Bongkrekic Acid
Atractyloside
Mitochondrial ADP, ATP Translocases
A class of nucleotide translocases found abundantly in mitochondria that function as integral components of the inner mitochondrial membrane. They facilitate the exchange of ADP and ATP between the cytosol and the mitochondria, thereby linking the subcellular compartments of ATP production to those of ATP utilization.
Burkholderia gladioli
Mitochondria
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
Mitochondrial Swelling
Mitochondrial Membrane Transport Proteins
Oligomycins
A closely related group of toxic substances elaborated by various strains of Streptomyces. They are 26-membered macrolides with lactone moieties and double bonds and inhibit various ATPases, causing uncoupling of phosphorylation from mitochondrial respiration. Used as tools in cytochemistry. Some specific oligomycins are RUTAMYCIN, peliomycin, and botrycidin (formerly venturicidin X).
Intracellular Membranes
Permeability
Cyclosporine
Caspase 9
A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Caspase 9 is activated during cell stress by mitochondria-derived proapoptotic factors and by CARD SIGNALING ADAPTOR PROTEINS such as APOPTOTIC PROTEASE-ACTIVATING FACTOR 1. It activates APOPTOSIS by cleaving and activating EFFECTOR CASPASES.
Cytochrome c Group
Membrane Potentials
The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).
Apoptosis
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Caspases
A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.
Adenosine Triphosphate
Mitochondria, Liver
Mitochondria in hepatocytes. As in all mitochondria, there are an outer membrane and an inner membrane, together creating two separate mitochondrial compartments: the internal matrix space and a much narrower intermembrane space. In the liver mitochondrion, an estimated 67% of the total mitochondrial proteins is located in the matrix. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p343-4)
Adenosine Diphosphate
Caspase 3
Proto-Oncogene Proteins c-bcl-2
Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
Induction of apoptosis by valinomycin: mitochondrial permeability transition causes intracellular acidification. (1/100)
In order to determine whether disruption of mitochondrial function could trigger apoptosis in murine haematopoietic cells, we used the potassium ionophore valinomycin. Valinomycin induces apoptosis in the murine pre-B cell line BAF3, which cannot be inhibited by interleukin-3 addition or Bcl-2 over-expression. Valinomycin triggers rapid loss of mitochondrial membrane potential. This precedes cytoplasmic acidification, which leads to cysteine-active-site protease activation, DNA fragmentation and cell death. Bongkrekic acid, an inhibitor of the mitochondrial permeability transition, prevents acidification and subsequent induction of apoptosis by valinomycin. (+info)Death signals from the B cell antigen receptor target mitochondria, activating necrotic and apoptotic death cascades in a murine B cell line, WEHI-231. (2/100)
B cell antigen receptor (BCR)-mediated cell death has been proposed as a mechanism for purging the immune repertoire of anti-self specificities during B cell differentiation in bone marrow. Mitochondrial alterations and activation of caspases are required for certain aspects of apoptotic cell death, but how the mitochondria and caspases contribute to BCR-mediated cell death is not well understood. In the present study, we used the mouse WEHI-231 B cell line to demonstrate that mitochondrial alterations and activation of caspases are indeed participants in BCR-mediated cell death. The peptide inhibitor of caspases, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk), blocked cleavage of poly(ADP-ribose) polymerase and various manifestation of nuclear apoptosis such as nuclear fragmentation, hypodiploidy and DNA fragmentation, indicating that signals from the BCR induced the activation of caspases. In addition, z-VAD-fmk delayed apoptosis-associated changes in cellular reduction-oxidation potentials as determined by hypergeneration of superoxide anion, as well as exposure of phosphatidylserine residues in the outer plasma membrane. By contrast, although z-VAD-fmk retarded cytolysis, it was incapable of preventing disruption of the plasma membrane even under the same condition in which it completely blocked nuclear apoptosis. Mitochondrial membrane potential loss was also not blocked by z-VAD-fmk. Bongkrekic acid, a specific inhibitor of mitochondrial permeability transition pores, suppressed not only the mitochondrial membrane potential but also the change of plasma membrane permeability. Overexpression of Bcl-xL prevented mitochondrial dysfunction, nuclear apoptosis and membrane permeability cell death triggered by BCR signal transduction. These observations indicate that death signals from BCR may first cause mitochondrial alterations followed by activation of both necrotic and apoptotic cascades. (+info)Over-expression of Bcl-2 does not protect cells from hypericin photo-induced mitochondrial membrane depolarization, but delays subsequent events in the apoptotic pathway. (3/100)
