Bromobenzenes
Puerto Rico
Soil
Public Health
Questionnaires
Inhibition of glutathione synthesis with propargylglycine enhances N-acetylmethionine protection and methylation in bromobenzene-treated Syrian hamsters. (1/69)
The finding that liver necrosis caused by the environmental glutathione (GSH)-depleting chemical, bromobenzene (BB) is associated with marked impairment in O- and S-methylation of BB metabolites in Syrian hamsters raises questions concerning the role of methyl deficiency in BB toxicity. N-Acetylmethionine (NAM) has proven to be an effective antidote against BB toxicity when given after liver GSH has been depleted extensively. The mechanism of protection by NAM may occur via a replacement of methyl donor and/or via an increase of GSH synthesis. If replacement of the methyl donor is an important process, then blocking the resynthesis of GSH in the methyl-repleted hamsters should not decrease NAM protection. This hypothesis was examined in this study. Propargylglycine (PPG), an irreversible inhibitor of cystathionase, was used to inhibit the utilization of NAM for GSH resynthesis. Two groups of hamsters were pretreated with an intraperitoneal (ip) dose of PPG (30 mg/kg) or saline 24 h before BB administration (800 mg/kg, ip). At 5 h after BB treatment, an ip dose of NAM (1200 mg/kg) was given. Light microscopic examinations of liver sections obtained 24 h after BB treatment indicated that NAM provided better protection (P < 0.05) in the PPG + BB + NAM group than in the BB + NAM group. Liver GSH content, however, was lower in the PPG + BB + NAM group than in the BB + NAM group. The Syrian hamster has a limited capability to N-deacetylated NAM. The substitution of NAM with methionine (Met; 450 mg/kg) resulted in a higher level of GSH in the BB + Met group than in the BB + NAM group (P < 0.05). The enhanced protection by PPG in the PPG + BB + NAM group was accompanied by higher (P < 0.05) urinary excretions of specificO- and S-methylated bromothiocatechols than in the BB + NAM group. The results suggest that NAM protection occurs primarily via a replacement of the methyl donor and that methyl deficiency occurring in response to GSH repletion plays a potential role in BB toxicity. (+info)The role of biotransformation in chemical-induced liver injury. (2/69)
The role of drug metabolism in chemical-induced liver injury is reviewed. Parameters for studying the formation of chemically reactive metabolites are discussed and the factors that alter the formation and covalent binding of reactive metabolites are selectively emphasized. Some of the experimental work that led to these concepts is discussed, especially the chemical toxicology of the hepatic injury produced by acetaminophen, bromobenzene, furosemide, isoniazid and iproniazid. (+info)Hepatoprotection by dimethyl sulfoxide. I. Protection when given twenty-four hours after chloroform or bromobenzene. (3/69)
Dimethyl sulfoxide (DMSO) has previously been reported to protect against hepatotoxicity resulting from chloroform (CHCl3) or bromobenzene (BB) when given 10 hr after the toxicant. The object of these studies was to further demonstrate the latent protective ability of DMSO by administering it at a much later time (24 hr) following toxicant exposure. In addition, a more detailed evaluation of the lesions was performed to better characterize the lesion progression and resolution. Male Sprague-Dawley rats received a hepatotoxic oral dose of either CHCl3 (1.0 ml/kg) or BB (0.5 ml/kg) and then received 2 ml/kg DMSO intraperitoneally 24 hr later. With both toxicants, limited centrilobular lesions were already present by the time DMSO was administered. Without treatment, liver injury rapidly progressed so that by 48 hr it occupied 40-50% of the liver, with accompanying large increases in plasma alanine aminotransferase (ALT) activity. Administration of DMSO greatly attenuated lesion development for both toxicants; the area injured was reduced by more than 4-fold, accompanied by a decrease in 48 hr ALT activity of 8-16-fold. The ability of DMSO to intervene in the development of liver injury at such a late time appears to be unique and may provide insight into therapies for acute xenobiotic-induced hepatitis. (+info)Nuclear localization of biliverdin reductase in the rat kidney: response to nephrotoxins that induce heme oxygenase-1. (4/69)
