Receptor, Metabotropic Glutamate 5
Receptors, Metabotropic Glutamate
NADH, NADPH Oxidoreductases
Cytochrome P-450 CYP1A2
Magnetic Resonance Spectroscopy
Chemistry Techniques, Synthetic
Gram-Negative Facultatively Anaerobic Rods
Chromatography, High Pressure Liquid
Indicators and Reagents
Cardiovascular Physiological Processes
Excitatory Amino Acid Antagonists
Green Chemistry Technology
Dose-Response Relationship, Drug
Cytochrome P-450 Enzyme System
Nitrate Reductase (NAD(P)H)
Bicyclo Compounds, Heterocyclic
Heterocyclic Compounds, 2-Ring
Spectrometry, Mass, Electrospray Ionization
Mixed Function Oxygenases
Gas Chromatography-Mass Spectrometry
Inhibitory Concentration 50
Molecular Sequence Data
Phagocyte Bactericidal Dysfunction
Drug Screening Assays, Antitumor
Transformation mediated by RhoA requires activity of ROCK kinases. (1/8964)BACKGROUND: The Ras-related GTPase RhoA controls signalling processes required for cytoskeletal reorganisation, transcriptional regulation, and transformation. The ability of RhoA mutants to transform cells correlates not with transcription but with their ability to bind ROCK-I, an effector kinase involved in cytoskeletal reorganisation. We used a recently developed specific ROCK inhibitor, Y-27632, and ROCK truncation mutants to investigate the role of ROCK kinases in transcriptional activation and transformation. RESULTS: In NIH3T3 cells, Y-27632 did not prevent the activation of serum response factor, transcription of c-fos or cell cycle re-entry following serum stimulation. Repeated treatment of NIH3T3 cells with Y-27632, however, substantially disrupted their actin fibre network but did not affect their growth rate. Y-27632 blocked focus formation by RhoA and its guanine-nucleotide exchange factors Dbl and mNET1. It did not affect the growth rate of cells transformed by Dbl and mNET1, but restored normal growth control at confluence and prevented their growth in soft agar. Y-27632 also significantly inhibited focus formation by Ras, but had no effect on the establishment or maintenance of transformation by Src. Furthermore, it significantly inhibited anchorage-independent growth of two out of four colorectal tumour cell lines. Consistent with these data, a truncated ROCK derivative exhibited weak ability to cooperate with activated Raf in focus formation assays. CONCLUSIONS: ROCK signalling is required for both the establishment and maintenance of transformation by constitutive activation of RhoA, and contributes to the Ras-transformed phenotype. These observations provide a potential explanation for the requirement for Rho in Ras-mediated transformation. Moreover, the inhibition of ROCK kinases may be of therapeutic use. (+info)
Regulation and function of family 1 and family 2 UDP-glucuronosyltransferase genes (UGT1A, UGT2B) in human oesophagus. (2/8964)Human UDP-glucuronosyltransferases (UGTs) are expressed in a tissue-specific fashion in hepatic and extrahepatic tissues [Strassburg, Manns and Tukey (1998) J. Biol. Chem. 273, 8719-8726]. Previous work suggests that these enzymes play a protective role in chemical carcinogenesis [Strassburg, Manns and Tukey (1997) Cancer Res. 57, 2979-2985]. In this study, UGT1 and UGT2 gene expression was investigated in human oesophageal epithelium and squamous-cell carcinoma in addition to the characterization of individual UGT isoforms using recombinant protein. UGT mRNA expression was characterized by duplex reverse transcriptase-PCR analysis and revealed the expression of UGT1A7, UGT1A8, UGT1A9 and UGT1A10 mRNAs. UGT1A1, UGT1A3, UGT1A4, UGT1A5 and UGT1A6 transcripts were not detected. UGT2 expression included UGT2B7, UGT2B10 and UGT2B15, but UGT2B4 mRNA was absent. UGT2 mRNA was present at significantly lower levels than UGT1 transcripts. This observation was in agreement with the analysis of catalytic activities in oesophageal microsomal protein, which was characterized by high glucuronidation rates for phenolic xenobiotics, all of which are classical UGT1 substrates. Whereas UGT1A9 was not regulated, differential regulation of UGT1A7 and UGT1A10 mRNA was observed between normal oesophageal epithelium and squamous-cell carcinoma. Expression and analysis in vitro of recombinant UGT1A7, UGT1A9, UGT1A10, UGT2B7 and UGT2B15 demonstrated that