Hypericin (HY) is a powerful photo-inducer of apoptosis in Jurkat cells as measured by caspase-3 activation, cell shrinkage, phosphatidylserine (PS) exposure and the appearance of hypoploid DNA. These processes are preceded by rapid Bcl-2-independent mitochondrial transmembrane depolarization and a drop in cytoplasmic pH. Pre-incubation of cells with inhibitors of the mitochondrial permeability transition pore, such as cyclosporin A or bongkrekic acid, does not protect cells from mitochondrial membrane potential (deltapsim) decrease. However, monitoring of mitochondrial entrapped calcein by confocal fluorescence imaging gives clear evidence of HY photo-induced mitochondrial permeability. This should be considered as the result of a non-specific alteration of mitochondrial membrane integrity brought about by lipid peroxidation. Nevertheless, synthesis of the anti-apoptotic protein Bcl-2 appears to delay the subsequent time course of PS exposure and to reduce caspase-3 activation and the fraction of cells which become hypoploid. We interpret this partially protective effect as the consequence of a direct interaction of Bcl-2 with cytosolic cytochrome c previously released from mitochondria upon deltapsim decrease and/or of Bcl-2 inhibition of the deleterious retro-effect of caspase-3 on the mitochondrial permeability transition pore and/or the mitochondrial membrane components. (+info)Antibody evidence for different conformational states of ADP, ATP translocator protein isolated from mitochondria. (4/100)
Consistent with the previously proposed reorientation mechanism for the ADP,ATP translocator protein of mitochondria, evidence has now been obtained for the existence of two distinct conformational states of the isolated translocator protein. Previous studies indicated that when the mitochondrial translocator protein is in the c-state(i.e., when its binding site faces the cytosol side) the protein binds primarily the ligand carboxyatractylate (CAT), and when the translocator protein is in the m-state(i.e., when its binding site faces the mitochondrial matrix) the translocator protein binds primarily bongkrekate. Direct evidence for this formulation has now come from the application of antibodies to the isolated translocator protein-ligand complex. Two antibodies were produced against the ADP,ATP translocator protein isolated from beef heart mitochondria. One antibody, which was produced against the protein isolated as the CAT-binding protein complex, was found to be highly specific for that complex and did not react with the protein in the conformation state conferred by the bongkrekate ligand. This antibody did not cover the CAT-binding site, as evidenced by the exchange of unlabeled CAT with [35S]CAT bound to the translocator protein. However, the same antibody inhibited a transition of the protein from the c-state to the m-state, as evidenced by an inhibition of the displacement of[35S]CAT by bongkrekate (added jointly with ADP). It appears, therefore, that the antibody immobilized the translocator protein in the c-state. The second antibody produced against the (somewhat less pure) ADP,ATP translocator protein, isolated as the bongkrekate-binding protein complex, did not react with the CAT-binding protein. Thus, the second antibody appeared to be specific for the translocator protein in the m-state. Neither antibody inhibited mitochondrial ADP,ATP transport. (+info)Mitochondrial and extramitochondrial apoptotic signaling pathways in cerebrocortical neurons. (5/100)
In cultured cerebrocortical neurons, mild excitotoxic insults or staurosporine result in apoptosis. We show here that N-methyl-d-aspartate (NMDA) receptor-mediated, but not staurosporine-mediated, apoptosis is preceded by depolarization of the mitochondrial membrane potential (Deltapsi(m)) and ATP loss. Both insults, however, release cytochrome c (Cyt c) into the cytoplasm. What prompts mitochondria to release Cyt c and the mechanism of release are as yet unknown. We examined the effect of inhibition of the adenine nucleotide translocator (ANT), a putative component of the mitochondrial permeability transition pore. Inhibition of the mitochondrial ANT with bongkrekic acid (BA) prevented NMDA receptor-mediated apoptosis of cerebrocortical neurons. Concomitantly, BA prevented Deltapsi(m) depolarization, promoted recovery of cellular ATP content, and blocked caspase-3 activation. However, in the presence of BA, Cyt c was still released. Because BA prevented NMDA-induced caspase-3 activation and apoptosis, the presence of Cyt c in the neuronal cytoplasm is not sufficient for the induction of caspase activity or apoptosis. In contrast to these findings, BA was ineffective in preventing staurosporine-induced activation of caspases or apoptosis. Additionally, staurosporine-induced, but not NMDA-induced, apoptosis was associated with activation of caspase-8. These results indicate that, in cerebrocortical cultures, excessive NMDA receptor activation precipitates neuronal apoptosis by means of mitochondrial dysfunction, whereas staurosporine utilizes a distinct pathway. (+info)Mitochondrial amplification of death signals determines thymidine kinase/ganciclovir-triggered activation of apoptosis. (6/100)
