Clinical Toxicology

Clinical Toxicology

  • Witold Orlik added an answer:
    How can one estimate the health cost of workers due to exposure ?

    plz suggest me that what methodology should i  use to evaluate the adverse health effect of workers working in toxic waste?

    Witold Orlik

    Hello Muhammad,

    I was able to provide information on more "general" level. Unfortunately I am not an expert within your research domain. So if I want to be honest, my ability to help you with regard to more sophisticated "angles" of your task is somewhat limited. 


  • Maria Gabriella Verso added an answer:
    Why isn’t clinical toxicology a more significant part of medical school education?
    With abundant evidence in the literature that many health afflictions result from toxicant exposures, and with published NHANES data from CDC that most people have bioaccumulated numerous persistent toxicants within their body, why are medical students not taught about clinical toxicology and approaches to investigate and treat toxicant-related health problems?
    Maria Gabriella Verso

    In Italy Occupational and environmental Medicine, with clinical toxicology,  is a fundamental subject of the degree course in Medicine and Surgery and is subject of study in almost all the Degree Courses of the Medical Schools (to become nurses, midwives, rehabilitation technicians etc) .

  • Kari Radha Krishna Murthy added an answer:
    I´m currently doing a study about scorpionism in Ecuador, Panamá and Uruguay, but there is little information. Does anyone know something?

    Due to a poor record of this accidents in Latin America, there´s little information about this public health problem. I´m looking for numbers of incidence and mortality by scorpion sting in Ecuador, Panmá and Uruguay.

    Kari Radha Krishna Murthy

    Dear Dr,

    I am working on scorpion envenoming syndrome for the last 40 years. We advocate the use of insulin-glucose infusion , continuous infusion of regular crystalline insulin should be given at the rate of 0.3 U/g glucose and glucose at the rate of 0.1 g/kg body weight /hour for 48-72 hours, with supplementation of potassium as needed and maintenance of fluid, electrolytes and acid-base balance. Administration of insulin-glucose infusion to scorpion sting victims appears to the physiological basis for the control of the metabolic response when that has become a determinant to survival. My e-mail id:, Kindly give your e-mail id. I will send copies of all my research publications to you.

    With best wishes,

    (Dr. K. Radha Krishna Murthy)

  • Priyamvada Sharma added an answer:
    Can anybody suggest me information about “Chronic Methanol Poisoning Effects"?

    Can anyone suggest me any information about “Chronic Methanol Poisoning or Repeated Exposure to Methyl Alcohol or its Metabolites and its effects in human health” either in published or unpublished works (gray literature).

    I searched PubMed many times but, I did not find almost anything.  

    Priyamvada Sharma

     In case of methanol poisoning Formic acid, ethoxy acetic acid, methoxy acetic acid and glycolic acid are measured in different biological fluids using gas chromatography mass spectrometer .   You can get idea from the article

    J Pharm Biomed Anal. 2015 Oct 10;114:16-21. doi: 10.1016/j.jpba.2015.04.039. Epub 2015 May 6.
    Identification and quantification of acidosis inducing metabolites in cases of alcohols intoxication by GC-MS for emergency toxicology.

  • Alessandro Protti asked a question:
    Have you ever witnessed linezolid-induced lactic acidosis?

    We've recently had a case. Systemic oxygen consumption and extraction progressive decreased while refractory lactic acidosis progressive developed (likely due to mitochondrial "poisoning"). Anyone willing to share data on other cases to write something interesting together? 

  • Simon C Johnson added an answer:
    What is rapamycin dose for live animals?

    i want to use rapamycin in my control group of hamsters infected with prion...whats the recommended dose?


    Simon C Johnson

    We recently characterized the dose response profile of rapamycin in mice, this may be helpful for you:

  • Mustafa I Elbashir added an answer:
    Anyone aware of any work/research on off-gassing from patients who have ingested cyanide?

    Interested in any:

    Case reports/research or animal models etc.

    Mustafa I Elbashir

    sorry Dr Muhaammad I have no idea on the topic

  • Prabhat Kumar Upadhyay added an answer:
    Magnesium chloride works more intracellularly than magnesium sulphate. What are the impacts on clinical effects?

    Magnesiumchloride has more intra cellular effects while magnesiumsulphate has more extra cellular effects. This explains that magnesium sulphate is clinical less effective but why is it then also more toxic as the toxicity effects are primarily intracellular?

    intravenous given magnesium reduces the opioid requirements per operative by reducing the sympathetic outflow.

