A potent mutagen and carcinogen. This compound and its metabolite 4-HYDROXYAMINOQUINOLINE-1-OXIDE bind to nucleic acids. It inactivates bacteria but not bacteriophage.
Quinolines substituted in any position by one or more nitro groups.
Tumors or cancer of the TONGUE.
A potent mutagen and carcinogen. It is a reduction product of 4-NITROQUINOLINE-1-OXIDE. It binds with nucleic acids and inactivates both bacteria and bacteriophage.
Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.
Compounds having the nitro group, -NO2, attached to carbon. When attached to nitrogen they are nitramines and attached to oxygen they are NITRATES.
A muscular organ in the mouth that is covered with pink tissue called mucosa, tiny bumps called papillae, and thousands of taste buds. The tongue is anchored to the mouth and is vital for chewing, swallowing, and for speech.
A flavanone glycoside found in CITRUS fruit peels.
Chemical agents that increase the rate of genetic mutation by interfering with the function of nucleic acids. A clastogen is a specific mutagen that causes breaks in chromosomes.
A proteolytic enzyme obtained from Streptomyces griseus.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
Quinolines substituted in any position by one or more amino groups.
Tumors or cancer of the MOUTH.
Quinolines are heterocyclic aromatic organic compounds consisting of a two-nitrogened benzene ring fused to a pyridine ring, which have been synthesized and used as building blocks for various medicinal drugs, particularly antibiotics and antimalarials.
A circumscribed benign epithelial tumor projecting from the surrounding surface; more precisely, a benign epithelial neoplasm consisting of villous or arborescent outgrowths of fibrovascular stroma covered by neoplastic cells. (Stedman, 25th ed)
Polyamines are organic compounds with more than one amino group, involved in various biological processes such as cell growth, differentiation, and apoptosis, and found to be increased in certain diseases including cancer.
Agents that reduce the frequency or rate of spontaneous or induced tumors independently of the mechanism involved.
A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)
Pathological processes that tend eventually to become malignant. (From Dorland, 27th ed)
The reconstruction of a continuous two-stranded DNA molecule without mismatch from a molecule which contained damaged regions. The major repair mechanisms are excision repair, in which defective regions in one strand are excised and resynthesized using the complementary base pairing information in the intact strand; photoreactivation repair, in which the lethal and mutagenic effects of ultraviolet light are eliminated; and post-replication repair, in which the primary lesions are not repaired, but the gaps in one daughter duplex are filled in by incorporation of portions of the other (undamaged) daughter duplex. Excision repair and post-replication repair are sometimes referred to as "dark repair" because they do not require light.
A CALCIUM-independent subtype of nitric oxide synthase that may play a role in immune function. It is an inducible enzyme whose expression is transcriptionally regulated by a variety of CYTOKINES.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
F344 rats are an inbred strain of albino laboratory rats (Rattus norvegicus) that have been widely used in biomedical research due to their consistent and reliable genetic background, which facilitates the study of disease mechanisms and therapeutic interventions.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
Binary compounds of oxygen containing the anion O(2-). The anion combines with metals to form alkaline oxides and non-metals to form acidic oxides.
A transferase that catalyzes the addition of aliphatic, aromatic, or heterocyclic FREE RADICALS as well as EPOXIDES and arene oxides to GLUTATHIONE. Addition takes place at the SULFUR. It also catalyzes the reduction of polyol nitrate by glutathione to polyol and nitrite.
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
That portion of the electromagnetic spectrum immediately below the visible range and extending into the x-ray frequencies. The longer wavelengths (near-UV or biotic or vital rays) are necessary for the endogenous synthesis of vitamin D and are also called antirachitic rays; the shorter, ionizing wavelengths (far-UV or abiotic or extravital rays) are viricidal, bactericidal, mutagenic, and carcinogenic and are used as disinfectants.
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in NERVE TISSUE.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
Inorganic oxides that contain nitrogen.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A mild astringent and topical protectant with some antiseptic action. It is also used in bandages, pastes, ointments, dental cements, and as a sunblock.

Functional analysis of the promoter of the yeast SNQ2 gene encoding a multidrug resistance transporter that confers the resistance to 4-nitroquinoline N-oxide. (1/242)

The yeast gene SNQ2, which encodes a multidrug resistance ABC superfamily protein, is required for resistance to the mutagen 4-nitroquinoline N-oxide (4-NQO). The expression of the SNQ2 gene is under the control of a regulatory network that involves the transcription factor Yrr1p, as well as Pdr1p/Pdr3p (Cui et al., Mol. Microbiol., 29, 1307-1315 (1998)). By 5'-deletion analysis of the promoter by using SNQ2-lacZ fusion constructs, four regions: -745 to -639 (region I), -639 to -578 (region II), -548 to -533 (region III) and -533 to -485 (region IV) were found to be important for SNQ2 expression. Genetic analysis suggested that the site in region IV was responsible for the Yrr1p-mediated SNQ2 expression. A consensus motif known for the binding of Pdr1p/Pdr3p (PDRE) was not found in region IV.  (+info)

Inhibition of DNA replicon initiation by 4-nitroquinoline 1-oxide, adriamycin, and ethyleneimine. (2/242)

The effects of three widely differing chemical carcinogens, 4-nitroquinoline 1-oxide, Adriamycin, and ethyleneimine, on DNA replication were studied by pulse labeling of DNA with [3H]thymidine and sedimentation analysis with alkaline sucrose gradients. At doses that reduced the rate of DNA synthesis to 30 to 60% of control values, only ethyleneimine produced damage that resulted in lower molecular weights of parental DNA. All three chemicals inhibited replicon initiation, but to differing extents. Inhibition of replicon initiation was the first clearly identified effect of 4-nitroquinoline 1-oxide and was the main cause of inhibition of DNA synthesis. Ethyleneimine caused severe inhibition of replicon initiation, but blocks to chain elongation also contributed significantly to the inhibition of overall DNA synthesis. Adriamycin affected replicon initiation to a small but significant extent; the primary cause of inhibition of DNA synthesis by this drug was a slowing of the rate of chain elongation. These results indicate that inhibition of replicon initiation is an important mechanism for the action of DNA-damaging agents in mammalian cells and strengthen the concept that control of DNA replication depends on the structural integrity of a chromosomal subunit that consists of several replicons.  (+info)

Inverse correlation between p53 protein levels and DNA repair efficiency in human fibroblast strains treated with 4-nitroquinoline 1-oxide: evidence that lesions other than DNA strand breaks trigger the p53 response. (3/242)

