Molecular Docking Simulation
Synthesis of anacardic acids, 6-[8(Z),11(Z)-pentadecadienyl]salicylic acid and 6-[8(Z),11(Z),14-pentadecatrienyl]salicylic acid. (1/24)11-Chloro-3-methoxy-2-undecenal was synthesized from 8-bromooctanol, and an annelation reaction with this aldehyde and ethyl acetoacetate proceeded to give the ethyl 6-(8-chlorooctyl)salicylate. Ethyl 6-(8-chlorooctyl)salicylate was converted to ethyl 6-(7-formylheptyl)-2-methoxybenzoate through the iodide after protection of the phenolic hydroxyl group. Finally, the Wittig reaction with the aldehyde and triphenylphosphonium iodides in the presence of BuLi gave the methoxybenzoates, and then treatments of these methoxybenzoates with BBr3 in CH2Cl2 and 10% NaOH in ethanol gave 6-18(Z),11(Z)-pentadecadienyllsalicylic acid (anacardic acid 3) and 6-[8(Z),11(Z),14-pentadecatrienyl]salicylic acid (anacardic acid 4) which were isolated from plants of the anacardiaceae. (+info)
Anacardic acid-mediated changes in membrane potential and pH gradient across liposomal membranes. (2/24)We have previously shown that anacardic acid has an uncoupling effect on oxidative phosphorylation in rat liver mitochondria using succinate as a substrate (Life Sci. 66 (2000) 229-234). In the present study, for clarification of the physicochemical characteristics of anacardic acid, we used a cyanine dye (DiS-C3(5)) and 9-aminoacridine (9-AA) to determine changes of membrane potential (DeltaPsi) and pH difference (DeltapH), respectively, in a liposome suspension in response to the addition of anacardic acid to the suspension. The anacardic acid quenched DiS-C3(5) fluorescence at concentrations higher than 300 nM, with the degree of quenching being dependent on the log concentration of the acid. Furthermore, the K(+) diffusion potential generated by the addition of valinomycin to the suspension decreased for each increase in anacardic acid concentration used over 300 nM, but the sum of the anacardic acid- and valinomycin-mediated quenching was additively increasing. This indicates that the anacardic acid-mediated quenching was not due simply to increments in the K(+) permeability of the membrane. Addition of anacardic acid in the micromolar range to the liposomes with DeltaPsi formed by valinomycin-K(+) did not significantly alter 9-AA fluorescence, but unexpectedly dissipated DeltaPsi. The DeltaPsi preformed by valinomycin-K(+) decreased gradually following the addition of increasing concentrations of anacardic acid. The DeltaPsi dissipation rate was dependent on the pre-existing magnitude of DeltaPsi, and was correlated with the logarithmic concentration of anacardic acid. Furthermore, the initial rate of DeltapH dissipation increased with logarithmic increases in anacardic acid concentration. These results provide the evidence for a unique function of anacardic acid, dissimilar to carbonylcyanide p-trifluoromethoxyphenylhydrazone or valinomycin, in that anacardic acid behaves as both an electrogenic (negative) charge carrier driven by DeltaPsi, and a 'proton carrier' that dissipates the transmembrane proton gradient formed. (+info)
Small molecule modulators of histone acetyltransferase p300. (3/24)Histone acetyltransferases (HATs) are a group of enzymes that play a significant role in the regulation of gene expression. These enzymes covalently modify the N-terminal lysine residues of histones by the addition of acetyl groups from acetyl-CoA. Dysfunction of these enzymes is often associated with the manifestation of several diseases, predominantly cancer. Here we report that anacardic acid from cashew nut shell liquid is a potent inhibitor of p300 and p300/CBP-associated factor histone acetyltranferase activities. Although it does not affect DNA transcription, HAT-dependent transcription from a chromatin template was strongly inhibited by anacardic acid. Furthermore, we describe the design and synthesis of an amide derivative N-(4-chloro-3-trifluoromethyl-phenyl)-2-ethoxy-6-pentadecyl-benzamide (CTPB) using anacardic acid as a synthon, which remarkably activates p300 HAT activity but not that of p300/CBP-associated factor. Although CTPB does not affect DNA transcription, it enhances the p300 HAT-dependent transcriptional activation from in vitro assembled chromatin template. However, it has no effect on histone deacetylase activity. These compounds would be useful as biological switching molecules for probing into the role of p300 in transcriptional studies and may also be useful as new chemical entities for the development of anticancer drugs. (+info)
Characterization of xanthine oxidase inhibition by anacardic acids. (4/24)Anacardic acid, 6[8(Z), 11(Z), 14-pentadecatrienyl]salicylic acid, inhibits generation of superoxide radicals by xanthine oxidase. This inhibition does not follow a hyperbolic inhibition, depends on anacardic acid concentrations, but follows a sigmoidal inhibition. The inhibition was analyzed by using a Hill equation, and slope factor and EC(50) were 4.3+/-0.5 and 53.6+/-5.1 microM, respectively. In addition, anacardic acid inhibited uric acid formation by xanthine oxidase cooperatively. Slope factor and EC(50) were 1.7+/-0.5 and 162+/-10 microM, respectively. The results indicate that anacardic acid binds to allosteric sites near the xanthine-binding domain in xanthine oxidase. Salicylic acid moiety and alkenyl side chain in anacardic acid are associated with the cooperative inhibition and hydrophobic binding, respectively. (+info)