    Prabhat Kumar Upadhyay

    Simple reasons of acidosis because different abilities of chloride and sulphate ions upon interations with cellular parts and phsiological pH changes drastcally....

    Follow this.......Roche, Block, sonie and wilson.....Inoganic med chem book

  • MOHAMMAD Nabavi added an answer:
    What makes titanium implants toxic and cause allergic and autoimmune reactions?
    Dental implants are made of titanium because of biocompatibililty. Dental implants give titanium toxicity allergic and autoimune reactions.
    MOHAMMAD Nabavi

     this is a good article Nikola:

  • Amulya Nidhi Shrivastava added an answer:
    How we usually determine the neurotoxicity of certain Antibody?

    I am working to determine the proper therapeutic dose for certain antibody  so I need to know how we can evaluate the toxicity using a validated method ? 

    Please, could anybody also provide me with a published article about this? 

    Amulya Nidhi Shrivastava

    • Source
      [Show abstract] [Hide abstract]
      ABSTRACT: Prion infections cause lethal neurodegeneration. This process requires the cellular prion protein (PrP(C); ref. 1), which contains a globular domain hinged to a long amino-proximal flexible tail. Here we describe rapid neurotoxicity in mice and cerebellar organotypic cultured slices exposed to ligands targeting the α1 and α3 helices of the PrP(C) globular domain. Ligands included seven distinct monoclonal antibodies, monovalent Fab1 fragments and recombinant single-chain variable fragment miniantibodies. Similar to prion infections, the toxicity of globular domain ligands required neuronal PrP(C), was exacerbated by PrP(C) overexpression, was associated with calpain activation and was antagonized by calpain inhibitors. Neurodegeneration was accompanied by a burst of reactive oxygen species, and was suppressed by antioxidants. Furthermore, genetic ablation of the superoxide-producing enzyme NOX2 (also known as CYBB) protected mice from globular domain ligand toxicity. We also found that neurotoxicity was prevented by deletions of the octapeptide repeats within the flexible tail. These deletions did not appreciably compromise globular domain antibody binding, suggesting that the flexible tail is required to transmit toxic signals that originate from the globular domain and trigger oxidative stress and calpain activation. Supporting this view, various octapeptide ligands were not only innocuous to both cerebellar organotypic cultured slices and mice, but also prevented the toxicity of globular domain ligands while not interfering with their binding. We conclude that PrP(C) consists of two functionally distinct modules, with the globular domain and the flexible tail exerting regulatory and executive functions, respectively. Octapeptide ligands also prolonged the life of mice expressing the toxic PrP(C) mutant, PrP(Δ94-134), indicating that the flexible tail mediates toxicity in two distinct PrP(C)-related conditions. Flexible tail-mediated toxicity may conceivably play a role in further prion pathologies, such as familial Creutzfeldt-Jakob disease in humans bearing supernumerary octapeptides.
      Nature 07/2013; 501(7465). DOI:10.1038/nature12402
  • Venkata Harsha Vardhan Boddeda added an answer:
    What are simple assays done for toxicological studies of a compound on zebrafish embryos?

    I'm testing a compound (plant extract) on zebrafish embryos. Please suggest a few simple yet effective assays to test toxicity at cellular level. 

    Venkata Harsha Vardhan Boddeda

    You can follow the Fish embryotoxicity tests which have been given by OECD guidlines. 6hpf embryos should be taken and should be treated with test drug. 

    You can also perform cardiotoxicity and hepatotoxicity on 72hpf larvae. 

    You can do teratogenicity and also you can give scoring system in zebrafish based on structural malformations. 

    Check these links.

    + 1 more attachment

  • Arik Eisenkraft added an answer:
    Which laboratorial methods can be used to search botulinum toxin in food and patients blood or feces to replace the mouse bioassay?

    In Brazil we follow the recommendation of the CDC. However, the result of bioassay take much time, can not be used for a fast diagnosis, and causes animal cruelty.

    Arik Eisenkraft

    Hi Nidia,

    Of course! I'll be happy to help.


  • Michele Barone added an answer:
    For febrile patients with acute hepatitis there is no safe antipyretic. Is there an acceptable dose of paracetamol ? is measuring drug level useful ?