UGT1A7, UGT1A9 and UGT1A10 catalysed the glucuronidation of 7-hydroxybenzo(alpha)pyrene, as well as other environmental carcinogens, such as 2-hydroxyamino-1-methyl-6-phenylimidazo-(4, 5-beta)-pyridine. Although UGT1A9 was not regulated in the carcinoma tissue, the five-fold reduction in 7-hydroxybenzo(alpha)pyrene glucuronidation could be attributed to regulation of UGT1A7 and UGT1A10. These data elucidate an individual regulation of human UGT1A and UGT2B genes in human oesophagus and provide evidence for specific catalytic activities of individual human UGT isoforms towards environmental carcinogens that have been implicated in cellular carcinogenesis. (+info)
Insulin-like growth factors I and II are unable to form and maintain their native disulfides under in vivo redox conditions. (3/8964)Insulin-like growth factor (IGF) I does not quantitatively form its three native disulfide bonds in the presence of 10 mM reduced and 1 mM oxidized glutathione in vitro [Hober, S. et al. (1992) Biochemistry 31, 1749-1756]. In this paper, we show (i) that both IGF-I and IGF-II are unable to form and maintain their native disulfide bonds at redox conditions that are similar to the situation in the secretory vesicles in vivo and (ii) that the presence of protein disulfide isomerase does not overcome this problem. The results indicate that the previously described thermodynamic disulfide exchange folding problem of IGF-I in vitro is also present in vivo. Speculatively, we suggest that the thermodynamic disulfide exchange properties of IGF-I and II are biologically significant for inactivation of the unbound growth factors by disulfide exchange reactions to generate variants destined for rapid clearance. (+info)
delta-Aminolevulinate synthetases in the liver cytosol fraction and mitochondria of mice treated with allylisopropylacetamide and 3,5-dicarbethoxyl-1,4-dihydrocollidine. (4/8964)Hepatic delta-aminolevulinate (ALA) synthetase was induced in mice by the administration of allylisopropylacetamide (AIA) and 3,5-dicarbethoxy-1,4-dihydrocollidine (DDC). In both cases, a significant amount of ALA synthetase accumulated in the liver cytosol fraction as well as in the mitochondria. The apparent molecular weight of the cytosol ALA synthetase was estimated to be 320,000 by gel filtration, but when the cytosol ALA synthetase was subjected to sucrose density gradient centrifugation, it showed a molecular weight of 110,000. In the mitochondria, there were two different sizes of ALA synthetase with molecular weights of 150,000 and 110,000, respectively; the larger enzyme was predominant in DDC-treated mice, whereas in AIA-treated mice and normal mice the enzyme existed mostly in the smaller form. When hemin was injected into mice pretreated with DDC, the molecular size of the mitochondrial ALA synthetase changed from 150,000 to 110,000. The half-life of ALA synthetase in the liver cytosol fraction was about 30 min in both the AIA-treated and DDC-treated mice. The half-life of the mitochondrial ALA synthetase in AIA-treated mice and normal mice was about 60 min, but in DDC-treated mice the half-life was as long as 150 min. The data suggest that the cytosol ALA synthetase of mouse liver is a protein complex with properties very similar to those of the cytosol ALA synthetase of rat liver, which has been shown to be composed of the enzyme active protein and two catalytically inactive binding proteins, and that ALA synthetase may be transferred from the liver cytosol fraction to the mitochondria with a size of about 150,000 daltons, followed by its conversion to enzyme with a molecular weight of 110,000 within the mitochondria. The process of intramitochondrial enzyme degradation seems to be affected in DDC-treated animals. (+info)