Ionizing radiation-induced stabilization and the resultant transient accumulation of the p53 tumor suppressor protein is impaired in cells from ataxia telangiectasia (AT) patients, indicating a key role for ATM, the gene mutated in AT, upstream in the radiation-responsive p53 signaling pathway. Activation of this pathway is generally assumed to be triggered by DNA strand breaks produced directly following genotoxic stress or indirectly during excision repair of DNA lesions. The aim of this study was to identify the triggering signal for induction of p53 in diploid human dermal fibroblasts treated with 4-nitroquinoline 1-oxide (4NQO), a model environmental carcinogen that produces both DNA strand breaks (like ionizing radiation) and alkali-stable bulky DNA lesions (like UV light). 4NQO treatment of fibroblasts cultured from normal and AT donors and those from patients with the UV-hypersensitivity disorder xeroderma pigmentosum (XP, complementation groups A, E and G) resulted in up-regulation of p53 protein. In normal fibroblasts, there was no temporal relationship between the incidence of DNA strand breaks and levels of p53 protein; >90% of strand breaks and alkali-labile sites were repaired over 2 h following treatment with 1 microM 4NQO, whereas approximately 3 h of post-treatment incubation was required to demonstrate a significant rise in p53 protein. In contrast, exposure of normal fibroblasts to gamma-rays resulted in a rapid up-regulation of p53 and the level peaked at 2 h post-irradiation. XP cells with a severe deficiency in the nucleotide excision repair pathway showed abnormally high levels of p53 protein in response to 4NQO treatment, indicating that lesions other than incision-associated DNA strand breaks trigger p53 up-regulation. We observed a consistent, inverse correlation between the ability of the various fibroblast cultures to induce p53 following 4NQO treatment and their DNA repair efficiencies. Treatment with 0.12 microM 4NQO, for example, caused a >2-fold up-regulation of p53 in excision repair-deficient (AT, XPA and XPG) strains without eliciting any effect on p53 levels in repair-proficient (normal and XPE) strains. We conclude that up-regulation of p53 by 4NQO is mediated solely by an ATM-independent mechanism and that the p53 response is primarily triggered by persistent alkali-stable 4NQO-DNA adducts.  (+info)

Development of a new bioluminescent mutagenicity assay based on the Ames test. (4/242)

A newly developed rapid mutagenicity assay based on the adenosine triphosphate (ATP)-bioluminescence technique and the Ames test is described. Salmonella typhimurium strains TA98 and TA100 were exposed in an appropriate liquid medium to the direct mutagens 4-nitroquinoline-N-oxide and methyl methanesulphonate, respectively, and to the indirect mutagen 2-aminoanthracene. Both auxotrophic and prototrophic growth were monitored throughout the incubation period as variations in the intracellular ATP levels by means of the luciferin-luciferase assay. After 9-12 h of incubation a dose-response increase in the levels of ATP was readily detected. In order to demonstrate that this increase was due to the growth of revertant bacteria, aliquots from each culture were plated on minimal agar plates. A very good correlation between the changes in ATP levels and the appearance of revertant colonies on the plates was found. Given the rapidity of this method as compared with conventional mutagenicity assays, it has potential for industrial and environmental applications. Other potential applications are also discussed.  (+info)

Enzymatic and DNA binding properties of purified WRN protein: high affinity binding to single-stranded DNA but not to DNA damage induced by 4NQO. (5/242)

Mutations in the WRN gene result in Werner syndrome, an autosomal recessive disease in which many characteristics of aging are accelerated. A probable role in some aspect of DNA metabolism is suggested by the primary sequence of the WRN gene product. A recombinant His-tagged WRN protein (WRNp) was overproduced in insect cells using the baculovirus system and purified to near homogeneity by several chromatographic steps. This purification scheme removes both nuclease and topoisomerase contaminants that persist following a single Ni(2+)affinity chromatography step and allows for unambiguous interpretation of WRNp enzymatic activities on DNA substrates. Purified WRNp has DNA-dependent ATPase and helicase activities consistent with its homology to the RecQ subfamily of proteins. The protein also binds with higher affinity to single-stranded DNA than to double-stranded DNA. However, WRNp has no higher affinity for various types of DNA damage, including adducts formed during 4NQO treatment, than for undamaged DNA. Our results confirm that WRNp has a role in DNA metabolism, although this role does not appear to be the specific recognition of damage in DNA.  (+info)

Regulation of the ribonucleotide reductase small subunit gene by DNA-damaging agents in Dictyostelium discoideum. (6/242)

In Escherichia coli, yeast and mammalian cells, the genes encoding ribonucleotide reductase, an essential enzyme for de novo DNA synthesis, are up-regulated in response to DNA damaging agents. We have examined the response of the rnrB gene, encoding the small subunit of ribonucleotide reductase in Dictyostelium discoideum, to DNA damaging agents. We show here that the accumulation of rnrB transcript is increased in response to methyl methane sulfonate, 4-nitroquinoline-1-oxide and irradiation with UV-light, but not to the ribonucleotide reductase inhibitor hydroxyurea. This response is rapid, transient and independent of protein synthesis. Moreover, cells from different developmental stages are able to respond to the drug in a similar fashion, regardless of the basal level of expression of the rnrB gene. We have defined the cis -acting elements of the rnrB promoter required for the response to methyl methane sulfonate and 4-nitroquinoline-1-oxide by deletion analysis. Our results indicate that there is one element, named box C, that can confer response to both drugs. Two other boxes, box A and box D, specifically conferred response to methyl methane sulfonate and 4-nitroquinoline-1-oxide, respectively.  (+info)

Rsp5 ubiquitin-protein ligase mediates DNA damage-induced degradation of the large subunit of RNA polymerase II in Saccharomyces cerevisiae. (7/242)

Rsp5 is an E3 ubiquitin-protein ligase of Saccharomyces cerevisiae that belongs to the hect domain family of E3 proteins. We have previously shown that Rsp5 binds and ubiquitinates the largest subunit of RNA polymerase II, Rpb1, in vitro. We show here that Rpb1 ubiquitination and degradation are induced in vivo by UV irradiation and by the UV-mimetic compound 4-nitroquinoline-1-oxide (4-NQO) and that a functional RSP5 gene product is required for this effect. The 26S proteasome is also required; a mutation of SEN3/RPN2 (sen3-1), which encodes an essential regulatory subunit of the 26S proteasome, partially blocks 4-NQO-induced degradation of Rpb1. These results suggest that Rsp5-mediated ubiquitination and degradation of Rpb1 are components of the response to DNA damage. A human WW domain-containing hect (WW-hect) E3 protein closely related to Rsp5, Rpf1/hNedd4, also binds and ubiquitinates both yeast and human Rpb1 in vitro, suggesting that Rpf1 and/or another WW-hect E3 protein mediates UV-induced degradation of the large subunit of polymerase II in human cells.  (+info)