Biliverdin reductase catalyzes the reduction of biliverdin, the product of heme oxygenase (HO) activity, to bilirubin. The reductase is unique among all enzymes characterized to date in being dual pH/cofactor-dependent. Until now the enzyme was assumed to be a noninducible cytosolic protein. This report, for the first time, demonstrates induction and nuclear localization of reductase in rat kidney in response to HO-1 inducers: bacterial lipopolysaccharide (LPS) and bromobenzene. The study also demonstrates that nuclear localization requires an intact nuclear localization signal and is responsive to cGMP. Specifically 16 h after treatment of rats (i.p.) with LPS (5 mg/kg), there was an increase in nuclear biliverdin reductase as determined by immunostaining, Western blotting, and activity analysis. Induction and nuclear localization of the reductase in kidney was also observed in bromobenzene-treated rats (2 mmol/kg, s.c., 24 h). The reductase message levels, however, were not increased in response to either treatment, suggesting post-transcriptional activation of the reductase by LPS and bromobenzene. The mechanism of nuclear transport of the reductase was examined using HeLa cells transfected with the hemagglutinin-tagged reductase construct. When cells were treated with 8-Br-cGMP the protein translocated into the nucleus. Mutation of the putative nuclear localization signal domain of the reductase blocked nuclear transport of the protein. We suggest the significance of nuclear localization of the reductase may relate to: 1) chain-breaking antioxidant activity of bilirubin; 2) inhibition of superoxide formation by bilirubin; and 3) modulation of the signal transduction pathways. (+info)Unique gene expression patterns in liver and kidney associated with exposure to chemical toxicants. (5/69)
DNA arrays containing 260 unique genes involved in phase I and II metabolism, heat shock, DNA repair, inflammation, transcription, and housekeeping were used to examine gene expression patterns in liver and kidney in response to five classes of chemicals (polyaromatic hydrocarbons: benzo(a)pyrene, 3-methylcholanthrene; DNA alkylators: dimethylnitrosamine, ethylnitrosourea; peroxisome proliferators: diethylhexylphthalate, clofibrate; heavy metals: CdCl(2), HgCl(2); and oxidative stressors: CCl(4), bromobenzene). Time course experiments in mice were carried out in both tissues for each chemical and dose-response studies were used to further evaluate several of these chemicals. Each pair of chemicals yielded a similar pattern of gene expression distinct from the other four classes of chemicals. Both peroxisome proliferators up-regulated Cyp4a10, acyl-CoA thioesterase, and insulin-like growth factor binding protein-1, whereas the DNA alkylators altered the expression of monokine induced by gamma-interferon, the metallothioneins, p21, and several acute phase proteins. For each of the five classes of chemicals tested, several genes that were induced or repressed were common in each chemical exposure, whereas other genes were unique for that specific class of compound. Both time and dose are important factors in differentiating between chemical classes. Likewise, comparison of changes in messenger RNA expression between the kidney and liver of treated animals indicates that gene arrays may be useful in determining the comparative toxicity of chemicals in various tissues but that exposure to uncharacterized chemicals will have to be monitored in several tissues. (+info)Alpha-glutathione S-transferase in the assessment of hepatotoxicity--its diagnostic utility in comparison with other recognized markers in the Wistar Han rat. (6/69)
