Carcinogenicity Tests
Carcinogens
Neoplasms, Experimental
Mutagenicity Tests
Rats, Inbred F344
Mutagens
Toxicity Tests, Chronic
Evaluation of the chronic toxicity and oncogenicity of N,N-diethyl-m-toluamide (DEET). (1/865)
Chronic toxicity and/or oncogenicity studies were conducted in rats, mice, and dogs with the insect repellent DEET. DEET was mixed in the diet and administered to CD rats for two years at concentrations that corresponded to dosage levels of 10, 30 or 100 mg/kg/day for males and 30, 100, or 400 mg/kg/day for females; to CD-1 mice for 18 months at dosage levels of 250, 500, or 1000 mg/kg/day; and to dogs for one year, via gelatin capsules, at dosage levels of 30, 100, or 400 mg/kg/day. In the rodent studies, each group consisted of 60 animals of each sex, and two concurrent independent control groups, each containing 60 animals/sex were included in each study. Each group in the dog study consisted of four male and four female dogs and one control group was included in the study. Treatment-related effects were observed at the highest dose level in all three studies. For rats, the effects included decreases in body weight and food consumption and an increase in serum cholesterol in females only. In mice, the effects observed were decreases in body weight and food consumption in both sexes. The effects observed in dogs included increased incidences of emesis and ptyalism, and levels of transient reduction in hemoglobin and hematocrit, increased alkaline phosphatase (males only), decreased cholesterol, and increased potassium. One male dog in the high-dose group also exhibited ataxia, tremors, abnormal head movements, and/or convulsions on several occasions during the study. The highest no-observed-effect levels (NO-ELs) for rats, mice and dogs were determined to be 100, 500, and 100 mg/kg/day, respectively. No specific target organ toxicity or oncogenicity was observed in any of the studies. (+info)Administration of an unconjugated bile acid increases duodenal tumors in a murine model of familial adenomatous polyposis. (2/865)
Intestinal carcinogenesis involves the successive accumulation of multiple genetic defects until cellular transformation to an invasive phenotype occurs. This process is modulated by many epigenetic factors. Unconjugated bile acids are tumor promoters whose presence in intestinal tissues is regulated by dietary factors. We studied the role of the unconjugated bile acid, chenodeoxycholate, in an animal model of familial adenomatous polyposis. Mice susceptible to intestinal tumors as a result of a germline mutation in Apc (Min/+ mice) were given a 10 week dietary treatment with 0.5% chenodeoxycholate. Following this, the mice were examined to determine tumor number, enterocyte proliferation, apoptosis and beta-catenin expression. Intestinal tissue prostaglandin E2 (PGE2) levels were also assessed. Administration of chenodeoxycholate in the diet increased duodenal tumor number in Min/+ mice. Promotion of duodenal tumor formation was accompanied by increased beta-catenin expression in duodenal cells, as well as increased PGE2 in duodenal tissue. These data suggest that unconjugated bile acids contribute to periampullary tumor formation in the setting of an Apc mutation. (+info)Malignant transformation of p53-deficient astrocytes is modulated by environmental cues in vitro. (3/865)
The early incidence of p53 mutation in astrocytomas suggests that it plays an important role in astrocyte transformation. Astrocytes isolated from homozygous p53 knockout mice grow rapidly, lack contact inhibition, and are immortal. Here we tested whether the loss of p53 is sufficient for progression to tumorigenicity of astrocytes. We grew primary astrocytes under three conditions for over 120 population doublings and assessed their antigenic phenotype, chromosome number, and expression of glioma-associated genes as well as their ability to form colonies in soft agarose and tumors s.c. and intracranially in nude mice. Under two conditions (10% FCS and 0.5% FCS plus 20 ng/ml EGF), cells acquired the ability to form colonies in soft agarose and tumors in nude mice, and this was accompanied by the expression of genes, including epidermal growth factor receptor, platelet-derived growth factor receptor alpha and beta, protein kinase Cdelta, and vascular endothelial growth factor, which are known to be aberrantly regulated in human astrocytomas. Under the third condition (0.5% FCS plus 10 ng/ml basic fibroblast growth factor), astrocytes gained the ability to form colonies in soft agarose and had abnormal chromosome numbers similar to cells in the first two conditions but did not form tumors in nude mice or overexpress glioma-associated genes. These data provide experimental evidence for the idea that the malignant progression initiated by the loss of p53 may be subject to modulation by extracellular environmental influences. (+info)Expression of AML1-d, a short human AML1 isoform, in embryonic stem cells suppresses in vivo tumor growth and differentiation. (4/865)