The ATPase domain but not the acidic region of Cockayne syndrome group B gene product is essential for DNA repair. (8/242)

Cockayne syndrome (CS) is a human genetic disorder characterized by UV sensitivity, developmental abnormalities, and premature aging. Two of the genes involved, CSA and CSB, are required for transcription-coupled repair (TCR), a subpathway of nucleotide excision repair that removes certain lesions rapidly and efficiently from the transcribed strand of active genes. CS proteins have also been implicated in the recovery of transcription after certain types of DNA damage such as those lesions induced by UV light. In this study, site-directed mutations have been introduced to the human CSB gene to investigate the functional significance of the conserved ATPase domain and of a highly acidic region of the protein. The CSB mutant alleles were tested for genetic complementation of UV-sensitive phenotypes in the human CS-B homologue of hamster UV61. In addition, the CSB mutant alleles were tested for their ability to complement the sensitivity of UV61 cells to the carcinogen 4-nitroquinoline-1-oxide (4-NQO), which introduces bulky DNA adducts repaired by global genome repair. Point mutation of a highly conserved glutamic acid residue in ATPase motif II abolished the ability of CSB protein to complement the UV-sensitive phenotypes of survival, RNA synthesis recovery, and gene-specific repair. These data indicate that the integrity of the ATPase domain is critical for CSB function in vivo. Likewise, the CSB ATPase point mutant failed to confer cellular resistance to 4-NQO, suggesting that ATP hydrolysis is required for CSB function in a TCR-independent pathway. On the contrary, a large deletion of the acidic region of CSB protein did not impair the genetic function in the processing of either UV- or 4-NQO-induced DNA damage. Thus the acidic region of CSB is likely to be dispensable for DNA repair, whereas the ATPase domain is essential for CSB function in both TCR-dependent and -independent pathways.  (+info)

4-Nitroquinoline-1-oxide is a chemical compound that is often used in laboratory research as a carcinogenic agent. Its molecular formula is C6H4N2O3, and it is known to cause DNA damage and mutations, which can lead to the development of cancer. It is primarily used in scientific research to study the mechanisms of carcinogenesis and to test the effectiveness of potential cancer treatments.

It is important to note that 4-Nitroquinoline-1-oxide is not a medication or a treatment for any medical condition, and it should only be handled by trained professionals in a controlled laboratory setting.

I'm sorry for any confusion, but "Nitroquinolines" is not a recognized term in medical or pharmacological sciences. It seems to be a chemical category that consists of compounds containing a quinoline nucleus (a heterocyclic aromatic compound) with one or more nitro groups attached to it.

Quinoline derivatives have been explored for their potential medicinal properties, including antimalarial and antibacterial activities. However, the term "Nitroquinolines" does not specifically refer to a medical definition or a particular therapeutic application. If you're looking for information on specific quinoline-based compounds with nitro groups, I would be happy to help if you could provide more context or details.

Tongue neoplasms refer to abnormal growths or tumors that develop in the tongue tissue. These growths can be benign (non-cancerous) or malignant (cancerous).

Benign tongue neoplasms may include entities such as papillomas, fibromas, or granular cell tumors. They are typically slow growing and less likely to spread to other parts of the body.

Malignant tongue neoplasms, on the other hand, are cancers that can invade surrounding tissues and spread to other parts of the body. The most common type of malignant tongue neoplasm is squamous cell carcinoma, which arises from the thin, flat cells (squamous cells) that line the surface of the tongue.

Tongue neoplasms can cause various symptoms such as a lump or thickening on the tongue, pain or burning sensation in the mouth, difficulty swallowing or speaking, and unexplained bleeding from the mouth. Early detection and treatment are crucial for improving outcomes and preventing complications.

4-Hydroxyaminoquinoline-1-oxide, also known as 4HAQ or acriflavine hydroxylamine, is a chemical compound that has been used in research to study the mechanisms of DNA damage and mutagenesis. It is an aromatic heterocyclic amine and is known to be a potent mutagen and carcinogen.

The compound works by forming adducts with DNA, particularly at guanine residues, leading to mispairing during replication and the introduction of mutations. It has been used as a tool in molecular biology to study the effects of DNA damage on cellular processes such as transcription, replication, and repair.

It is important to note that 4HAQ is not used clinically in medicine due to its toxicity and carcinogenic properties.

Carcinogens are agents (substances or mixtures of substances) that can cause cancer. They may be naturally occurring or man-made. Carcinogens can increase the risk of cancer by altering cellular DNA, disrupting cellular function, or promoting cell growth. Examples of carcinogens include certain chemicals found in tobacco smoke, asbestos, UV radiation from the sun, and some viruses.

It's important to note that not all exposures to carcinogens will result in cancer, and the risk typically depends on factors such as the level and duration of exposure, individual genetic susceptibility, and lifestyle choices. The International Agency for Research on Cancer (IARC) classifies carcinogens into different groups based on the strength of evidence linking them to cancer:

Group 1: Carcinogenic to humans
Group 2A: Probably carcinogenic to humans
Group 2B: Possibly carcinogenic to humans
Group 3: Not classifiable as to its carcinogenicity to humans
Group 4: Probably not carcinogenic to humans

This information is based on medical research and may be subject to change as new studies become available. Always consult a healthcare professional for medical advice.

Nitro compounds, also known as nitro derivatives or nitro aromatics, are organic compounds that contain the nitro group (-NO2) bonded to an aromatic hydrocarbon ring. They are named as such because they contain a nitrogen atom in a -3 oxidation state and are typically prepared by the nitration of aromatic compounds using nitric acid or a mixture of nitric and sulfuric acids.

Nitro compounds have significant importance in organic chemistry due to their versatile reactivity, which allows for various chemical transformations. They can serve as useful intermediates in the synthesis of other chemical products, including dyes, pharmaceuticals, and explosives. However, some nitro compounds can also be hazardous, with potential health effects such as skin and respiratory irritation, and they may pose environmental concerns due to their persistence and potential toxicity.

It is important to handle nitro compounds with care, following appropriate safety guidelines and regulations, to minimize risks associated with their use.