Inhibition of histone acetyltransferase activity by anacardic acid sensitizes tumor cells to ionizing radiation. (5/24)Histone acetyltransferases (HATs) regulate transcription, chromatin structure and DNA repair. Here, we utilized a novel HAT inhibitor, anacardic acid, to examine the role of HATs in the DNA damage response. Anacardic acid inhibits the Tip60 HAT in vitro, and blocks the Tip60-dependent activation of the ATM and DNA-PKcs protein kinases by DNA damage in vivo. Further, anacardic acid sensitizes human tumor cells to the cytotoxic effects of ionizing radiation. These results demonstrate a central role for HATs such as Tip60 in regulating the DNA damage response. HAT inhibitors provide a novel therapeutic approach for increasing the sensitivity of tumors to radiation therapy. (+info)
Characterization of novel inhibitors of histone acetyltransferases. (6/24)Modification of proteins by histone acetyltransferases (HAT) or histone deacetylases plays an important role in the control of gene expression, and its dysregulation has been linked to malignant transformation and other diseases. Although histone deacetylase inhibitors have been extensively studied and several are currently in clinical trials, there is little information available on inhibitors of HATs (HATi). Starting from the natural product lead HATi anacardic acid, a series of 28 analogues was synthesized and investigated for HAT-inhibitory properties and effects on cancer cell growth. The compounds inhibited up to 95% HAT activity in vitro, and there was a clear correlation between their inhibitory potency and cytotoxicity toward a broad panel of cancer cells. Interestingly, all tested compounds were relatively nontoxic to nonmalignant human cell lines. Western blot analysis of MCF7 breast carcinoma cells treated with HATi showed significant reduction in acetylation levels of histone H4. To directly show effect of the new compounds on HAT activity in vivo, MCF7 cells were cotransfected with the p21 promoter fused to firefly luciferase and a full-length p300 acetyltransferase, and luciferase activity was determined following treatment with HATi. Significant inhibition of p300 activity was detected after treatment with all tested compounds except one. Effects of the new HATi on protein acetylation and HAT activity in vivo make them a suitable tool for discovery of molecular targets of HATs and, potentially, for development of new anticancer therapeutics. (+info)
Anacardic acid (6-nonadecyl salicylic acid), an inhibitor of histone acetyltransferase, suppresses expression of nuclear factor-kappaB-regulated gene products involved in cell survival, proliferation, invasion, and inflammation through inhibition of the inhibitory subunit of nuclear factor-kappaBalpha kinase, leading to potentiation of apoptosis. (7/24)(+info)
Histone acetyltransferase inhibitor anacardic acid causes changes in global gene expression during in vitro Plasmodium falciparum development. (8/24)(+info)
CNV can cause vision loss and blindness if left untreated. It can also increase the risk of complications such as cataracts, glaucoma, and corneal ulcers.
There are several treatment options for CNV, including:
1. Anti-vascular endothelial growth factor (VEGF) injections: These medications can help reduce the growth of new blood vessels and preserve vision.
2. Photodynamic therapy: This involves the use of a light-sensitive medication and low-intensity laser to damage and shrink the new blood vessels.
3. Corneal transplantation: In severe cases, a corneal transplant may be necessary to replace the damaged or diseased cornea with a healthy one.
4. Surgical removal of the neovascularized tissue: This can be done through a surgical procedure called vitrectomy, where the new blood vessels are removed and the eye is filled with a gas or oil bubble.
Early detection and treatment of CNV are crucial to prevent vision loss and improve outcomes. Ophthalmologists use a range of diagnostic tests such as imaging studies and visual acuity assessments to diagnose and monitor the progression of the condition.
1. Causes: The immune system mistakenly identifies proteins in nuts as harmful, triggering the release of histamine and other chemicals that cause allergic symptoms.
2. Symptoms: Mild symptoms may include hives, itching, swelling, stomach cramps, diarrhea, and difficulty breathing. Severe reactions can lead to anaphylaxis, a life-threatening condition that requires immediate medical attention.
3. Common nut allergens: The most common allergenic proteins in nuts are from tree nuts (such as walnuts, almonds, and pecans) and peanuts.