The human AML1 gene encodes a heterodimeric transcription factor which plays an important role in mammalian hematopoiesis. Several alternatively spliced AML1 mRNA species were identified, some of which encode short protein products that lack the transactivation domain. When transfected into cells these short isoforms dominantly suppress transactivation mediated by the full length AML1 protein. However, their biological function remains obscure. To investigate the role of these short species in cell proliferation and differentiation we generated embryonic stem (ES) cells overexpressing one of the short isoforms, AML1-d, as well as cells expressing the full length isoforms AML1-b and AML2. The in vitro growth rate and differentiation of the transfected ES cells were unchanged. However, overexpression of AML1-d significantly affected the ES cells' ability to form teratocarcinomas in vivo in syngeneic mice, while a similar overexpression of AML1-b and AML2 had no effect on tumor formation. Histological analysis revealed that the AML1-d derived tumors were poorly differentiated and contained numerous apoptotic cells. These data highlight the pleiotropic effects of AML1 gene products and demonstrate for the first time an in vivo growth regulation function for the short isoform AML1-d. (+info)Marriage of a medium-term liver model to surrogate markers--a practical approach for risk and benefit assessment. (5/865)
The need for a reliable medium-term alternative to traditional long-term rodent test protocols for carcinogen risk assessment is pressing given the immense variety of compounds being developed for introduction into the human environment. The established lack of a complete correlation between mutagenicity and carcinogenicity means that recourse must be made to an in vivo model. Optimally, this model should be able to detect not only complete carcinogenic or promoting potential but also any ability to inhibit neoplasia. In order to be effective, it must take into account the available detailed knowledge on mechanisms of action of carcinogens and modulating agents. The Ito model, for which a uniquely comprehensive set of background data has already been accumulated, has a solid scientific basis; this model utilizes quantitative data for glutathione S transferase-positive foci as the preneoplasia-based surrogate end point (PSE). A very practical candidate for routine application, its predictive power, its flexibility, and its capacity to incorporate a range of mechanism-based surrogate end points (MSEs) provide a powerful tool for attainment of the twin goals of detecting carcinogenic agents and identifying promising chemopreventors. (+info)Comparison of the effectiveness of adenovirus vectors expressing cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21(WAF1/CIP1) and p27KIP1 in inducing cell cycle arrest, apoptosis and inhibition of tumorigenicity. (6/865)
Cell cycle regulatory proteins are important candidates for therapeutic tumour suppressors. Adenovirus vectors were constructed to overexpress cyclin kinase inhibitors p16INK4A, p18INK4C, p19INK4D, p21(WAF1/CIP1) and p27KIP1 under the control of the murine cytomegalovirus immediate early gene promoter. These vectors directed the efficient expression of each of the cyclin kinase inhibitors and induced growth arrest, inhibited DNA synthesis, and prevented phosphorylation of the retinoblastoma protein (pRb) in cell lines expressing functional pRb. In pRb-deficient cells, expression of the cyclin kinase inhibitors was not effective in inhibiting DNA replication or growth arrest. Interestingly, three of the cyclin kinase inhibitors, p16, p18 and p27 were found to induce apoptotic death in transduced HeLa and A549 cells. When the vectors were tested for their ability to inhibit tumorigenicity in a polyomavirus middle T antigen model of murine breast carcinoma, expression of the cyclin kinase inhibitors resulted in a delay in tumour formation that varied from several weeks for the p19 expressing vector to greater than 25 weeks for the p27 expressing vector. When tumours were injected directly with the adenovirus vectors expressing the cyclin kinase inhibitors, only treatment with the vector expressing p16 resulted in a delay in tumour growth. (+info)Tumorigenic conversion resulting from inhibition of apoptosis in a nontumorigenic HeLa-derived hybrid cell line. (7/865)