In medical terms, the tongue is a muscular organ in the oral cavity that plays a crucial role in various functions such as taste, swallowing, and speech. It's covered with a mucous membrane and contains papillae, which are tiny projections that contain taste buds to help us perceive different tastes - sweet, salty, sour, and bitter. The tongue also assists in the initial process of digestion by moving food around in the mouth for chewing and mixing with saliva. Additionally, it helps in forming words and speaking clearly by shaping the sounds produced in the mouth.

Hesperidin is a flavonoid, specifically a type of flavanone glycoside, that is commonly found in citrus fruits such as oranges, lemons, and grapefruits. It is particularly abundant in the peel and membranes of these fruits. Hesperidin has been studied for its potential health benefits, including its antioxidant, anti-inflammatory, and cardiovascular protective properties. However, more research is needed to fully understand its effects and potential therapeutic uses.

Mutagens are physical or chemical agents that can cause permanent changes in the structure of genetic material, including DNA and chromosomes, leading to mutations. These mutations can be passed down to future generations and may increase the risk of cancer and other diseases. Examples of mutagens include ultraviolet (UV) radiation, tobacco smoke, and certain chemicals found in industrial settings. It is important to note that not all mutations are harmful, but some can have negative effects on health and development.

Pronase is not a medical term itself, but it is a proteolytic enzyme mixture derived from the bacterium Streptomyces griseus. The term "pronase" refers to a group of enzymes that can break down proteins into smaller peptides and individual amino acids by hydrolyzing their peptide bonds.

Pronase is used in various laboratory applications, including protein degradation, DNA and RNA isolation, and the removal of contaminating proteins from nucleic acid samples. It has also been used in some medical research contexts to study protein function and structure, as well as in certain therapeutic settings for its ability to break down proteins.

It is important to note that pronase is not a drug or a medical treatment itself but rather a laboratory reagent with potential applications in medical research and diagnostics.

Nitric Oxide Synthase (NOS) is a group of enzymes that catalyze the production of nitric oxide (NO) from L-arginine. There are three distinct isoforms of NOS, each with different expression patterns and functions:

1. Neuronal Nitric Oxide Synthase (nNOS or NOS1): This isoform is primarily expressed in the nervous system and plays a role in neurotransmission, synaptic plasticity, and learning and memory processes.
2. Inducible Nitric Oxide Synthase (iNOS or NOS2): This isoform is induced by various stimuli such as cytokines, lipopolysaccharides, and hypoxia in a variety of cells including immune cells, endothelial cells, and smooth muscle cells. iNOS produces large amounts of NO, which functions as a potent effector molecule in the immune response, particularly in the defense against microbial pathogens.
3. Endothelial Nitric Oxide Synthase (eNOS or NOS3): This isoform is constitutively expressed in endothelial cells and produces low levels of NO that play a crucial role in maintaining vascular homeostasis by regulating vasodilation, inhibiting platelet aggregation, and preventing smooth muscle cell proliferation.

Overall, NOS plays an essential role in various physiological processes, including neurotransmission, immune response, cardiovascular function, and respiratory regulation. Dysregulation of NOS activity has been implicated in several pathological conditions such as hypertension, atherosclerosis, neurodegenerative diseases, and inflammatory disorders.

Aminoquinolines are a class of drugs that contain a quinoline chemical structure and an amino group. They are primarily used as antimalarial agents, with the most well-known members of this class being chloroquine and hydroxychloroquine. These drugs work by inhibiting the parasite's ability to digest hemoglobin in the red blood cells, which is necessary for its survival and reproduction.

In addition to their antimalarial properties, aminoquinolines have also been studied for their potential anti-inflammatory and immunomodulatory effects. They have been investigated as a treatment for various autoimmune diseases, such as rheumatoid arthritis and lupus, although their use in these conditions is not yet widely accepted.

It's important to note that aminoquinolines can have significant side effects, including gastrointestinal symptoms, retinopathy, and cardiac toxicity. They should only be used under the close supervision of a healthcare provider, and their use may be contraindicated in certain populations, such as pregnant women or individuals with preexisting heart conditions.

A mouth neoplasm refers to an abnormal growth or tumor in the oral cavity, which can be benign (non-cancerous) or malignant (cancerous). Malignant mouth neoplasms are also known as oral cancer. They can develop on the lips, gums, tongue, roof and floor of the mouth, inside the cheeks, and in the oropharynx (the middle part of the throat at the back of the mouth).

Mouth neoplasms can have various causes, including genetic factors, tobacco use, alcohol consumption, and infection with human papillomavirus (HPV). Symptoms may include a lump or thickening in the oral soft tissues, white or red patches, persistent mouth sores, difficulty swallowing or speaking, and numbness in the mouth. Early detection and treatment of mouth neoplasms are crucial for improving outcomes and preventing complications.

Quinolines are a class of organic compounds that consist of a bicyclic structure made up of a benzene ring fused to a piperidine ring. They have a wide range of applications, but they are perhaps best known for their use in the synthesis of various medications, including antibiotics and antimalarial drugs.

Quinolone antibiotics, such as ciprofloxacin and levofloxacin, work by inhibiting the bacterial enzymes involved in DNA replication and repair. They are commonly used to treat a variety of bacterial infections, including urinary tract infections, pneumonia, and skin infections.

Quinoline-based antimalarial drugs, such as chloroquine and hydroxychloroquine, work by inhibiting the parasite's ability to digest hemoglobin in the red blood cells. They are commonly used to prevent and treat malaria.

It is important to note that quinolines have been associated with serious side effects, including tendinitis and tendon rupture, nerve damage, and abnormal heart rhythms. As with any medication, it is important to use quinolines only under the supervision of a healthcare provider, and to follow their instructions carefully.

A papilloma is a benign (noncancerous) tumor that grows on a stalk, often appearing as a small cauliflower-like growth. It can develop in various parts of the body, but when it occurs in the mucous membranes lining the respiratory, digestive, or genitourinary tracts, they are called squamous papillomas. The most common type is the skin papilloma, which includes warts. They are usually caused by human papillomavirus (HPV) infection and can be removed through various medical procedures if they become problematic or unsightly.

Polyamines are organic compounds with more than one amino group (-NH2) and at least one carbon atom bonded to two or more amino groups. They are found in various tissues and fluids of living organisms and play important roles in many biological processes, such as cell growth, differentiation, and apoptosis (programmed cell death). Polyamines are also involved in the regulation of ion channels and transporters, DNA replication and gene expression. The most common polyamines found in mammalian cells are putrescine, spermidine, and spermine. They are derived from the decarboxylation of amino acids such as ornithine and methionine. Abnormal levels of polyamines have been associated with various pathological conditions, including cancer and neurodegenerative diseases.

