material for 2-ME in DNA extraction processes.
Regards
Mohammad
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I am not an expert in DNA extraction but a search of PubMed found a publication of possible interest to you. It is "Toxic reagents and expensive equipment: are they really necessary for the extraction of good quality fungal DNA?" ( ). An excerpt is "This study clearly demonstrates that it is possible to obtain high yields of pure DNA from pigmented conidia without the use of strong and expensive cell disrupting procedures and of toxic reagents."
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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
Staining:
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.
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TMB has been used as a hydrogen donor chromogen in combination with hydrogen peroxide (H2O2) as a hydrogen acceptor for detection of tracer horseradish peroxidase (HRP). Indeed this reaction is highly sensitive to detect a small quantity of the tracer, but it has some drawbacks in that its colored reaction product fades rapidly and sometime forms crystals.
Thus, tendency of TMB solution to produce crystalline artifacts that appear as a random clumps of crystals has been observed while observing the slide under the microscope. If the cells are not much dense then you can apply cover slip that may take away these crystals and then carefully count your cells in a crystal free areas of the slide.
Good luck
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Hi All,
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?
Thank you.
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Fromm your experimental setup it seems you are inducing toxicity in various cell lines and trying to analyze cell viability, ROS levels etc. I would suggest you to analyze Nitric oxide (NO) level along with ROS to confirm whether your protein is inducing stress-mediated cell toxicity. Once it is confirmed that ROS and/or NO are elevated, then you can check antioxidant enzymes like SOD, Catalase etc to correlate the cellular antioxidant enzymes with ROS as well as NO level that may signal downstream pathways to initiate cell toxicity including apoptosis, autophagy, necroptosis ans well as necrosis depending upon the extent of oxidative stress insult.
Once you finish the above parameters then you can check the pro-apoptotic and apoptotic markers such as p53, Bax/BCl2, upstream as well as downstream caspases (Caspase 9, Caspase-3 etc) and DNA damage by agarose gel electrophoresis. Its always better to have morphological changes at the level of cell in vitro (I mean morphological apoptotic features such as blabbing, shrinkage, cytoplamsmic fragmentation etc) that can be very useful to correlate the .biochemical well as molecular data as described above.
Although there are several other important parameters that could be analyzed but you have to see that whether your lab facilities/resources allow you to conduct proteomic and genomic level analysis. Good luck
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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
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rabbits, rats, mice, dogs, cats, primates, hamsters, guinea pigs, birds, and fish.
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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。
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Hello!
Could anyone provide and advice regarding if its better to use in your PDE calculation the doses expressed in mg/m2 or if its better to convert the doses on a mg/kg basis. I saw that is possible to convert the dose expressed in mg/m2 to mg/kg by dividing the Animal Dose by Km value (according to FDA guidance for industry) , is this a correct approach?
I was wondering this because firstly i took in consider to multiply in the PDE formula the animal dose (mg/m2) from preclinical studies with average body surface for humans (1.62m2) before applying the adjustments factor, and i dont know if this or the previous one is the correct approach.
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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.
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Dear Ademi
Please kindly follow the attached document and also my papers regarding the toxicity......,hope they will be helpful !
this site can help you too : https://cfpub.epa.gov/ecotox/
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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.
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See this article, it might be helpful
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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?
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When NaOH dissolved in water good amount of heat is evolved and pH of solution increases.
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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 ?
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congo red is histological stain for amyliodosis
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Dear all,
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?
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Dear all,
I addressed the problem by mixing and matching solutions, variables to transduction. I tested, cell confluence at transduction, condition media, MOI values, cell passage number and transduction type (reverse plating, add on top, spinfection)
I found that the most effective changes I made was ensuring 'health' of cells by adding 30%+ conditioned media during and after transduction, as well as using spinfection on the myoblasts, following protocol from (Himeda, Jones and Jones, 2016) with some alterations on time of viral incubation.
Conditioned media makes a big difference, thank you for suggestions!
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I was wondering if LB broth would be harmful if ingested. The ingredients don't seem particularly toxic, but many safety sheet warn against drinking it. If anyone could help me with my query I would be very thankful.
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Nawel Zaatout that's the SDS for the powder. Any finely powdered substance has those safety concerns if inhaled. The standard LB broth (tryptone/casein, yeast extract and NaCl) shouldn't be different to a very concentrated soup or stock used for cooking. And many of the oldest classic culture media, esp. the undefined non-selective ones are more or less the same as they would be made out of readily available produce.
Obviously, those sold nowadays haven't cleared food safety regulations so I wouldn't recommend their consumption.
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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?
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Irshad A Hajam thank you so much dear Irshad
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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.
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Check out Qiagen
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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?
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Thanks again and again for your valuable answers.
The Arabian Gulf countries use the desalination plants, which is more fast and efficient than the rest methods. Even the distillation technique needs a lot of efforts and people to run it, the matter that make the first technique is more reliable but with environmental risks.