The diagnostic utility of alpha-glutathione S-transferase (alphaGST) in the assessment of acute hepatotoxicity was compared with a range of markers including alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Rats were given a single oral dose of either alpha-naphthylisothiocynate (AN IT), bromobenzene (BrB). or thioacetamide (TAM) at concentrations previously shown to induce marked hepatotoxicity. The progression of each hepatic lesion was monitored by the measurement of a battery of markers, including alphaGST, in plasma collected at time points ranging from 3 h to 7 days after dosing. alphaGST was seen to increase significantly at 24 h (ANIT/BrB) and 3 h (TAM) postdosing, corresponding with histopathological findings. For each compound, when the degree of insult was most severe, fold increases in alphaGST were greater than those seen with ALT and AST, yet lower than those seen with glutamate dehydrogenase (BrB and ANIT). sorbitol dehydrogenase (TAM), or total bilirubin and bile acids (ANIT). Elevations in alphaGST were also detected no earlier than any other marker. AlphaGST in the rat was shown to be a valid marker of hepatotoxicity; however, its measurement offered no additional information in detecting either the time of onset/recovery or the severity of each type of hepatic injury induced. (+info)Enhancing effect of zinc on hepatoprotectivity of epigallocatechin gallate in isolated rat hepatocytes. (7/69)
The influence of metal ions (Fe2+, Cu2+, Zn2+) on the hepatoprotective activity of epigallocatechin gallate (EGCG) against hepatotoxin-induced cell injury was investigated. Primary cultures of rat hepatocytes were treated with a well-known hepatotoxin, bromobenzene (BB), in the presence of EGCG only or EGCG plus each metal ion. After 24 h, 0.02 mM EGCG did not show protective activity on the cultured hepatocytes. In contrast, the hepatocytes were protected against BB in the presence of 0.02 mM EGCG and 0.02 mM zinc. The addition of only zinc could not protect hepatocytes against BB. These results suggest that the formation of the zinc-EGCG complex is very important in the enhancement of the hepatoprotective activity of EGCG. The complexation of EGCG with zinc was confirmed by UV-VIS absorption spectroscopy. (+info)Effect of non-steroidal anti-inflammatory ophthalmic solution on intraocular pressure reduction by latanoprost. (8/69)
AIM: To investigate the effects of a non-steroidal anti-inflammatory drug (NSAID) ophthalmic solution on latanoprost induced intraocular pressure (IOP) reduction using normal volunteers. METHODS: This study was conducted as a prospective and observer masked clinical trial. 13 normal volunteers were enrolled. After measurement of basal IOP and ophthalmic examination, latanoprost ophthalmic solution was initially administered to both eyes once daily. Four weeks later, an NSAID ophthalmic solution, sodium 2-amino-3-(4-bromobenzoyl) phenylacetate sesquihydrate (refer to bromfenac sodium hydrate), was co-administered to one randomly selected eye (NSAID group) twice daily for 2 weeks. The other eye was employed as a control (non-NSAID group). After withdrawal of the NSAID ophthalmic solution, latanoprost ophthalmic solution was continuously administered for another 2 weeks and was then withdrawn. After a 4 week washout, only bromfenac sodium hydrate ophthalmic solution was administered to the eyes of the NSAID group for 2 weeks. During the study period, ophthalmic examination, including IOP measurement was performed in an observer masked fashion. RESULTS: Before initiation of bromfenac sodium hydrate, baseline IOPs of the non-NSAID group and the NSAID group were 15.73 (SD 1.97) mm Hg and 15.86 (2.06) mm Hg, respectively (p=0.88). Although latanoprost ophthalmic solution significantly reduced IOP in both groups, co-administration of bromfenac sodium hydrate significantly inhibited latanoprost induced IOP reduction compared with the non-NSAID group. The IOPs of the non-NSAID and NSAID groups were 10.18 (1.17) mm Hg and 11.63 (1.35) mm Hg with a 2 week co-administration, respectively (p <0.01). Withdrawal of bromfenac sodium hydrate ophthalmic solution diminished the difference between the two groups. Re-administration of bromfenac sodium ophthalmic solution only did not affect IOP. CONCLUSION: These results indicate that NSAID ophthalmic solution may interfere with IOP reduction by latanoprost ophthalmic solution in normal volunteers and that we should take this into account when treating patients with glaucoma using latanoprost ophthalmic solution. (+info)Bromobenzenes are a group of chemical compounds that consist of a benzene ring (a cyclic structure with six carbon atoms and alternating double bonds) substituted with one or more bromine atoms. The simplest and most common member of this group is bromobenzene itself, which contains a single bromine atom attached to a benzene ring.