Anticarcinogenic agents are substances that prevent, inhibit or reduce the development of cancer. They can be natural or synthetic compounds that interfere with the process of carcinogenesis at various stages, such as initiation, promotion, and progression. Anticarcinogenic agents may work by preventing DNA damage, promoting DNA repair, reducing inflammation, inhibiting cell proliferation, inducing apoptosis (programmed cell death), or modulating immune responses.

Examples of anticarcinogenic agents include chemopreventive agents, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and retinoids; phytochemicals found in fruits, vegetables, and other plant-based foods; and medications used to treat cancer, such as chemotherapy, radiation therapy, and targeted therapies.

It is important to note that while some anticarcinogenic agents have been shown to be effective in preventing or reducing the risk of certain types of cancer, they may also have potential side effects and risks. Therefore, it is essential to consult with a healthcare professional before using any anticarcinogenic agent for cancer prevention or treatment purposes.

Squamous cell carcinoma is a type of skin cancer that begins in the squamous cells, which are flat, thin cells that form the outer layer of the skin (epidermis). It commonly occurs on sun-exposed areas such as the face, ears, lips, and backs of the hands. Squamous cell carcinoma can also develop in other areas of the body including the mouth, lungs, and cervix.

This type of cancer usually develops slowly and may appear as a rough or scaly patch of skin, a red, firm nodule, or a sore or ulcer that doesn't heal. While squamous cell carcinoma is not as aggressive as some other types of cancer, it can metastasize (spread) to other parts of the body if left untreated, making early detection and treatment important.

Risk factors for developing squamous cell carcinoma include prolonged exposure to ultraviolet (UV) radiation from the sun or tanning beds, fair skin, a history of sunburns, a weakened immune system, and older age. Prevention measures include protecting your skin from the sun by wearing protective clothing, using a broad-spectrum sunscreen with an SPF of at least 30, avoiding tanning beds, and getting regular skin examinations.

A precancerous condition, also known as a premalignant condition, is a state of abnormal cellular growth and development that has a higher-than-normal potential to progress into cancer. These conditions are characterized by the presence of certain anomalies in the cells, such as dysplasia (abnormal changes in cell shape or size), which can indicate an increased risk for malignant transformation.

It is important to note that not all precancerous conditions will eventually develop into cancer, and some may even regress on their own. However, individuals with precancerous conditions are often at a higher risk of developing cancer compared to the general population. Regular monitoring and appropriate medical interventions, if necessary, can help manage this risk and potentially prevent or detect cancer at an early stage when it is more treatable.

Examples of precancerous conditions include:

1. Dysplasia in the cervix (cervical intraepithelial neoplasia or CIN)
2. Atypical ductal hyperplasia or lobular hyperplasia in the breast
3. Actinic keratosis on the skin
4. Leukoplakia in the mouth
5. Barrett's esophagus in the digestive tract

Regular medical check-ups, screenings, and lifestyle modifications are crucial for individuals with precancerous conditions to monitor their health and reduce the risk of cancer development.

DNA repair is the process by which cells identify and correct damage to the DNA molecules that encode their genome. DNA can be damaged by a variety of internal and external factors, such as radiation, chemicals, and metabolic byproducts. If left unrepaired, this damage can lead to mutations, which may in turn lead to cancer and other diseases.

There are several different mechanisms for repairing DNA damage, including:

1. Base excision repair (BER): This process repairs damage to a single base in the DNA molecule. An enzyme called a glycosylase removes the damaged base, leaving a gap that is then filled in by other enzymes.
2. Nucleotide excision repair (NER): This process repairs more severe damage, such as bulky adducts or crosslinks between the two strands of the DNA molecule. An enzyme cuts out a section of the damaged DNA, and the gap is then filled in by other enzymes.
3. Mismatch repair (MMR): This process repairs errors that occur during DNA replication, such as mismatched bases or small insertions or deletions. Specialized enzymes recognize the error and remove a section of the newly synthesized strand, which is then replaced by new nucleotides.
4. Double-strand break repair (DSBR): This process repairs breaks in both strands of the DNA molecule. There are two main pathways for DSBR: non-homologous end joining (NHEJ) and homologous recombination (HR). NHEJ directly rejoins the broken ends, while HR uses a template from a sister chromatid to repair the break.

Overall, DNA repair is a crucial process that helps maintain genome stability and prevent the development of diseases caused by genetic mutations.

Nitric Oxide Synthase Type II (NOS2), also known as Inducible Nitric Oxide Synthase (iNOS), is an enzyme that catalyzes the production of nitric oxide (NO) from L-arginine. Unlike other isoforms of NOS, NOS2 is not constitutively expressed and its expression can be induced by various stimuli such as cytokines, lipopolysaccharides, and bacterial products. Once induced, NOS2 produces large amounts of NO, which plays a crucial role in the immune response against invading pathogens. However, excessive or prolonged production of NO by NOS2 has been implicated in various pathological conditions such as inflammation, septic shock, and neurodegenerative disorders.

Deoxyribonucleic acid (DNA) is the genetic material present in the cells of organisms where it is responsible for the storage and transmission of hereditary information. DNA is a long molecule that consists of two strands coiled together to form a double helix. Each strand is made up of a series of four nucleotide bases - adenine (A), guanine (G), cytosine (C), and thymine (T) - that are linked together by phosphate and sugar groups. The sequence of these bases along the length of the molecule encodes genetic information, with A always pairing with T and C always pairing with G. This base-pairing allows for the replication and transcription of DNA, which are essential processes in the functioning and reproduction of all living organisms.

F344 is a strain code used to designate an outbred stock of rats that has been inbreeded for over 100 generations. The F344 rats, also known as Fischer 344 rats, were originally developed at the National Institutes of Health (NIH) and are now widely used in biomedical research due to their consistent and reliable genetic background.

Inbred strains, like the F344, are created by mating genetically identical individuals (siblings or parents and offspring) for many generations until a state of complete homozygosity is reached, meaning that all members of the strain have identical genomes. This genetic uniformity makes inbred strains ideal for use in studies where consistent and reproducible results are important.

F344 rats are known for their longevity, with a median lifespan of around 27-31 months, making them useful for aging research. They also have a relatively low incidence of spontaneous tumors compared to other rat strains. However, they may be more susceptible to certain types of cancer and other diseases due to their inbred status.