Selective antiaggressive effects of alnespirone in resident-intruder test are mediated via 5-hydroxytryptamine1A receptors: A comparative pharmacological study with 8-hydroxy-2-dipropylaminotetralin, ipsapirone, buspirone, eltoprazine, and WAY-100635. (5/8964)The present study characterized the effects of the novel, selective, and potent 5-hydroxytryptamine1A (serotonin) (5-HT1A) receptor agonist, alnespirone [S-20499, (S)-N-4-[5-methoxychroman-3-yl)propylamino)butyl- 8-azaspiro-(4,5)-diacetamide, hydrochloride] on offensive and defensive resident-intruder aggression in wild-type rats and compared its actions with those of the prototypical full 5-HT1A agonist 8-hydroxy-2- dipropylaminotetralin (8-OH-DPAT), the partial 5-HT1A agonists ipsapirone and buspirone, and the mixed 5-HT1A/1B agonist eltoprazine. All five agonists exerted effective dose-dependent decreases of offensive aggressive behavior in resident rats; 8-OH-DPAT was the most potent (ID50 = 0.074 mg/kg), followed by eltoprazine (0.24), buspirone (0.72), ipsapirone (1.08), and alnespirone (1.24). However, in terms of selectivity of the antiaggressive effects as determined by the absence of decrements in social interest and general motor activity, alnespirone appeared to be superior. In the defensive aggression test, neither alnespirone nor any of the other four agonists changed defensive behaviors in the intruder rats. The involvement of 5-HT1A receptors in the antiaggressive actions of these drugs was confirmed by showing that the selective 5-HT1A receptor antagonist WAY-100635 (N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2- pyridinyl)cyclohexanecarboxamide trihydrochloride), which was inactive alone, fully prevented the antiaggressive effects of alnespirone, 8-OH-DPAT, and buspirone and partly reversed those of ipsapirone and eltoprazine. The data clearly indicate that alnespirone effectively suppresses offensive aggression with an advantageous profile of action compared with other full or partial 5-HT1A agonists. These selective antiaggressive actions of alnespirone are mediated by stimulating 5-HT1A receptors, presumably the somatodendritic autoreceptors at the raphe nuclei. Furthermore, the data provide evidence for a major involvement of these 5-HT1A receptors in the modulation of aggressive behavior by 8-OH-DPAT, ipsapirone, buspirone, and eltoprazine. (+info)
Development of muscarinic analgesics derived from epibatidine: role of the M4 receptor subtype. (6/8964)Epibatidine, a neurotoxin isolated from the skin of Epipedobates tricolor, is an efficacious antinociceptive agent with a potency 200 times that of morphine. The toxicity of epibatidine, because of its nonspecificity for both peripheral and central nicotinic receptors, precludes its development as an analgesic. During the synthesis of epibatidine analogs we developed potent antinociceptive agents, typified by CMI-936 and CMI-1145, whose antinociception, unlike that of epibatidine, is mediated via muscarinic receptors. Subsequently, we used specific muscarinic toxins and antagonists to delineate the muscarinic receptor subtype involved in the antinociception evoked by these agents. Thus, the antinociception produced by CMI-936 and CMI-1145 is inhibited substantially by 1) intrathecal injection of the specific muscarinic M4 toxin, muscarinic toxin-3; 2) intrathecally administered pertussis toxin, which inhibits the G proteins coupled to M2 and M4 receptors; and 3) s.c. injection of the M2/M4 muscarinic antagonist himbacine. These results demonstrate that the antinociception elicited by these epibatidine analogs is mediated via muscarinic M4 receptors located in the spinal cord. Compounds that specifically target the M4 receptor therefore may be of substantial value as alternative analgesics to the opiates. (+info)
The ras oncogene-mediated sensitization of human cells to topoisomerase II inhibitor-induced apoptosis. (7/8964)BACKGROUND: Among the inhibitors of the enzyme topoisomerase II (an important target for chemotherapeutic drugs) tested in the National Cancer Institute's In Vitro Antineoplastic Drug Screen, NSC 284682 (3'-hydroxydaunorubicin) and NSC 659687 [9-hydroxy-5,6-dimethyl-1-(N-[2(dimethylamino)ethyl]carbamoyl)-6H-pyrido -(4,3-b)carbazole] were the only compounds that were more cytotoxic to tumor cells harboring an activated ras oncogene than to tumor cells bearing wild-type ras alleles. Expression of the multidrug resistance proteins P-glycoprotein and MRP (multidrug resistance-associated protein) facilitates tumor cell resistance to topoisomerase II inhibitors. We investigated whether tumor cells with activated ras oncogenes showed enhanced sensitivity to other topoisomerase II inhibitors in the absence of the multidrug-resistant phenotype. METHODS: We studied 20 topoisomerase II inhibitors and