Although tumorigenicity in nude mice is one of the most important transformed phenotypes, its mechanism has been little analyzed. To understand the molecular basis of tumorigenicity, we characterized nontumorigenic CGL1 and tumorigenic CGL4 cell lines, both of which were originated from a common ancestral HeLa-human diploid fibroblast hybrid cell clone and retained a malignant state except tumorigenicity. When injected into nude mice, nontumorigenic CGL1 cells underwent apoptosis, but tumorigenic CGL4 cells did not. In vitro, CGL1 was also less resistant to various apoptotic stimuli than CGL4. These results suggested that inhibition of apoptosis may lead to tumorigenicity. To examine this hypothesis, we introduced antiapoptotic genes into the CGL1 cell line and injected the resulting clones into nude mice. The results showed that the ectopic expression of Bcl-2 or E1B19k, but not of crmA, converted CGL1 cells to tumorigenicity, suggesting strongly that this phenotype may be conferred by evasion of apoptosis. (+info)Increased oncogenicity of subclones of SV40 large T-induced neuroectodermal tumor cell lines after loss of large T expression and concomitant mutation in p53. (8/865)
A model for medulloblastoma-like primitive neuroectodermal tumors was established in rat using retrovirally transduced SV40 large T antigen (LT) as an inducing agent (O. D. Wiestler et al., Brain Pathol., 2: 47-59, 1992). A cell line isolated from such a tumor and clonal derivatives thereof were biologically and molecularly characterized. In the parental tumor cell line, TZ870, which had been selected for G418 resistance, virtually all cells expressed LT and wild-type p53, which were complexed to each other. When plated in soft agar, these cells grew relatively slowly and formed disperse colonies. However, when grown without selection pressure, these cells reproducibly gave rise to LT-negative and G418-sensitive derivatives, LT-0 cells. Surprisingly, these latter cells exhibited a higher degree of malignancy both in vitro, growing readily to large colonies in soft agar, and in vivo, where they gave rise to a rapidly growing malignant tumor. Clonal selection from TZ870 cells revealed two types of clones: in one type, LT expression was stably maintained, even without selection pressure, whereas the other type lost the LT coding sequences. All LT-negative clones exhibited the same phenotype as the LT-0 cells. Reexpression of LT had no effect. However, LT no longer formed complexes with p53, and p53 was metabolically stable, suggesting that it had been mutated. Sequence analyses and diagnostic restriction digests of the p53 gene revealed that (a) both the parental LT-transformed cells and their derivatives contained only one complete p53 allele and (b) all LT-positive clones expressed wild-type p53, whereas all LT-negative clones expressed a mutant allele with a common mutation at Cys-174-->Tyr, indicating their clonal origin. We assume that the loss of LT coding sequences is the consequence of the p53 mutation, perhaps by inducing genomic instability, and that both the p53 mutation and additional genetic alterations that accompany the loss of LT coding sequences might contribute to enhanced malignancy. (+info)Carcinogenicity tests are a series of experiments designed to determine whether a substance has the potential to cause cancer in living organisms. These tests are typically performed on animals, such as mice or rats, and involve exposing them to the substance for an extended period of time to see if it causes any changes in their cells that could lead to the development of cancer. There are several different types of carcinogenicity tests, including in vitro tests, which are performed in a laboratory setting using cells grown in a dish, and in vivo tests, which involve exposing animals to the substance and monitoring them for signs of cancer. Carcinogenicity tests are an important part of the process of evaluating the safety of new drugs, chemicals, and other substances before they are approved for use in humans. By identifying substances that have the potential to cause cancer, these tests help to protect public health and reduce the risk of cancer-related illnesses.
Carcinogens are substances or agents that have the potential to cause cancer. They can be found in various forms, including chemicals, radiation, and biological agents. Carcinogens can be classified into two categories: 1. Direct carcinogens: These are substances that can directly damage DNA and cause mutations, leading to the development of cancer. Examples of direct carcinogens include tobacco smoke, asbestos, and ultraviolet radiation. 2. Indirect carcinogens: These are substances that do not directly damage DNA but can cause cancer by promoting the growth and survival of cancer cells. Examples of indirect carcinogens include certain hormones, viruses, and certain chemicals found in food and water. Carcinogens can cause cancer by disrupting the normal functioning of cells, leading to uncontrolled growth and division. Exposure to carcinogens can occur through various means, including inhalation, ingestion, or skin contact. The risk of developing cancer from exposure to carcinogens depends on several factors, including the type and duration of exposure, the individual's age and overall health, and their genetic makeup.