It's important to note that while F344 rats are often used as a standard laboratory rat strain, there can still be some genetic variation between individual animals within the same strain, particularly if they come from different suppliers or breeding colonies. Therefore, it's always important to consider the source and history of any animal model when designing experiments and interpreting results.

Fibroblasts are specialized cells that play a critical role in the body's immune response and wound healing process. They are responsible for producing and maintaining the extracellular matrix (ECM), which is the non-cellular component present within all tissues and organs, providing structural support and biochemical signals for surrounding cells.

Fibroblasts produce various ECM proteins such as collagens, elastin, fibronectin, and laminins, forming a complex network of fibers that give tissues their strength and flexibility. They also help in the regulation of tissue homeostasis by controlling the turnover of ECM components through the process of remodeling.

In response to injury or infection, fibroblasts become activated and start to proliferate rapidly, migrating towards the site of damage. Here, they participate in the inflammatory response, releasing cytokines and chemokines that attract immune cells to the area. Additionally, they deposit new ECM components to help repair the damaged tissue and restore its functionality.

Dysregulation of fibroblast activity has been implicated in several pathological conditions, including fibrosis (excessive scarring), cancer (where they can contribute to tumor growth and progression), and autoimmune diseases (such as rheumatoid arthritis).

I'm sorry for any confusion, but "oxides" is not a term that has a specific medical definition. Oxides are a class of chemical compounds that contain at least one oxygen atom and one other element. They can be formed through the process of oxidation, which involves the combination of oxygen with another substance.

In a broader sense, you might encounter the term "oxide" in a medical context when discussing various materials or substances used in medical devices, treatments, or research. For instance, titanium dioxide is a common ingredient in medical-grade sunscreens due to its ability to block and scatter UV light. However, it's important to note that the term "oxides" itself doesn't have a direct connection to medicine or human health.

Glutathione transferases (GSTs) are a group of enzymes involved in the detoxification of xenobiotics and endogenous compounds. They facilitate the conjugation of these compounds with glutathione, a tripeptide consisting of cysteine, glutamic acid, and glycine, which results in more water-soluble products that can be easily excreted from the body.

GSTs play a crucial role in protecting cells against oxidative stress and chemical injury by neutralizing reactive electrophilic species and peroxides. They are found in various tissues, including the liver, kidneys, lungs, and intestines, and are classified into several families based on their structure and function.

Abnormalities in GST activity have been associated with increased susceptibility to certain diseases, such as cancer, neurological disorders, and respiratory diseases. Therefore, GSTs have become a subject of interest in toxicology, pharmacology, and clinical research.

DNA damage refers to any alteration in the structure or composition of deoxyribonucleic acid (DNA), which is the genetic material present in cells. DNA damage can result from various internal and external factors, including environmental exposures such as ultraviolet radiation, tobacco smoke, and certain chemicals, as well as normal cellular processes such as replication and oxidative metabolism.

Examples of DNA damage include base modifications, base deletions or insertions, single-strand breaks, double-strand breaks, and crosslinks between the two strands of the DNA helix. These types of damage can lead to mutations, genomic instability, and chromosomal aberrations, which can contribute to the development of diseases such as cancer, neurodegenerative disorders, and aging-related conditions.

The body has several mechanisms for repairing DNA damage, including base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair. However, if the damage is too extensive or the repair mechanisms are impaired, the cell may undergo apoptosis (programmed cell death) to prevent the propagation of potentially harmful mutations.

According to the medical definition, ultraviolet (UV) rays are invisible radiations that fall in the range of the electromagnetic spectrum between 100-400 nanometers. UV rays are further divided into three categories: UVA (320-400 nm), UVB (280-320 nm), and UVC (100-280 nm).

UV rays have various sources, including the sun and artificial sources like tanning beds. Prolonged exposure to UV rays can cause damage to the skin, leading to premature aging, eye damage, and an increased risk of skin cancer. UVA rays penetrate deeper into the skin and are associated with skin aging, while UVB rays primarily affect the outer layer of the skin and are linked to sunburns and skin cancer. UVC rays are the most harmful but fortunately, they are absorbed by the Earth's atmosphere and do not reach the surface.

Healthcare professionals recommend limiting exposure to UV rays, wearing protective clothing, using broad-spectrum sunscreen with an SPF of at least 30, and avoiding tanning beds to reduce the risk of UV-related health problems.

Nitric Oxide Synthase Type III (NOS-III), also known as endothelial Nitric Oxide Synthase (eNOS), is an enzyme responsible for the production of nitric oxide (NO) in the endothelium, the lining of blood vessels. This enzyme catalyzes the conversion of L-arginine to L-citrulline, producing NO as a byproduct. The release of NO from eNOS plays an important role in regulating vascular tone and homeostasis, including the relaxation of smooth muscle cells in the blood vessel walls, inhibition of platelet aggregation, and modulation of immune function. Mutations or dysfunction in NOS-III can contribute to various cardiovascular diseases such as hypertension, atherosclerosis, and erectile dysfunction.

Neoplastic cell transformation is a process in which a normal cell undergoes genetic alterations that cause it to become cancerous or malignant. This process involves changes in the cell's DNA that result in uncontrolled cell growth and division, loss of contact inhibition, and the ability to invade surrounding tissues and metastasize (spread) to other parts of the body.

Neoplastic transformation can occur as a result of various factors, including genetic mutations, exposure to carcinogens, viral infections, chronic inflammation, and aging. These changes can lead to the activation of oncogenes or the inactivation of tumor suppressor genes, which regulate cell growth and division.

The transformation of normal cells into cancerous cells is a complex and multi-step process that involves multiple genetic and epigenetic alterations. It is characterized by several hallmarks, including sustained proliferative signaling, evasion of growth suppressors, resistance to cell death, enabling replicative immortality, induction of angiogenesis, activation of invasion and metastasis, reprogramming of energy metabolism, and evading immune destruction.

Neoplastic cell transformation is a fundamental concept in cancer biology and is critical for understanding the molecular mechanisms underlying cancer development and progression. It also has important implications for cancer diagnosis, prognosis, and treatment, as identifying the specific genetic alterations that underlie neoplastic transformation can help guide targeted therapies and personalized medicine approaches.

Nitric Oxide Synthase Type I, also known as NOS1 or neuronal nitric oxide synthase (nNOS), is an enzyme that catalyzes the production of nitric oxide (NO) from L-arginine. It is primarily expressed in the nervous system, particularly in neurons, and plays a crucial role in the regulation of neurotransmission, synaptic plasticity, and cerebral blood flow. NOS1 is calcium-dependent and requires several cofactors for its activity, including NADPH, FAD, FMN, and calmodulin. It is involved in various physiological and pathological processes, such as learning and memory, seizure susceptibility, and neurodegenerative disorders.