Other members of the bromobenzenes family include dibromobenzene (with two bromine atoms), tribromobenzene (with three bromine atoms), and tetrabromobenzene (with four bromine atoms). These compounds are used in various industrial applications, such as in the production of flame retardants, dyes, pharmaceuticals, and agrochemicals.
It is important to note that bromobenzenes can be harmful or toxic to humans and other organisms, and should be handled with care. Exposure to high levels of these compounds can cause a range of health effects, including irritation of the skin, eyes, and respiratory tract, headaches, dizziness, nausea, and damage to the liver and kidneys.
I'm sorry for any confusion, but "Puerto Rico" is not a medical term. It is a territorial possession of the United States, located in the northeastern Caribbean Sea. It includes the main island of Puerto Rico and various smaller islands. If you have any questions about a medical topic, please provide more details so I can try to help answer your question.
I'm sorry for any confusion, but "soil" is not a term that has a medical definition. Soil is defined as the top layer of earth in which plants grow, a mixture of organic material, clay, sand, and silt. If you have any questions related to medicine or health, I would be happy to try to help answer them for you.
I believe there may be some confusion in your question as "translations" is not a term that has a specific medical definition. However, if you are referring to the process of "translation" in the context of medicine and biomedical research, it refers to the process of converting scientific findings or medical information from one language to another, while maintaining accuracy, clarity, and the original meaning. This is particularly important in the field of international clinical trials, medical publications, and cross-cultural healthcare communication.
If you meant something different by 'translations', please provide more context so I can give a more accurate response.
Public health is defined by the World Health Organization (WHO) as "the art and science of preventing disease, prolonging life and promoting human health through organized efforts of society." It focuses on improving the health and well-being of entire communities, populations, and societies, rather than individual patients. This is achieved through various strategies, including education, prevention, surveillance of diseases, and promotion of healthy behaviors and environments. Public health also addresses broader determinants of health, such as access to healthcare, housing, food, and income, which have a significant impact on the overall health of populations.
In the context of medicine, "translating" often refers to the process of turning basic scientific discoveries into clinical applications that can directly benefit patients. This is also known as "translational research." It involves taking findings from laboratory studies and experiments, and finding ways to use that knowledge in the development of new diagnostic tools, treatments, or medical practices.
The goal of translation is to bridge the gap between scientific discovery and clinical practice, making sure that new advances in medicine are both safe and effective for patients. This process can be complex and challenging, as it requires collaboration between researchers, clinicians, regulatory agencies, and industry partners. It also involves rigorous testing and evaluation to ensure that any new treatments or interventions are both safe and effective.
A questionnaire in the medical context is a standardized, systematic, and structured tool used to gather information from individuals regarding their symptoms, medical history, lifestyle, or other health-related factors. It typically consists of a series of written questions that can be either self-administered or administered by an interviewer. Questionnaires are widely used in various areas of healthcare, including clinical research, epidemiological studies, patient care, and health services evaluation to collect data that can inform diagnosis, treatment planning, and population health management. They provide a consistent and organized method for obtaining information from large groups or individual patients, helping to ensure accurate and comprehensive data collection while minimizing bias and variability in the information gathered.
Hispanic Americans, also known as Latino Americans, are individuals in the United States who are of Spanish-speaking origin or whose ancestors came from Spain, Mexico, Cuba, the Caribbean, Central and South America. This group includes various cultures, races, and nationalities. It is important to note that "Hispanic" refers to a cultural and linguistic affiliation rather than a racial category. Therefore, Hispanic Americans can be of any race, including White, Black, Asian, Native American, or mixed races.