In the medical field, "Neoplasms, Experimental" refers to the study of neoplasms (abnormal growths of cells) in experimental settings, such as in laboratory animals or in vitro cell cultures. These studies are typically conducted to better understand the underlying mechanisms of neoplasms and to develop new treatments for cancer and other types of neoplastic diseases. Experimental neoplasms may be induced by various factors, including genetic mutations, exposure to carcinogens, or other forms of cellular stress. The results of these studies can provide valuable insights into the biology of neoplasms and help to identify potential targets for therapeutic intervention.
"Carcinogens, Environmental" refers to substances or agents in the environment that have the potential to cause cancer in humans or animals. These substances can be found in various forms, including air, water, soil, and food, and can be naturally occurring or man-made. Examples of environmental carcinogens include: 1. Radon gas 2. Polycyclic aromatic hydrocarbons (PAHs) 3. Asbestos 4. Benzene 5. Formaldehyde 6. Dioxins and furans 7. Mercury 8. Lead 9. Chromium 10. Nickel Exposure to environmental carcinogens can occur through various routes, including inhalation, ingestion, and skin contact. The risk of developing cancer from exposure to environmental carcinogens depends on several factors, including the duration and intensity of exposure, the individual's age, sex, and overall health, and the specific type of cancer being considered.
Umu Chromotest
Chlornaphazine
SOS chromotest
Sudan I
2,4-DB
Liquid Paper
Mirex
4-Chloro-o-toluidine
Prallethrin
Bioassay
2-Amino-1-methyl-6-phenylimidazo(4,5-b)pyridine
Mineral wool
Intratracheal instillation
Furylfuramide
Louise M. Ryan
Dimethyl tetrachloroterephthalate
Ethylbenzene
Genotoxicity
HMX
Safe Drinking Water Act
Animals and tobacco smoke
Benzoyl peroxide
Séralini affair
Naphthalene poisoning
Nickel(II) sulfate
Mifepristone
2-Butoxyethanol
Chlormadinone acetate
Electromagnetic radiation and health
Central Institute for Experimental Animals
Quality and Study Design Considerations for Carcinogenicity Testing with the rasH2™ Mouse | Taconic Biosciences
IARC Publications Website - Directories of Agents Being Tested for Carcinogenicity
Results of search for 'su:{Carcinogenicity tests.}'
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WHO HQ Library catalog
Multiple-endpoint in vitro carcinogenicity test in human cell line TK6 distinguishes carcinogens from non-carcinogens and...
Testosterone (IARC Summary & Evaluation, Volume 6, 1974)
Toxic Neuropathy: Practice Essentials, Background, Pathophysiology
Hexamethylene Diisocyanate (HDI) | ToxFAQs™ | ATSDR
NIOSHTIC-2 Search Results - Full View
Vahle J[au] - Search Results - PubMed
Presentations at 11th World Congress on Alternatives and Animal Use
Daniel Nathans - Profiles in Science
EUR-Lex - 02008R0429-20210327 - EN - EUR-Lex
Biblio | Linus Pauling Institute | Oregon State University
Gardasil Contamination: EMA Steps Up to the Plate, FDA drops the Ball - SaneVax, Inc.
Peer Review: List of Hazardous Drugs in Healthcare Settings 2019 | NIOSH | CDC
Sodium Benzoate - Cosmetics Info
Registration Dossier - ECHA
Toxins | Free Full-Text | Multi-Mycotoxin Screening Reveals the Occurrence of 139 Different Secondary Metabolites in Feed and...
Sodium thiocyanate - Safety Data Sheet
DailyMed - ZIANA- clindamycin phosphate and tretinoin gel
3.1 Isofetamid | Therapeutic Goods Administration (TGA)
Portal LIS - Localizador de Informação em Saúde
Registration Dossier - ECHA
Klor-Con M: Package Insert - Drugs.com
Merck and Ridgeback Biotherapeutics Provide Update on New Clinical and Non-Clinical Studies of LAGEVRIO™ (molnupiravir) - Merck...