I'm sorry for any confusion, but "Pyridines" is not a medical term. It is a chemical term that refers to a class of organic compounds with the chemical structure of a six-membered ring containing one nitrogen atom and five carbon atoms (heterocyclic aromatic compound).

In a biological or medical context, pyridine derivatives can be found in various natural and synthetic substances. For example, some medications contain pyridine rings as part of their chemical structure. However, "Pyridines" itself is not a medical term or condition.

Nitrogen oxides (NOx) are a group of highly reactive gases, primarily composed of nitric oxide (NO) and nitrogen dioxide (NO2). They are formed during the combustion of fossil fuels, such as coal, oil, gas, or biomass, and are emitted from various sources, including power plants, industrial boilers, transportation vehicles, and residential heating systems. Exposure to NOx can have adverse health effects, particularly on the respiratory system, and contribute to the formation of harmful air pollutants like ground-level ozone and fine particulate matter.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Zinc oxide is an inorganic compound with the formula ZnO. It exists as a white, odorless, and crystalline powder. In medicine, zinc oxide is used primarily as a topical agent for the treatment of various skin conditions, including diaper rash, minor burns, and irritations caused by eczema or psoriasis.

Zinc oxide has several properties that make it useful in medical applications:

1. Antimicrobial activity: Zinc oxide exhibits antimicrobial properties against bacteria, viruses, and fungi, which can help prevent infection and promote wound healing.
2. Skin protectant: It forms a physical barrier on the skin, protecting it from external irritants, friction, and moisture. This property is particularly useful in products like diaper rash creams and sunscreens.
3. Astringent properties: Zinc oxide can help constrict and tighten tissues, which may reduce inflammation and promote healing.
4. Mineral sunscreen agent: Zinc oxide is a common active ingredient in physical (mineral) sunscreens due to its ability to reflect and scatter UV light, protecting the skin from both UVA and UVB radiation.

Zinc oxide can be found in various medical and skincare products, such as creams, ointments, pastes, lotions, and powders. It is generally considered safe for topical use, but it may cause skin irritation or allergic reactions in some individuals.