Bromobenzene
Cyanation
Iodobenzene
Double bond rule
Metal-halogen exchange
Pentaphenylantimony
Chlorobenzene
Dibromophenols
Chelidonine
2,4-Dibromophenol
Bromotoluene
George Samuel Hurst
Owen Webster
Rodney S. Ruoff
Phenylmagnesium bromide
Benzoic acid
Aryl halide
Pentaphenylphosphorus
Ether
NanoPutian
Electrophilic aromatic directing groups
Diphenylmercury
Phenylsodium
Bis(2-ethylhexyl)tetrabromophthalate
List of MeSH codes (D02)
Mesityl bromide
Tetrabromonickelate
Benzothiophene
Benzhydryl compounds
Frustrated Lewis pair
Bromobenzene - Wikipedia
Explain 1-bromobenzene without using a grignard reaction
Bromobenzene
organic chemistry - Why is bromobenzene more stable than benzene? - Chemistry Stack Exchange
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Solubility Differences of Halocarbon Isomers in Ionic Liquid [emim][Tf2N] | Journal of Chemical & Engineering Data
Bromine2
- Bromobenzene is prepared by the action of bromine on benzene in the presence of Lewis acid catalysts such as aluminium chloride or ferric bromide. (wikipedia.org)
- I understand that due to resonance in bromine to benzene in bromobenzene increase the stability but such an enormous amount of energy can't only be dealt by resonance. (stackexchange.com)
Benzene2
- Why is bromobenzene more stable than benzene? (stackexchange.com)
- Benzene is 45 kJ/mol more energetic than bromobenzene. (stackexchange.com)
C6H5Br1
- Bromobenzene is an aryl halide, C6H5Br. (wikipedia.org)
Reaction2
- How would you prepare methyl,phenyl,ketone starting with 1-bromobenzene without using a grignard reaction. (expertsmind.com)
- In this lab, a Grignard reagent will be prepared through the reaction of magnesium turnings and bromobenzene. (ipl.org)
Spectrum1
- Inelastic Neutron Scattering spectrum of Bromobenzene, C₆H₅Br, measured on the TFXA instrument. (stfc.ac.uk)
Manufacture2
- Bromobenzene is used as a precursor in the manufacture of phencyclidine. (wikipedia.org)
- The investigation into Hubbard began in October 2019 when authorities learned of a shipment of four drums of bromobenzene from China to a beauty supply company that he owned, said Mrozek, adding that bromobenzene has a number of applications, including being used to manufacture PCP. (nbclosangeles.com)
F3441
- 6 - 48-Hour Evaluation of the Toxicity (C20410) of Bromobenzene (108-86-1) in F344/N Rats Exposed via Gavage. (nih.gov)
Phenyl1
- Bromobenzene is used to introduce a phenyl group into other compounds. (wikipedia.org)
Glutathione1
- Two-dimensional J-resolved nuclear magnetic resonance spectral study of two bromobenzene glutathione conjugates. (nih.gov)
Reagent1
- The labelled version of Bromobenzene, used as a general reagent in palladium-catalyzed reactions and in the synthesis of Grignard reagents. (clearsynthcdmo.com)
Rats1
- The application of two-dimensional J-resolved nuclear magnetic resonance spectroscopy to determine the structure of two bile metabolites isolated from rats injected interperitoneally with bromobenzene is described. (nih.gov)
Vivo1
- Accordingly, the severity of liver necrosis has been compared with the formation of metabolites of bromobenzene and with covalent binding of metabolites in vivo and in vitro after various pretreatment regimens that alter hepatotoxicity. (karger.com)
Liver1
- Bromobenzene-Induced Liver Necrosis. (karger.com)
Formula1
- The molecular formula, chemical abstracts service number, registry of toxic effects of chemical substances number, production figures and economic trends, uses, and producer and user data are given for bromobenzene (108861) and polybrominated-biphenyls without the number information. (cdc.gov)
Data1
- These data provide direct kinetic evidence that 3,4-bromobenzene oxide is the reactive hepatotoxic metabolite. (karger.com)
Manufacturer1
- Longshen is the Bromobenzene manufacturer of China. (hzpdfum.cn)
Study1
- An overview of Genetic Toxicology Mammalian Cell Cytogenetics study conclusions related to Bromobenzene (108-86-1). (nih.gov)