individual cell lines with or without activated ras oncogenes and with varying degrees of multidrug resistance. RESULTS: In the absence of multidrug resistance, human tumor cell lines with activated ras oncogenes were uniformly more sensitive to most topoisomerase II inhibitors than were cell lines containing wild-type ras alleles. The compounds NSC 284682 and NSC 659687 were especially effective irrespective of the multidrug resistant phenotype. The ras oncogene-mediated sensitization to topoisomerase II inhibitors was far more prominent with the non-DNA-intercalating epipodophyllotoxins than with the DNA-intercalating inhibitors. This difference in sensitization appears to be related to a difference in apoptotic sensitivity, since the level of DNA damage generated by etoposide (an epipodophyllotoxin derivative) in immortalized human kidney epithelial cells expressing an activated ras oncogene was similar to that in the parental cells, but apoptosis was enhanced only in the former cells. CONCLUSIONS: Activated ras oncogenes appear to enhance the sensitivity of human tumor cells to topoisomerase II inhibitors by potentiating an apoptotic response. Epipodophyllotoxin-derived topoisomerase II inhibitors should be more effective than the DNA-intercalating inhibitors against tumor cells with activated ras oncogenes. (+info)
Raf-1 is activated by the p38 mitogen-activated protein kinase inhibitor, SB203580. (8/8964)SB203580 (4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imi dazole) is widely used as a specific inhibitor of p38 mitogen-activated protein kinase (MAPK). Here, we report that SB203580 activates the serine/threonine kinase Raf-1 in quiescent smooth muscle cells in a dose-dependent fashion. The concentrations of SB203580 required lie above those necessary to inhibit p38 MAPK and we were unable to detect basal levels of active p38 MAPK. SB203580 does not directly activate Raf-1 in vitro, and fails to activate Ras, MEK, and ERK in intact cells. In vitro, however, SB203580-stimulated Raf-1 activates MEK1 in a coupled assay. We conclude that activation of Raf-1 by SB203580 is not mediated by an inhibition of p38 MAPK, is Ras-independent, and is uncoupled from MEK/ERK signaling. (+info)
The exact cause of acatalasia is not known, but it is thought to be related to genetic mutations that affect the function or expression of the catalase enzyme. The disorder is usually diagnosed in infancy or early childhood, and treatment typically involves managing the symptoms with a high-calorie diet, vitamin supplements, and antioxidants. In some cases, bone marrow transplantation may be considered as a potential treatment option.
Here are some key points to consider when discussing acatalasia in the medical field:
* Acatalasia is a rare congenital disorder that affects the small intestine and is characterized by the absence or underdevelopment of catalase enzyme.
* The exact cause of acatalasia is not known, but it is thought to be related to genetic mutations that affect the function or expression of the catalase enzyme.
* Symptoms of acatalasia include diarrhea, abdominal pain, and failure to gain weight or grow at the expected rate.
* Treatment typically involves managing the symptoms with a high-calorie diet, vitamin supplements, and antioxidants.
* Bone marrow transplantation may be considered as a potential treatment option in some cases.
In summary, acatalasia is a rare genetic disorder that affects the small intestine and is characterized by the absence or underdevelopment of the catalase enzyme, leading to an accumulation of hydrogen peroxide in the body and a range of symptoms including diarrhea, abdominal pain, and failure to gain weight or grow at the expected rate. Treatment typically involves managing the symptoms with a high-calorie diet, vitamin supplements, and antioxidants, and bone marrow transplantation may be considered as a potential treatment option in some cases.
Types of Intestinal Neoplasms:
1. Adenomas: These are benign tumors that grow on the inner lining of the intestine. They can become malignant over time if left untreated.
2. Carcinomas: These are malignant tumors that develop in the inner lining of the intestine. They can be subdivided into several types, including colon cancer and rectal cancer.