    There is a clear reduced dose for paracetamol for stable cirrhotic, but for acute compromisation of liver function such severe acute hepatitis or post agressive liver resection no clear data about a safe adjusted  antipyretic drug use according to liver function. Can monitoring paracetamol level prevent its hepatotoxicity in such citation?

    Michele Barone

    Febrile patients with acute hepatitis can take different types of antipyretic without problems. However, you should avoid cortisone in case of acute viral hepatitis, and paracetamol in case of signs of hepatic insufficiency. Finally, in presence of alterations of coagulation cascade I would avoid NSAIDs.

  • Federico Emiliano Ghio added an answer:
    Is anyone willing to share data on SvO2 (or ScvO2) and cardiac output in patients with lactic acidosis and documented metformin intoxication?

    I'm interested in confirming that metformin intoxication is associated with diminished oxygen extraction and consumption (secondary to mitochondrial "poisoning"?). This can be the primary explanation for concomitant lactic acidosis.

    Federico Emiliano Ghio

    Dear Alessandro, i think your hypotesis is right. In fact Metformin reduces pyruvate dehydrogenase activity and mitochondrial transport of reducing agents, and thus enhances anaerobic metabolism. This shift to anaerobic metabolism, in the presence of reduced insulin, increases production of precursors for the Krebs cycle. Consequently, there is a decreased ability to channel those precursors into aerobic metabolism, which, in turn, results in increased metabolism of pyruvate to lactate and increases net lactic acid production. Greetings, Federico

  • Manikanta Murahari added an answer:
    Can anyone suggest a protocol for MTT or SRB assay of nanoformulation?

    We have prepared a nanoformulation of anticancer drug and performed MTT and SRB assay of API, nanoformulation and placebo (nanoformulation without drug) at concentrations of 5-100 ug/ml. 

    OD readings were observed at a range of 2-3 for all the concentrations for MTT assay. We thought that MTT is interfering with the formulation components and tried with SRB assay.

    In SRB assay, we found OD of placebo was more than control

    For nanoformulation OD readings were also more than control but less than placebo

    Can anyone suggest the interpretation of results or share any protocol for the same



    Manikanta Murahari

    We also tried to wash with PBS, because of incubation for 24-48 hrs the particles are settling on the plate and we couldnt wash the wells efficiently. 

  • Hossein Rahmani added an answer:
    Can anyone suggest me the effect of catalytic domain of diptheria toxin on CHO cells ?

    we are planning to express the catalytic domain of diphtheria toxin with signal sequence  (without translocation and binding domain)  in CHO cells. will cells die due the effect of toxin. Since the toxin will not be processed by furin or lysosomal enzymes.    

  • Adejuwon Adeneye added an answer:
    What are the limitations and (dis)advantages of the up and down method for the determination of the median lethal dose (LD50)?

    Are there any limitations of the up and down method? (mabye the broad of the LD50 and not an exact value) 

    in which cases should this test be performed? 

    And are there already better alternatives available or in development? 

    thank you in advance

    Adejuwon Adeneye

    Hi Laurence, Up and Down Procedure (consisting of limit dose test and main test) as stipulated in OECD Guidelines on Acute Oral Toxicity Testing (425) remains the standard in vivo acute oral toxicity measures for determining approximate median LD50 of a chemical substance/chemical/drug with an unknown or closely related drugs of unknown LD50 value. It has the advantage of using few experimental animals which are dosed sequentially depending on its short-term and long-term outcome. This acute oral toxicity test also cuts cost since it involves the use of few experimental animals. However, it has its limitations which include:

    1. The test is restricted to female, nulliparous mice and rats only;

    2. The test requires close and long term close and strict monitoring for up to two weeks for each experimental animal for you to determine the short- and long-term outcomes;

    3. Finally, the test requires an algorithm of strict steps which although simple but could be cumbersome;

    4. It provides an estimated LD50 value and not the exact value

    Overall, it remains the gold standard for determining the LD50 values of an orally administered substance/chemical/drug with an an unknown toxicity profile. You can check my published article using this procedure: Adeneye AA et al. Journal of Ethnopharmacology 105: 374-379 (see attached).

    Best wishes!

  • Stephen Treimer added an answer:
    How can I determine amount of paraquat in water by UV spectroscopy?

    please provide method and materials.

    Stephen Treimer


  • Ahmed Ezat El Zowalaty added an answer:
    Is organic mercury a more toxic that metallic and ionic mercury?