29 CFR § 1910.1048 - Formaldehyde. | Electronic Code of Federal Regulations (e-CFR) | US Law | LII / Legal Information Institute
Kynmobi (Apomorphine Hydrochloride Sublingual Film): Uses, Dosage, Side Effects, Interactions, Warning
Genotoxicity8
- For genotoxicity effects, we look at in vivo testing over in vitro testing. (cdc.gov)
- Although, genotoxicity tests for these ingredients were mostly negative, there were some assays that were positive. (cosmeticsinfo.org)
- There was no evidence that isofetamid was carcinogenic in mice and rats, and isofetamid was tested for genotoxicity in an adequate range of in vitro and in vivo assays and was negative. (tga.gov.au)
- Conclusion on genotoxicity A total of 12 benzyl derivatives in the group have been tested for genotoxicity. (europa.eu)
- The HESI GTTC is pleased to share its newest publication, " Error-corrected next-generation sequencing to advance nonclinical genotoxicity and carcinogenicity testing ," published in Nature Reviews Drug Discovery . (hesiglobal.org)
- The work group has evaluated the current testing paradigm for genotoxicity assessment of nanomaterials and is publishing the findings and recommendations for modifying the tests as needed. (hesiglobal.org)
- The classification is based on the similarities of these chemicals to other carcinogenic aromatic amines regarding how they are activated to DNA-binding electrophiles, their genotoxicity, and their target organs of carcinogenicity in chronic animal bioassays. (who.int)
- Genotoxicity/mutagenicity/carcinogenicity and microbial effects are the other parameters that characterize biocompatibility 8 . (bvsalud.org)
Mutagenicity3
- The high correlation between the Umu Chromotest and traditional Ames test for mutagenicity supports it as a reasonable alternative for early-stage testing of the thousands of new pharmaceutical, agricultural and industrial chemicals synthesized every year. (wikipedia.org)
- 2002. Modulation of heterocyclic amine-induced mutagenicity and carcinogenicity: an 'A-to-Z' guide to chemopreventive agents, promoters, and transgenic models. . (oregonstate.edu)
- In evaluating mutagenicity for potentially hazardous drugs, responses from multiple test systems are needed before precautions can be required for handling such agents. (cdc.gov)
Toxicity and carcinogenicity2
Carcinogens1
- A novel, integrated in vitro carcinogenicity test to identify genotoxic and non-genotoxic carcinogens using human lymphoblastoid cells by: Katherine Chapman, et al. (swan.ac.uk)
Genotoxic3
- Speakers included Koji Urano from the Central Institute of Experimental Animals in Japan (CIEA) and Marie McKeon of BioReliance Inc . Both speakers highlighted the increased utility of this model and how faster, more accurate nongenotoxic and genotoxic carcinogenicity testing helps pharmaceutical companies with strategic decision making in their drug development pipeline. (taconic.com)
- Salmonella typhimurium TA 1535 [pSK 1002] bacteria are exposed to potentially genotoxic test compounds in a 96-well microplate. (wikipedia.org)
- The intensity of the colour correlates with the amount of the induced protein and thus genotoxic potency of the test sample. (wikipedia.org)
Carcinogenic3
- 75% of mouse carcinogenicity studies submitted to the FDA utilize the rasH2™ mouse model (Tg.rasH2), a model accepted by the FDA as an alternative to the two-year in vivo bioassay for predicting human carcinogenic risk. (taconic.com)
- Results from a separate, non-clinical 6-month carcinogenicity study in mice demonstrated that LAGEVRIO was not carcinogenic. (merck.com)
- Additionally, Merck is reporting results from a recent carcinogenicity study in transgenic mice, which demonstrated that LAGEVRIO was not carcinogenic at any dose tested. (merck.com)
Toxicology1
- On 30 June 22, the Organisation for Economic Cooperation and Development (OECD) published Test #470: Mammalian Erythrocyte Pig-a Gene Mutation Assay , a Test Guideline (TG) that describes an in vivo gene mutation assay that can be combined with other genetic and general toxicology tests to promote the efficient use of animal resources. (hesiglobal.org)
Mice2
- Testosterone was tested by subcutaneous injection and/or implantation in mice, rats and hamsters. (inchem.org)