3. Lymphoma: This is a type of cancer that affects the immune system and can occur in the intestines.
4. Leiomyosarcomas: These are rare malignant tumors that develop in the smooth muscle layers of the intestine.
Causes and Risk Factors:
The exact cause of intestinal neoplasms is not known, but several factors can increase the risk of developing these growths. These include:
1. Age: The risk of developing intestinal neoplasms increases with age.
2. Family history: Having a family history of colon cancer or other intestinal neoplasms can increase the risk of developing these growths.
3. Inflammatory bowel disease: People with inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease, are at higher risk of developing intestinal neoplasms.
4. Genetic mutations: Certain genetic mutations can increase the risk of developing intestinal neoplasms.
5. Diet and lifestyle factors: A diet high in fat and low in fiber, as well as lack of physical activity, may increase the risk of developing intestinal neoplasms.
Intestinal neoplasms can cause a variety of symptoms, including:
1. Abdominal pain or discomfort
2. Changes in bowel habits, such as diarrhea or constipation
3. Blood in the stool
4. Weight loss
6. Loss of appetite
To diagnose intestinal neoplasms, a doctor may perform several tests, including:
1. Colonoscopy: A colonoscope is inserted through the rectum and into the colon to visualize the inside of the colon and detect any abnormal growths.
2. Biopsy: A small sample of tissue is removed from the colon and examined under a microscope for cancer cells.
3. Imaging tests: Such as X-rays, CT scans, or MRI scans to look for any abnormalities in the colon.
4. Blood tests: To check for certain substances in the blood that are associated with intestinal neoplasms.
The treatment of intestinal neoplasms depends on the type and location of the growth, as well as the stage of the cancer. Treatment options may include:
1. Surgery: To remove the tumor and any affected tissue.
2. Chemotherapy: To kill any remaining cancer cells with drugs.
3. Radiation therapy: To kill cancer cells with high-energy X-rays or other forms of radiation.
4. Targeted therapy: To use drugs that target specific molecules on cancer cells to kill them.
5. Immunotherapy: To use drugs that stimulate the immune system to fight cancer cells.
The prognosis for intestinal neoplasms depends on several factors, including the type and stage of the cancer, the location of the growth, and the effectiveness of treatment. In general, early detection and treatment improve the prognosis, while later-stage cancers have a poorer prognosis.
Intestinal neoplasms can cause several complications, including:
1. Obstruction: The tumor can block the normal flow of food through the intestine, leading to abdominal pain and other symptoms.
2. Bleeding: The tumor can cause bleeding in the intestine, which can lead to anemia and other complications.
3. Perforation: The tumor can create a hole in the wall of the intestine, leading to peritonitis (inflammation of the lining of the abdomen) and other complications.
4. Metastasis: The cancer cells can spread to other parts of the body, such as the liver or lungs, and cause further complications.
5. Malnutrition: The tumor can make it difficult for the body to absorb nutrients, leading to malnutrition and other health problems.
There is no sure way to prevent intestinal neoplasms, but there are several steps that may help reduce the risk of developing these types of cancer. These include:
1. Avoiding known risk factors: Avoiding known risk factors such as smoking, excessive alcohol consumption, and a diet high in processed meat can help reduce the risk of developing intestinal neoplasms.
2. Maintaining a healthy diet: Eating a balanced diet that is high in fruits, vegetables, and whole grains can help keep the intestines healthy and may reduce the risk of cancer.
3. Exercise regularly: Regular exercise can help maintain a healthy weight, improve digestion, and may reduce the risk of developing intestinal neoplasms.
4. Managing chronic conditions: Managing chronic conditions such as inflammatory bowel disease, diabetes, and obesity can help reduce the risk of developing intestinal neoplasms.
5. Screening tests: Regular screening tests such as colonoscopy, CT scan, or barium enema can help detect precancerous polyps or early-stage cancer, allowing for early treatment and prevention of advanced disease.
Early detection and diagnosis are crucial for effective treatment and survival rates for intestinal neoplasms. If you have any of the risk factors or symptoms mentioned above, it is essential to consult a doctor as soon as possible. A thorough examination and diagnostic tests can help determine the cause of your symptoms and recommend appropriate treatment.