    Toxicological Sciences - Medical Sciences

    Ahmed Ezat El Zowalaty

    Organic and inorganic mercury are much more toxic than metallic mercury

  • Istvan Ujvary added an answer:
    What evidence exists that novel synthetic cannabinoids may act in a clinically signficant fashion at receptor sites beyond CB1?


    The synthetic cannabinoids (SC) currently being marketed as alternatives to plant cannabis have a higher risk of adverse outcomes than phyto (plant) cannabinoids.

    The SC products on the market are much stronger agonists at the CB1 receptor than THC, and none contain a synthetic equivalent to the phyto-cannabinoid CBD, but is part of the increased risk also due to SC substances acting at other receptor sites?

    Istvan Ujvary

    It is an important question but, unfortunatelly, but there is no published data on effects on non-cannabinoid targets. None. Anything that has been mentioned here in the comments is mere speculation. In vitro studies, such as receptor profiling or enyzme screeing, are urgently needed. At a meeting organized by the European drug agency EMCDDA last year I gave a talk on new and some anticipated SCs as well as some similar structures but with different mode of action. Selected slides relevant to this topic can be found in the downloadable pdf file. Note that the list of structurally related substances such as etonitazene or indibuline, is incomplete. Furthermore, it would be interesting to test these latter 'non-cannnabinoid' compounds for CB receptor effect.

  • Phoebe Argyle added an answer:
    How to convert a toxic dose for a zebrafish to be equivalent to the one for rats?
    I want to use the toxic dose for a rat. I want to ask if I can use the dose without changing anything or do I need to make a certain conversion of the dose for zebrafish to be equivalent to the one for rats?
    Phoebe Argyle

    I agree with Gabriela above. It is not possible to convert the rat dose to a zebrafish dose as the methods of administration are different. In the past I have looked at relative toxicities between different treatments within one model (zebrafish or rat) e.g. chemical X is the most toxic out of X, Y, and Z for both zebrafish and rats. However it's not possible to directly compare g/g toxin/body weight to g/L toxin/solution concentration.

  • Vinuchakkaravarthy Thangaraj added an answer:
    Can phenytoin, carbamazepine and nevirapine form covalent bond with cellular proteins in native form or metabolite form?

    Can anyone help me in clearing my doubt whether the anticonvulsant drugs like phenytoin, carbamazepine and anti-retroviral drug nevirapine can act as haptens or can they form any covalent bond with any of the extracellular or intracellular proteins either in native form or in metaboilte/hapten form before/during exerting its mechanism of action or they can form any hapten-like molecule during conjugation process in kidney for elimination which can induce immune reaction? Any literature describing the phenomena has been published on this? Please share it here to me...

    Vinuchakkaravarthy Thangaraj

    Thank you Dr. Reza and Dr. Ali

  • Paul Dessauer added an answer:
    Synthetic cannabinoids- what evidence exists regarding potential for inducing acute or chronic problems with physical or mental health?

    A wide variety of synthetic cannabinoids (SC) are now being marketed as "safer" or "quasi legal" alternatives to plant cannabis.

    Anecdotally, it appears that these research chemicals are typically associated with a significantly higher risk of acute adverse responses (such as tachycardia, anxiety attacks and transient psychosis) than smoking "real" plant cannabis.
    As the majority of SC products being marketed contain chemicals that are much stronger cannabinoid receptor ligands than THC, (and some contain mixtures of more than one SC), and as these mixtures do not contain any equivalent to CBD, this is perhaps not surprising.

    Does anyone know of animal studies or case histories relevant to the potential of these chemicals to induce such acute problems?
    I am also keen to find any research that may indicate the potential for dependence, and likely withdrawal profiles upon abrupt abstinence from regular use, of these chemicals.

    <<< The intravenous administration of THC may be associated with a range of schizophrenia-like positive and negative symptoms in psychosis-free individuals (D’Souza et al., 2004).

    Conversely, the phytocannabinoid CBD presents with anxiolytic and antipsychotic properties (Zuardi et al., 2006), possibly because CBD may displace the binding of THC from CB-rs.

    In contrast, spice products contain no CBD, and the SC chemicals are full agonists at CB-rs and are characterized by both a receptors’ higher affinity and higher potency in comparison with THC (Fattore and Fratta, 2011; EMCDDA, 2011).
    Forrester et al. (2012) showed that a “cannabis”-associated psychopathological syndrome occurrence was less likely with marijuana than with SC, with 2% in the marijuana and 11.2% in the SC misusers’ group, having been identified as experiencing hallucinations and delusions.