- 1994). A Replicative DNA Synthesis assay using male B6C3F1 male mice given a single dose of 0, 400 or 800 mg/kg bw benzyl alcohol by gavage was negative at all doses tested (Miyagawa et al. (europa.eu)
Bioassay1
- 2017. A miRNA signature for an environmental heterocyclic amine defined by a multi-organ carcinogenicity bioassay in the rat. . (oregonstate.edu)
Monographs5
- The results of the recent IARC Monographs evaluation of the carcinogenicity of some aromatic amines and related compounds have now been published in The Lancet Oncology . (who.int)
- Aniline was previously evaluated as not classifiable as to its carcinogenicity to humans (Group 3), in IARC Monographs Volume 27, Supplement 7 . (who.int)
- The objective of the programme is to prepare, with the help of international working groups of experts, and to publish in the form of monographs, critical reviews and evaluations of evidence on the carcinogenicity of a wide range of human exposures. (who.int)
- The aim of the Monographs has been, from their inception, to evaluate evidence of carcinogenicity at any stage in the carcinogenesis process, independently of the underlying mechanisms. (who.int)
- The IARC Monographs are recognized as an authoritative source of information on the carcinogenicity of a wide range of human exposures. (who.int)
Studies4
- After discussing the model's history, from its development at CIEA to the ILSI/HESI validation in 2000 and increasing adoption in carcinogenicity studies, his talk focused on the quality control measures Taconic and CIEA have in place to ensure consistent quality of the rasH2™ mouse. (taconic.com)
- Marie McKeon focused on key study design considerations when using transgenic mouse models, particularly dose-range finding studies (usually conducted with the wild-type rasH2™ mouse) and twenty-six week carcinogenicity studies. (taconic.com)
- No carcinogenicity studies are available in people. (cdc.gov)
- Carcinogenicity studies, however, were negative. (cosmeticsinfo.org)
Assays1
- Cytotoxicity assays are the initial screening tests used to evaluate the biocompatibility of materials 7 . (bvsalud.org)
Evaluate2
- Could it be that since the FDA failed to require the manufacturer to test for, evaluate and quantify the risks of residual recombinant HPV DNA in Gardasil™ before granting approval for marketing the vaccine, they just decided to take their toys and go home? (sanevax.org)
- From 25 May to 12 June 2020, the International Agency for Research on Cancer (IARC) convened a working group of 19 scientists from 9 countries to evaluate the carcinogenicity of some aromatic amines and related compounds. (who.int)
Cancer2
- A substance with the ability to large amounts of chloroform, but these tests are useful for cause cancer. (cdc.gov)
- The Department of Health and Human Services, the International Agency for Research on Cancer, and the Environmental Protection Agency (EPA) have not classified hexamethylene diisocyanate as to its human carcinogenicity. (cdc.gov)
Cells3
- Recommendations, evaluation and validation of a semi-automated, fluorescent-based scoring protocol for micronucleus testing in human cells by: Gareth Jenkins, et al. (swan.ac.uk)
- The EPA evaluations include the type of cells affected and in vitro versus in vivo testing [51 Fed. (cdc.gov)
- In spite of the advantages of the in vitro tests, they are not able to mimic the orchestrated role of cells present inperiradicular region and the long-term cytotoxicity presented by the sealers. (bvsalud.org)
Vitro tests1
- However, adverse outcomes in several in vitro tests may be considered in our evaluation. (cdc.gov)
Human1
- Topics are selected on the basis of two main criteria: (a) there is evidence of human exposure, and (b) there is some evidence or suspicion of carcinogenicity. (who.int)
Dose2
- In addition to dose, for carcinogenicity testing we look for tumors in more than one species and sex. (cdc.gov)
- A Replicative DNA Synthesis assay using male Fischer 344 rats given a single dose of 0, 300 or 600 mg/kg bw benzyl alcohol by gavage was negative at all doses tested (Uno et al. (europa.eu)
Experimental1
- There was also sufficient evidence of carcinogenicity in experimental animals. (who.int)
Carcinogenesis1
- Structural correlates of carcinogenesis and mutagenesis : a guide to testing priorities? (who.int)
Assessment1