Phagocyte bactericidal dysfunction can be caused by a variety of factors, including genetic mutations, exposure to toxins, or infections with certain viruses or other pathogens that interfere with phagocyte function.
The consequences of phagocyte bactericidal dysfunction can include increased susceptibility to infections and the development of persistent or chronic infections, which can lead to a range of health problems and diseases.
Phagocyte bactericidal dysfunction is an important area of research in immunology and infectious disease, as understanding the mechanisms that control phagocyte function can help us develop new therapies and treatments for infections and other immune-related disorders.
There are several types of colonic neoplasms, including:
1. Adenomas: These are benign growths that are usually precursors to colorectal cancer.
2. Carcinomas: These are malignant tumors that arise from the epithelial lining of the colon.
3. Sarcomas: These are rare malignant tumors that arise from the connective tissue of the colon.
4. Lymphomas: These are cancers of the immune system that can affect the colon.
Colonic neoplasms can cause a variety of symptoms, including bleeding, abdominal pain, and changes in bowel habits. They are often diagnosed through a combination of medical imaging tests (such as colonoscopy or CT scan) and biopsy. Treatment for colonic neoplasms depends on the type and stage of the tumor, and may include surgery, chemotherapy, and/or radiation therapy.
Overall, colonic neoplasms are a common condition that can have serious consequences if left untreated. It is important for individuals to be aware of their risk factors and to undergo regular screening for colon cancer to help detect and treat any abnormal growths or tumors in the colon.
MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) poisoning is a type of toxicity that occurs when the brain is exposed to high levels of this substance. MPTP is a synthetic compound that was originally developed as a drug for treating Parkinson's disease, but it was found to be too toxic for human use.
MPTP poisoning can cause severe and irreversible damage to the brain's dopamine-producing neurons, leading to a condition called parkinsonism. Symptoms of MPTP poisoning include muscle rigidity, tremors, bradykinesia (slowness of movement), and changes in mood and cognitive function.
The diagnosis of MPTP poisoning is based on a combination of clinical findings and laboratory tests, including blood and urine analysis for the presence of MPTP or its metabolites. Treatment of MPTP poisoning typically involves supportive care, such as management of symptoms and prevention of complications, as well as medications to reduce dopamine levels in the brain.
MPTP poisoning can occur through intentional exposure (e.g., suicide attempt) or accidental exposure (e.g., ingestion of contaminated food or water). It is important for healthcare providers to be aware of the risks and signs of MPTP poisoning, as prompt diagnosis and treatment can help prevent long-term neurological damage and improve outcomes for affected individuals.
Boger pyridine synthesis
Pyridine nucleotide transhydrogenase
Pyridine nucleotide transferase
Pyridine (data page)
Kröhnke pyridine synthesis
Chichibabin pyridine synthesis
Hantzsch pyridine synthesis
Bohlmann-Rahtz pyridine synthesis
Transition metal pyridine complexes
Sulfur trioxide pyridine complex
Flavoprotein pyridine nucleotide cytochrome reductases
Pyridine nucleotide-disulphide oxidoreductase domain 1
Pyridine | ToxFAQs™ | ATSDR
CDC - NIOSH Pocket Guide to Chemical Hazards - Pyridine
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Carcinogenic effects of pyridine2
Sticks to soil particles1
- Pyridine sticks to soil particles. (cdc.gov)
- At present, there is a rise in the utilization of pyridine derivatives, such as beta picoline, to manufacture vitamin B3 and B6 for improving digestion, maintaining cholesterol levels, curing skin diseases, and reducing the risk of cardiovascular problems. (giiresearch.com)
- Moreover, there is an increase in the employment of pyridine as a raw material to produce insecticides, herbicides, and fungicides around the world. (giiresearch.com)
- Pyridine is extensively used in agrochemicals to manufacture herbicides, pesticides and insecticides. (giiresearch.com)
- Pyridine is also used in the production of insecticides chlorpyrifos and methyl chlorpyrifos, which are broad-spectrum insecticides. (tourismofrajasthan.com)