Regards
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Search for more details on anionic surfactant FFD-6 relatedness to antibiotics and its toxicity to aquatic ecosystems.
Kindly share your views.
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good question
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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
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Calculation of LC50 value by MTT assay seems to be the best way.we can take two concentrations below it and two above in it for some selected time of exposure
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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.
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Dear Dr Stanton,
These Days, I'm a bit curious about knowing more information regarding the use of Implantable Alzet Pump, that's why I would like to take a part and give you some information that might be useful.
Please have a look at these papers on the following link:
Regarding your second question, I suggest contacting the company providing this pump, maybe they have feedback on this issue.
all the best.
Regards.
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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.
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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?
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Hey, it might be too late but can you share the literature that refer to your statement "Then I looked into literature to find out that expression of T4, T5, Taq, Pfu DNA polymerases all confer toxicity to E. coli.". thankyou in advance..
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Hello everyone
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?
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Non!!: Not at all ... and "mercury amalgam" has long been FORBIDDEN, at least in the European Union, in the US and many other countries. Fight because your country prohibits it.
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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.
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You can use DMSO
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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?
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ofcourse you can measure many paramters without mice euthanization but it based on your lab. facilities for example:
you can measure neuro-behavioural tests, urine analysis with metabolic cages, blood analysis, cardiac indices by biopac and under anesthesia, growth and body weight indices and even effect on DNA extracted from blood, urine and microCt or other imaging modalities to visualize size and volume of each organ
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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?
Thank you.
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Dear Vishal, thank you for posting this very interesting technical question. There are various relevant references available rigth here on RG. For example, please have a look at the following potentially useful articles:
Development of Generalized QSAR Models for Predicting Cytotoxicity and Genotoxicity of Metal Oxides Nanoparticles
and
Nano-(Q)SAR for Cytotoxicity Prediction of Engineered Nanomaterials
Both articles have been posted by the authors as public full texts on RG, so you can freely download them as pdf files.
In this context also please see the following relevant paper:
What if the number of nanotoxicity data is too small for developing predictive Nano-QSAR models? An alternative read-across based approach for filling data gaps
Unfortunately this article has not (yet) been posted as public full text on RG. However, the author has an RG account (https://www.researchgate.net/profile/Agnieszka-Gajewicz-Skretna) so that there is a good chance that you can request the full text directly from the author via RG.
Good luck with your research and best wishes, Frank Edelmann
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Electrically decomposed solids
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Dear Abdullah, this is actually a very intersting and important technical question. Currnet research in this area is often directed toward the development of nitrogen-rich energetic compounds which are for example based on the azotetrazolate anion and related compounds. Such explosive materials have low toxicity and produce mainly elemental nitrogen as gaseous by-products. Thus I strongly suggest that you search the "Publications" section of RG for the term "nitrogen-rich energetic compounds":
This will provide you with a long list of relevant references which have been posted by RG members, many of them even as public full texts. Similarly you can also search for the term "azotetrazolate". A typical very useful article in this field is the following:
High-Energy Salts of 5,5’-Azotetrazole. I. Thermochemistry and Thermal Decomposition
This article is freely available as public full text on RG.
I hope this answers your question. Good luck with your research and best wishes, Frank Edelmann
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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.
Material:
  • 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).
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Hello Luca,
You can check on this paper for help.
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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?
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Hi there,
As you worked on triplicates, did you define the error bars for each time point? Is the observed difference significant?
What is the solvant used for your stocks of toxics? As the mix contains less YPD and a larger volume of toxics, I'm wondering if the global composition of the sample is the same as for the others.
Also I'm puzzled about the level for the stationnary phase: 0.7 is quite low for a culture run in rich media...
Anyway, having a quick look at the curves I would only say there is a delay in growth for the mix (but growth rate in exponential phase looks unchanged) but I would not conclude on the final state of the cultures.
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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.
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Thank you Mohamed Ben-Haddad . :)
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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?
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Thank you very much Kohei Torikai for the informations provided. As you say, chronic exposure may be a possible cause of toxicity which in the case of allergen-specific immunotherapy is important considering the potentially lifelong need for this kind of treatment. And in particular in cases where the animal has already chronic kidney disease for example.
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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!
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I think all the criteria are critical but Compound 1 is highly critical.
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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)?
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Dear colleague,
I think that not possible.
Changing the method of entering the pesticide (substance) or changing the solvent, the values will change LC50. Therefore, I recommend recalculating LC50 for oral feeding if the solvent is water and independently if the solvent is another substance (acetone).
All the best,
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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.
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Praveen Kumar Determine Cr(VI) by diphenylcarbazide (DPC) and then determine total Cr using ICP or AAS, if you have these instruments. DPC is specific to Cr (VI), while AAS/ICP measures total Cr (VI and III). subtract the difference, which gives Cr (III).
If you don't have access to these instrument, then try this method
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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.
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A number of previous studies have shown that calcium carbide is highly toxic due to its content of some toxic chemical like Arsenic and phosphorus which are well known to be hazardous.
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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.
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