- Her presentation concluded with suggestions for using the rasH2™ mouse model as part of the Weight of Evidence (WOE) when submitting a Carcinogenicity Assessment Document (CAD) and requesting a waiver of the two-year rat study from drug regulatory agencies. (taconic.com)
Pesticides1
- WHO is not responsible, and does not accept any liability, for the testing of pesticides for compliance with the specifications, nor for any methods recommended and/or used for testing compliance. (who.int)
Ames3
- Most large chemical manufacturers have the ability to screen 100 or more synthetic chemicals per year with the traditional Ames test, which requires the use of several Salmonella strains. (wikipedia.org)
- Benzyl alcohol was not mutagenic in several Ames tests with Salmonella typhimurium TA92, TA94, TA98, TA100, TA1535, TA1537, and TA1538 with and without metabolic activation (e.g. (europa.eu)
- Also the other related benzyl derivatives (benzaldehyde, benzoic acid and the benzoate salts) were negative when tested in in vitro Ames tests with or without metabolic activation. (europa.eu)
Micronucleus1
- 1990). A more recent in vitro micronucleus test (Fowler 2012) was negative. (europa.eu)
Salmonella1
- The umu test, using only a single Salmonella strain, could potentially test a greater range of new chemicals with the same resources. (wikipedia.org)
Evidence3
- therefore, no evidence for mutagenic carcinogenicity exists. (europa.eu)
- Title : Ethylene oxide (EtO) : evidence of carcinogenicity Corporate Authors(s) : National Institute for Occupational Safety and Health. (cdc.gov)
- The evaluations of IARC working groups are scientific, qualitative judgements about the evidence for or against carcinogenicity provided by the available data. (who.int)
Search1
- Results of search for 'su:{Carcinogenicity tests. (who.int)
Data1
- However, no historical control data was provided, though obtained data on the background incidence of left-sided umbilical artery in rat foetuses in four other testing laboratories indicated they were likely incidental to treatment. (tga.gov.au)
Results3
- Blood tests may show abnormal results. (ccohs.ca)
- Pet odor results based on testing with the most common odor sources found in dog and cat urine. (chemdry.com)
- The response pattern varied depending on time and type of cell line used for analysis, although the results indicate a higher cytotoxicity for EPH in short-term tests. (bvsalud.org)
Substances1
- However, there are problems with these tests: antibodies can react with other substances that look like hexamethylene diisocyanate in your blood and indicate that you have been exposed to hexamethylene diisocyanate when you have not been. (cdc.gov)
Multiple1
- Figures are an average across multiple tests. (chemdry.com)
Products2
- They are currently considering publishing a series of protocols for genetic toxicity testing of products containing nanomaterials. (hesiglobal.org)
- It is also identified in tobacco smoke and in wastewater and has been detected in drinking-water and during product testing of textiles and certain consumer products. (who.int)
Positive1
- S. typhimurium bacteria in the exponential phase of growth are exposed for 2 hours to decreasing concentrations of test sample in triplicate, including positive and negative controls, as well as blanks. (wikipedia.org)
Group1
- Standard liver function tests were applied to blood samples from 25 nickel-plating workers in Damietta, Egypt and 30 administrative workers as a reference group. (who.int)
Development1
- and to monitor and promote the development of innovative tests and testing strategies. (hesiglobal.org)
Blood1
- Allergicskinreactionstonickelarealso industryinDamiettacity,Egypt;this Blood tests common[3]. (who.int)
Items1
- The disperser was fed with the test/reference items under computerized control, i.e. with a feed back loop to the actual aerosol concentrations measured by an aerosol photometer. (europa.eu)
Role1
- These SOT sessions were a great prelude to the IQ Consortium webinar on progress toward revision of the ICH S1 Rodent Carcinogenicity Testing guidelines , which included presentations on industry experience with the rasH2™ mouse model, the quality of the rasH2™ mouse model, and what role this model can play in the future of carcinogenicity testing. (taconic.com)