- Pyridine is also the raw material of inulin, an indispensable active component in insecticidal aerosols, and one of the insecticides recommended by the World Health Organization for use in homes and public places. (tourismofrajasthan.com)
- Pyridine is very soluble in water. (cdc.gov)
- pyridine caused these effects because the patients were taking o Pyridine is very soluble in water. (cdc.gov)
- In the production of dyes, pyridine is mainly used to produce blue BB, blue RR, disperse blue S-RB, soluble reducing blue IBC, soluble reducing grey IBL, etc., with a small amount. (tourismofrajasthan.com)
- ToxFAQs Internet address via WWW is http://www.atsdr.cdc.gov/toxfaq.html breathed an unknown amount of pyridine for an unknown reported. (cdc.gov)
- In the pesticide industry, pyridine is mainly used in the production of herbicides paraquat and Dioxin, etc., which has been widely used in the world in recent years. (tourismofrajasthan.com)
- The Department of Health and Human Services, the International Agency for Research on Cancer, and the Environmental Protection Agency (EPA) have not classified pyridine as to its human carcinogenicity. (cdc.gov)
- ronmental Protection Agency (EPA) have not classified pyridine as to its human carcinogenicity. (cdc.gov)
- This minireview collects the results that we obtained in the recent years on luminescent compounds based on imidazo[1,5-a]pyridines, an interesting class of heterocycles characterized by relevant photophysical properties like high Stokes shift, good absolute quantum yields, good photostability and a λem modulable depending on the substituents on the heterocyclic ring. (uninsubria.it)
- The chemical sensor was based on the reaction of basic pyridine with certain chlorinated compounds to form an intense red color. (cdc.gov)
- It o Workers may be exposed in industries that make pyridine can be made from crude coal tar or from other chemicals. (cdc.gov)
- This, coupled with the rising demand for pyridine as a solvent to produce chemicals and adhesives, is propelling the growth of the market. (giiresearch.com)
- There are more than ten kinds of pyridine related to twenty kinds of chemicals produced in China. (tourismofrajasthan.com)
- There are also some drugs based on pyridine as raw material or solvent. (tourismofrajasthan.com)
- used to make many different products such as medicines, o People may breathe pyridine when it is released into the vitamins, food flavorings, paints, dyes, rubber products, air from burning cigarettes and from hot coffee. (cdc.gov)
- Animal studies and some limited case reports in people have noted liver damage from exposure to pyridine. (cdc.gov)
- These tests can't tell how much pyridine you were exposed to or if harmful health effects will occur from the exposure to pyridine. (cdc.gov)
- The Occupational Safety and Health Administration (OSHA) has set an occupational exposure limit of 5 parts of pyridine per million parts of workplace air (5 ppm) for an 8-hour workday over a 40-hour workweek. (cdc.gov)
- people have noted liver damage from exposure to pyridine. (cdc.gov)
- We do not know whether pyridine affects the ability of (OSHA) has set an occupational exposure limit of 5 parts of men and women to have children or whether it causes birth pyridine per million parts of workplace air (5 ppm) for an defects. (cdc.gov)
- Health (NIOSH) and the American Conference of Governmen tal and Industrial Hygienists (ACGIH) have established the The Department of Health and Human Services, the same guidelines as OSHA for pyridine exposure levels in the International Agency for Research on Cancer, and the Envi workplace. (cdc.gov)
- Exposures to pyridine (110861) and 4- phenyl-propylpyridine (2057490) had a combined average exposure of 7.0 parts per million (ppm) in the molding area. (cdc.gov)
- This quinolone agent is a derivative of pyridine carboxylic acid with broad-spectrum bactericidal effect. (medscape.com)
- The silver(I) and iodine(I) complexes of the 2-substituted pyridines 2-(diphenylmethyl)pyridine (1) and 2-(1,1-diphenylethyl)pyridine (2), along with their potential protonated side products, were synthesised to investigate the steric limitations of iodine(I) complex formation. (jyu.fi)
- The solid-state structures for the silver(I) and iodine(I) complexes were extensively compared to the literature and analysed by DFT to examine the influence of the sterically bulky pyridines and their anions. (jyu.fi)
- These peculiar features can be transferred to the corresponding complexes when imidazo[1,5-a]pyridines are used as ligands. (uninsubria.it)