    Those experiencing psychotic episodes related to Spice use are also reported to present with higher/more frequent levels of agitation and behavioral dyscontrol in comparison with those psychotic episodes described in marijuana misusers (Brakoulias, 2012). >>>

    “Spiceophrenia”: a systematic overview of “Spice”-related psychopathological issues and a case report

    Paul Dessauer

    I've just posted a related question here;

  • David Ogbonnaya Onu added an answer:
    Methadone poisoning in an addict?
    How to determine lethal methadone concentration in an addict when one doesn't know the amount of pills taken each day?
    David Ogbonnaya Onu

    I agree with the 2 responders about combining the severity of symptoms and hair analysis. The latter test quantifies the duration of Methadone use. Urine toxicological testing is only qualitative. 

  • Vincent Bloks added an answer:
    Can I give DMSO to a rat as a solvent?

    Hi all, please give me a hand. I am going to use glibenclamide (from Sigma) to treat diabetic rats as a positive control for my extract. I would like to know which solvent is suitable for dissolving glibenclamide before oral administration. I searched some papers and they use DMSO, however I don't know the concentration of DMSO. May I use the absolute one for rat feed? Or can I use another solvent (which, ?%). Thank you so much!

    Vincent Bloks

    perhaps dissolve in DMSO and then in oil ( cremaphore 10%) , perhaps that will work

  • Yvonne Hopf added an answer:
    Does anybody know a different solvent than DMSO for Everolimus?

    Background: it needs to be solved for IV administration to pavians and the current information we have is that it is soluble in DMSO (dimethylsulfoxid). If you don't know a different solvent maybe someone knows a little more about 'safe' concentrations for administration. Many thanks for your help!

    Yvonne Hopf

    Thanks David!

  • Ludwig Gruber added an answer:
    Does anyone know which plastic products contain the most phthalates?
    With phthalates being measured at higher levels in human biomarkers and being used increasingly in food containers and other products, has anyone examined the products that expose humans the most/least? Presumably those with the least amount of polyvinyl chloride, but is it so? Is there any relationship to the plastic recycle numbers?
    Ludwig Gruber
    Plasticised PVc is without doubt the most likely plastic material with high phthalate content. The exposure especially to DEHP from food consumption alone can be in the range of the TDI. And there are a number of other sources which contribute to the overall human exposure. Therefore there is indeed a problem, but we do not observe phthalates increasingly in food containers and other products as You suggest.

    Direct contact between PVC and food is not really the predominant scenario for phthalates contamination. It seems that the ubiquitous presence of the phthalates and their lipophilic character are more important.

    There is no direct relationship to the overall plastic recycle numbers, things are more complex. A contamination with phthalates is only likely for some kinds of plastics, and these are normally not used as food contact materials. Again, the high production numbers and the resulting ubiquitous presence of the phthalates are more important.
  • Rahman Maman added an answer:
    What are the current methods for determining the median lethal dose (LD50)? What are the advantages of these methods to "Lorke's Method"?
    Lorke's method has been used since 1983.
    Rahman Maman
    i wonder if the method (UDP) can be applied for the fishes since we know this oral administration for the rat/mice.. anyone can suggest me?
  • Richard Beasley asked a question:
    Should IRM drugs containing imiquimod be patient applied drugs?
    IRM's are very unpredictable and result in non-specific immune responses toward antigens and rogue cells that are not well defined nor well understood which can lead to catastrophic events occurring in certain segments of the patient population. Imiquimod is one such small-molecule IRM that causes over a dozen cytokines to be induced by their respective origin of production during their physical contacts with molecules of this drug. During treatments, the users cannot separate themselves from the physiological influences of the ongoing, out of sync, induction of this family of cascading cytokines being induced at unknown and unregulated levels within their bodies during each patient applied application of the drug. As with injection or IV chemo treatments where body weight and rate of drug deterioration after injection is factored into safety profiles for the individual patient, IRM's such as imiquimod do not possess this safety feature and are actually causing unknown or "free-wheeling" pharmacological effects within each user that are increasing the levels of cytokines during the weeks of treatments rather than systematically reducing them over time as we see in traditional chemotherapies. Drug induced autoimmunity is the number one possibility surrounding these IRM's.

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