4. Prevalence: Nut hypersensitivity is relatively rare but can be severe. According to Food Allergy Research & Education (FARE), around 1% of adults and 1.5% of children in the United States have a tree nut allergy, while peanut allergies affect about 1% of the population.
5. Diagnosis: A healthcare professional will typically conduct a physical examination, take a medical history, and perform diagnostic tests like skin prick testing or blood tests to confirm the presence of an immunoglobulin E (IgE) antibody response to nuts.
6. Treatment and management: The primary treatment for nut hypersensitivity is avoidance of nuts and products containing nuts. In severe cases, epinephrine injections may be necessary to treat anaphylaxis. Antihistamines, corticosteroids, and other medications may also be prescribed to manage symptoms.
7. Prognosis: While there is currently no cure for nut hypersensitivity, some individuals may outgrow their allergy over time. However, it's essential to maintain a strict avoidance diet to prevent accidental exposures and potentially life-threatening reactions.
8. Coexistence with other allergies: Nut allergies can coexist with other food allergies, such as peanut or soy allergies, or with non-food allergies like asthma or eczema. This increases the complexity of managing the condition and requires a comprehensive treatment plan.
9. Impact on quality of life: Nut hypersensitivity can have a significant impact on an individual's quality of life, affecting their social, emotional, and physical well-being. It can also limit their dietary choices and create anxiety about potential exposures.
10. Current research and future outlook: Ongoing research into the immunological mechanisms of nut allergies may lead to the development of novel treatments or prevention strategies. Additionally, there is hope for the development of a nut-specific immunotherapy, which could help desensitize individuals with nut allergies and potentially cure the condition.
List of phytochemicals in food
List of MeSH codes (D02)
The Inhibitory Effects of Anacardic Acid on Hepatitis C Virus Life Cycle | PLOS ONE
Anacardic Acid Inhibits the Catalytic Activity of Matrix Metalloproteinase-2 and Matrix Metalloproteinase-9 | Molecular...
Anacardic acid supplier | CAS 16611-84-0 | Focus Biomolecules
Natural Product Anacardic Acid from Cashew Nut Shells Stimulates Neutrophil Extracellular Trap Production and Bactericidal...
Small molecule modulators of histone acetyltransferase p300 - PubMed
Postoperative pain-from mechanisms to treatment : PAIN Reports
Pediatric Rhabdomyosarcoma - PubMed
Synthesis and Antimicrobial Activity of New Schiff Base Compounds Containing 2-Hydroxy-4-pentadecylbenzaldehyde Moiety
ALT cancer cells are specifically sensitive to lysine acetyl transferase inhibition | Oncotarget
Ehrlichia chaffeensis exploits host SUMOylation pathways to mediate effector-host interactions and promote intracellular...
MESH TREE NUMBER CHANGES - 2013 MeSH. August 27, 2012
NIOSHTIC-2 Search Results - Full View
Find Research outputs - Augusta University Research Profiles
Science.NaturalNews.com - Conduct powerful scientific research in mere seconds for your book, blog, website article or news...
Inhibition of histone acetylation by curcumin reduces alcohol-induced fetal cardiac apoptosis | Journal of Biomedical Science |...
Fresh Mangoes-6 pieces-Standard Shipping included. - GreatPlentifulShopUSA
NDF-RT Code NDF-RT Name
International Science & Engineering Fair - ACS Community
Division of AIDS Anti-HIV/OI/TB Therapeutics Database - Surveillance Memo
How does the farm-to-market process affect nutrition? When fruit is picked, how it's stored affects quality, nutrients
The Performance and Characterization of Polymeric Inclusion Membranes (PIMs) Containing 2-Nitro Phenyl Octyl Ether as...
Low Cell ChIP-Seq Optimization Module - Maximize Limited Samples
- Cardanol is a phenolic lipid obtained from anacardic acid, the main component of cashew nutshell liquid (CNSL), a byproduct of cashew nut processing. (kumarasamyindustries.com)
- 1H-NMR results showed anacardic acid as the main component of the extracts. (bvsalud.org)
- RESULTS: We report here the surprising observation that treatment of a human bronchial epithelial cell line, BEAS-2B cells, with the inhibitor histone deacetylase, trichostatin A, or the histone acetyltransferase inhibitor, anacardic acid, strongly inhibited induction of both IL-6 and IL-8 protein upon stimulation with organic dust. (cdc.gov)
- A group of 6-alkyl SALICYLIC ACIDS that are found in ANACARDIUM and known for causing CONTACT DERMATITIS . (nih.gov)
- 1. Genotoxic and cytostatic effects of 6-pentadecyl salicylic anacardic acid in transformed cell lines and peripheral blood mononuclear cells. (nih.gov)
- 6. Anacardic 6-pentadecyl salicylic acid induces apoptosis in breast cancer tumor cells, immunostimulation in the host and decreases blood toxic effects of taxol in an animal model. (nih.gov)