- Herein we report on the photoluminescent behavior of zinc(II) and silver(I) complexes with 1-pyridylimidazo[1,5-a]pyridines acting as N,N-bidentate, neutral ligands. (uninsubria.it)
- CYP1A2 and NAT2 genotype/phenotype relations and urinary excretion of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in a human dietary intervention study. (bvsalud.org)
- 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a mutagenic and carcinogenic heterocyclic amine formed during ordinary cooking , and is subsequently metabolically activated by cytochrome P4501A2 ( CYP1A2 ) and N- acetyltransferase 2 (NAT2). (bvsalud.org)
- Red wine consumption is inversely associated with 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine-DNA adduct levels in prostate. (cdc.gov)
- Pyridine is primarily released to the environment from industries that make and use this chemical. (cdc.gov)
- Pyridine (C5H5N) is a heterocyclic organic compound with a strong sour, putrid, and fish-like odor. (giiresearch.com)
- Pyridine is also an important pharmaceutical raw material. (tourismofrajasthan.com)
- Workers may be exposed in industries that make pyridine or use it to make other products by breathing it in air or by touching it. (cdc.gov)
- Besides this, the increasing usage of pyridine in the food and beverage (F&B) industry as a low-volume additive for flavoring products is offering lucrative growth opportunities to market players. (giiresearch.com)
- How can pyridine affect my health? (cdc.gov)
- For example, in the production of antihistamines and detoxification drugs, pyridine is used to absorb the chlorine produced. (tourismofrajasthan.com)
- How likely is pyridine to cause cancer? (cdc.gov)
- Headaches, giddiness, a desire to sleep, quickening of the pulse, and rapid breathing occurred in adults who breathed an unknown amount of pyridine for an unknown length of time. (cdc.gov)
- We do not know whether pyridine affects the ability of men and women to have children or whether it causes birth defects. (cdc.gov)
- These players are extensively investing in research and development (R&D) activities to produce pyridine with less toxicity, which is projected to strengthen the growth of the market. (giiresearch.com)
- In addition, pyridine is also used to produce propargyl and plant growth regulator. (tourismofrajasthan.com)
- The Food and Drug Administration (FDA) allows pyridine to be used as a flavoring agent in the preparation of foods. (cdc.gov)
- Mild skin irritation and eye irritation were seen in pyridine to be used as a flavoring agent in the preparation of rabbits when pyridine was placed on their skin or in their foods. (cdc.gov)
- People who live near hazardous waste sites or landfills where pyridine exists may be exposed to it by breathing contaminated air or by drinking contaminated water. (cdc.gov)
- Pyridine can also be o People who live near hazardous waste sites or landfills where pyridine exists may be exposed to it by breathing formed from the breakdown of many natural materials in the contaminated air or by drinking contaminated water. (cdc.gov)
- The global pyridine market size reached US$ 663.6 Million in 2022. (giiresearch.com)
- IMARC Group provides an analysis of the key trends in each sub-segment of the global pyridine market report, along with forecasts at the global and regional level from 2023-2028. (giiresearch.com)
- Pyridine N-Oxide holds the largest market share on account of its potential of reacting with both nucleophilic and electrophilic reagents. (giiresearch.com)
- However, it still remains a critical challenge to design and fabricate pyridine-containing block polymeric nano-assemblies in a large scale in aqueous media. (rsc.org)
- This facile strategy provides a new avenue to the scale-up preparation of smart and diversiform pyridine-containing polymer nanomaterials with potential applications in biomedicine. (rsc.org)
- Pyridine can also be formed from the breakdown of many natural materials in the environment. (cdc.gov)
- What happens to pyridine when it enters the environment? (cdc.gov)
- The EPA requires that discharges or accidental spills into the environment of 1,000 pounds or more of pyridine be reported. (cdc.gov)
- Pyridine-containing block copolymers are a special type of macromolecule, and they can self-assemble into highly-ordered nano-objects for a wide range of applications due to their multiple properties including hydrogen bond acceptance, pH sensitivity, facile functionalization and metal ion coordination. (rsc.org)