  • 4-Nitroquinoline 1-oxide (also known as 4-NQO, 4NQO, 4Nqo, NQO and NQNO) is a quinoline derivative and a tumorigenic compound used in the assessment of the efficacy of diets, drugs, and procedures in the prevention and treatment of cancer in animal models. (wikipedia.org)
  • 4-nitroquinoline 1-oxide (4NQO) is a quinoline, a carcinogenic and mutagenic chemical. (wikipedia.org)
  • Both 4NQO and its reduced metabolite 4-hydroxyaminoquinoline 1-oxide (4HAQO) bind covalently to cellular macromolecules such as nucleic acids and proteins. (wikipedia.org)
  • 4NQO's four electron reduction product, 4-hydroxyaminoquinoline 1-oxide (4HAQO), is believed to be a carcinogenic metabolite of 4NQO. (wikipedia.org)
  • Our previous reports have shown that two thirds of 4-nitroquinoline-1-oxide (4NQO)-induced murine oral squamous cell carcinomas (SCC) have Hras1 mutations. (jax.org)
  • To elucidate their role in immune cell recruitment during oral cancer development, we generated a mouse tongue cancer model using the carcinogen 4-nitroquinoline 1-oxide (4NQO) and investigated the carcinogenetic process and chemokine/cytokine gene expression kinetics in the mouse tongue. (immpact-international.org)
  • Previously, the extent of DNA repair (autoradiographic detection of unscheduled ³HTdR incorporation) in hamster and human cells following exposure to strongly, weakly and non-oncogenic isomers and derivatives of 4-nitroquinoline 1-oxide (4NQO) was examined. (ubc.ca)
  • Here, we used a model in which tumors were induced in rats using 4-nitroquinoline 1-oxide (4NQO), which mimicked tobacco-related HNSCC, and analyzed the expression profiles of microRNAs and mRNAs. (figshare.com)
  • Increased cell susceptibility to genotoxic xenobiotics was tested by challenging cell cultures with 4-nitroquinoline-N-oxide (4NQO) and evaluating the extent of primary DNA damage by comet assay. (unipg.it)
  • We used real-time quantitative PCR to analyze mtDNA integrity, damage repair, and induced mutations after exposure of human adult retinal pigment epithelial (ARPE)-19 cells to 4-nitroquinoline 1-oxide, a UV-mimetic and adduct-forming carcinogen, and tert-butyl hydroperoxide, an oxidant. (nih.gov)
  • They made use of albino Wistar rats that were induced to have oxidative stress using the potent carcinogen 4-nitroquinoline 1-oxide (4-NQO). (healing.news)
  • 1. Tumor-associated macrophage (TAM)-derived CCL22 induces FAK addiction in esophageal squamous cell carcinoma (ESCC). (nih.gov)
  • 8. Phospholipase C gamma 1 is a potential prognostic biomarker for patients with locally advanced and resectable oral squamous cell carcinoma. (nih.gov)
  • 9. Effect of DJ-1 overexpression on the proliferation, apoptosis, invasion and migration of laryngeal squamous cell carcinoma SNU-46 cells through PI3K/AKT/mTOR. (nih.gov)
  • Head and neck squamous cell carcinoma (HNSCC) is one of the most common cancers developed from mucosal linings of the upper aerodigestive tract ( 1 ). (aacrjournals.org)
  • This compound and its metabolite 4-HYDROXYAMINOQUINOLINE-1-OXIDE bind to nucleic acids. (nih.gov)
  • Furthermore, these genes also conferred resistance to UV-radiation, 4-nitroquinoline-N-oxide (4-NQO) and/or hydrogen peroxide (H 2 O 2 ), other stress conditions that induce oxidative stress, and damage in proteins and nucleic acids. (uai.cl)
  • Here, we demonstrate that five of six tumors with LOH have 4-8-fold amplification involving the distal portion of Chr 7 (7F4). (jax.org)
  • Four murine OSCC cell lines, designated MOC-L1 to MOC-L4, are established from tongue tumors induced by 4-nitroquinoline 1-oxide using the K14-EGFP- miR-211 transgenic mouse model. (biomedcentral.com)
  • 7. Inhibition of 4-nitroquinoline-1-oxide-induced oral carcinogenesis by dietary calcium. (nih.gov)
  • Using N -methyl- N ′-nitro- N -nitrosoguanidine, ultraviolet irradiation, ethyl methanesul- phonate or 4-nitroquinoline-1-oxide mutagenesis and an enrichment method for the isolation of auxotrophs, 25 mutants with defects in the adA locus were obtained after screening 41376 colonies. (microbiologyresearch.org)
  • 1995) In another study that complied with GLP, groups of three male and three female Sprague-Dawley rats were given [ 14 C-phenoxyphenyl]pyriproxyfen orally at a single dose of 2 mg/kg bw, and radiolabel in tissues was determined 2, 4, 8, 12, 24, 48, and 72 h after dosing. (inchem.org)
  • 15. The balance between 4-hydroxynonenal and intrinsic glutathione/glutathione S-transferase A4 system may be critical for the epidermal growth factor receptor phosphorylation of human esophageal squamous cell carcinomas. (nih.gov)
  • Moreover, we evaluated the relationship between glucose concentration and intracellular ROS, as well as the effects of glucose concentration on the induction of Nrf2-dependent genes such as Glutathione S-transferases, Heme‑oxygenase-1, and Glutathione peroxidase-4. (unipg.it)
  • It is a reduction product of 4-NITROQUINOLINE-1-OXIDE. (nih.gov)
  • The OSCC patients five-year survival rate is generally around 50% [ 1 ]. (biomedcentral.com)
  • At their November 16, 2000 meeting the Committee, by a vote of one in favor and five against, did not find that 4-methylquinoline had been "clearly shown through scientifically valid testing according to generally accepted principles to cause cancer. (nih.gov)
  • It is therefore concluded thatTrans-hex-2-en-1-ol was not mutagenic under the conditions of the test. (europa.eu)
  • DINP and 4-NP were mutagenic in the Ames assay and also induced significant levels of unscheduled DNA synthesis and DNA strand breakage. (scirp.org)
  • 2012). IncP-1 epsilon plasmids are important vectors of antibiotic resistance genes in agricultural systems: diversification driven by class 1 integron gene cassettes. (uai.cl)
  • In the UK a random screen of 20 organic man-made chemicals present in liquid effluents revealed that half appeared to interact with the oestrogen receptor [1] and results obtained from fifteen sewage treatment plants (STPs) showed that exposure of male trout to effluent resulted in a very pronounced increase in plasma vitellogenin concentration indicating exposure to a substance or substances oestrogenic to fish [2]. (scirp.org)
  • Significant induction in the percentage of cells containing micronuclei was observed after treatment with DINP, DEHP and 4-NP. (scirp.org)
  • The capacity of Trans-hex-2-en-1-ol to induce gene mutation in bacteria was evaluated during a GLP-compliant study performed in accordance with the OECD Testing Guideline 471. (europa.eu)
  • 4-Methylquinoline was assigned a final priority of `high' carcinogenicity concern and placed on the Final Candidate list of chemicals for Committee review on August 6, 1999. (nih.gov)
  • In experiment 1 the test item induced toxicity as weakened bacterial background lawns and/or substantial reductions in the revertant colony frequency of all of the Salmonella strains in both the presence and absence of S9-mix at 5,000 μg/plate. (europa.eu)
  • This includes 29 directly active proximate or ultimate carcinogens, 15 precarcinogens, that require metabolic activation, 16 non-oncogenic compounds and 4 chemicals of unknown carcinogenicity. (ubc.ca)
  • This document reviews the available scientific evidence on the carcinogenic potential of 4-methylquinoline. (nih.gov)
  • Carcinogenic and related properties of compounds structurally similar to 4-methylquinoline. (nih.gov)
  • In mice with EoE, we detect distinct expansion of 4 suprabasal populations coupled with depletion of 2 basal populations. (bvsalud.org)
  • By contrast, mice with ESCC display unique expansion of 2 basal populations and 1 suprabasal population, as well as depletion of 2 suprabasal populations. (bvsalud.org)
  • The dose range used for Experiment 2 was determined by the results of Experiment 1 and was 1.5 to 5000 µg/plate. (europa.eu)
  • Plate incorporation method (experiment 1) and pre-incubation method (experiment 2) were used. (europa.eu)
  • There were no increases in the frequency of revertant colonies recorded for any of the bacterial strains, with any dose of the test item, either with or without metabolic activation (S9-mix) in Experiment 1 (plate incorporation method). (europa.eu)
  • The following product was used in this experiment: LC3 Polyclonal Antibody from Thermo Fisher Scientific, catalog # 14600-1-AP. (thermofisher.com)
  • Similarly, a linear increase in micronucleus frequency was detected with 10(-3)-10(-1) M mercury ions. (nih.gov)
  • 1. A dose-related increase in mutant frequency over the dose range tested (De Serres and Shelby, 1979). (europa.eu)
  • OI blocks the VEGF signaling pathway by downregulating the expression levels of VEGF, HIF-1α and EGFR and inhibits the migration and invasion of HepG2 cells and the formation of new blood vessels. (biomedcentral.com)
  • With the Indian trumpet flower treatment, these effects of 4-NQO were successfully reversed. (healing.news)
  • More recently studies in the UK have reported a reduction in egg production in fish after exposure to wastewater treatment effluent [3] and that the life stage at which male fish are exposed can have dramatic consequences for sexual disruption [4]. (scirp.org)
  • The results of this study prove that extracts from the leaves of the Indian trumpet flower have antioxidant and hepatoprotective properties that allow them to work against 4-NQO induced damage in a dose-dependent manner. (healing.news)
  • 1-8 of 8 results for ""Ala Aghbali, A. (sagrado.edu)
  • Radiolabel was excreted predominantly in the faeces (90%) at both doses, urinary excretion representing 4-8% of the administered dose over 48 h. (inchem.org)
  • The main organic hydrolysis product is 1-butanol and therefore the properties are considered similar. (europa.eu)
  • 4. Statistical analysis of data as determined by UKEMS (Mahon et al. (europa.eu)
  • Diisononylphthalate (DINP), diethylhexylphthalate (DEHP), dibutylphthalate (DBP), diisododecylphthalate (DIDP) and 4-nonylphenol (4-NP) were oestrogenic in the yeast estrogen screen (YES) assay and potently oestrogenic in the MVLN and E-SCREEN assays at environmentally relevant concentrations. (scirp.org)
  • 10(-4) M, however, destroyed the cells. (nih.gov)
  • This is likely done through inhibition of the urate anion transporter (hURAT1) as well as the human organic anion transporter 4 (hOAT4). (illumina.com)