Previous clinical experience shows that the efficacy of suicide gene transfer in tumor therapy is limited, resulting from inefficient gene transfer or alternatively, from intrinsic resistance of the tumor in vivo. Herpes simplex virus thymidine kinase/ganciclovir (TK/GCV), a paradigmatic suicide gene therapy system, has been described to exert its cytotoxic effect, at least in part, by inducing apoptosis in target cells. Here, we report that mitochondria amplify TK/GCV-induced apoptosis by regulating p53 accumulation and the effector phase of apoptosis. Treatment with TK/GCV led to mitochondrial perturbations including loss of the mitochondrial membrane potential and release of cytochrome c from mitochondria into the cytosol, inducing caspase activation and nuclear fragmentation. Inhibition of TK/GCV-induced mitochondrial perturbations by Bcl-2 overexpression or by the mitochondrion-specific inhibitor bongkrekic acid also strongly inhibited TK/GCV-induced activation of caspases and apoptosis. TK/GCV-induced mitochondrial perturbations depended on caspase activity possibly initiated by death receptor signaling. Perturbation of mitochondrial function mediated accumulation of wild-type p53 protein, since Bcl-2 overexpression, bongkrekic acid, or inhibition of mitochondrial protein synthesis with chloramphenicol strongly reduced TK/GCV-induced accumulation of wild-type p53 protein. These findings suggest that TK/GCV therapy may be less efficient in tumors in which the mitochondrial amplification of TK/GCV-induced apoptosis is blocked, e.g., by Bcl-2 overexpression. Given the low efficacy of currently used gene therapy systems, our data on molecular mechanisms that regulate sensitivity or resistance toward TK/GCV-induced cytotoxicity might have important implications to improve the clinical application of suicide gene therapy. (+info)BNIP3 and genetic control of necrosis-like cell death through the mitochondrial permeability transition pore. (7/100)
Many apoptotic signaling pathways are directed to mitochondria, where they initiate the release of apoptogenic proteins and open the proposed mitochondrial permeability transition (PT) pore that ultimately results in the activation of the caspase proteases responsible for cell disassembly. BNIP3 (formerly NIP3) is a member of the Bcl-2 family that is expressed in mitochondria and induces apoptosis without a functional BH3 domain. We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. Surprisingly, BNIP3-mediated cell death is independent of Apaf-1, caspase activation, cytochrome c release, and nuclear translocation of apoptosis-inducing factor. However, cells transfected with BNIP3 exhibit early plasma membrane permeability, mitochondrial damage, extensive cytoplasmic vacuolation, and mitochondrial autophagy, yielding a morphotype that is typical of necrosis. These changes were accompanied by rapid and profound mitochondrial dysfunction characterized by opening of the mitochondrial PT pore, proton electrochemical gradient (Deltapsim) suppression, and increased reactive oxygen species production. The PT pore inhibitors cyclosporin A and bongkrekic acid blocked mitochondrial dysregulation and cell death. We propose that BNIP3 is a gene that mediates a necrosis-like cell death through PT pore opening and mitochondrial dysfunction. (+info)Bcl-2 independence of flavopiridol-induced apoptosis. Mitochondrial depolarization in the absence of cytochrome c release. (8/100)
The new chemotherapeutic agent, flavopiridol, presently in clinical trials, has been extensively studied yet little is known about its mechanism of action. In this study we show that the induction of apoptosis by flavopiridol is largely independent of Bcl-2. This is indicated by the observation that neither overexpression nor the antisense oligonucleotide-mediated down-regulation of Bcl-2 had any effect on flavopiridol-induced cell killing. Our results suggest that flavopiridol can induce apoptosis through different pathways of caspase activation with caspase 8 playing a pivotal role. In human lung carcinoma cells, which contain high levels of endogenous Bcl-2 and lack procaspase 8, flavopiridol treatment leads to mitochondrial depolarization in the absence of cytochrome c release, followed by the activation of caspase 3 and cell death. These results clearly differ from observations made with other anti-tumor drugs and might explain, at least in part, the unusual anti-tumor properties of flavopiridol. (+info)
Bongkrek acid
... (also known as bongkrekic acid) is a respiratory toxin produced in fermented coconut or corn contaminated by the ... The structure of bongkrekic acid bound to ADP/ATP translocase was solved in 2019, demonstrating that it binds to the substrate ... Garcia, R. A.; Hotchkiss, J. H.; Steinkraus, K. H. (1999). "The Effect of Lipids on Bongkrekic (Bongkrek) Acid Toxin Production ... Henderson, P. J. F.; Lardy, H. A. (1970). "Bongkrekic Acid: An Inhibitor of Adenine Nucleotide Translocase of Mitochondria" ( ...
Desulfonylation reactions
Shindo, Mitsuru; Sugioka, Tomoyuki; Umaba, Yuko; Shishido, Kozo (2004). "Total synthesis of (+)-bongkrekic acid". Tetrahedron ... Carboxylic acid derivatives, acetals, thioacetals, amines, alcohols, and isolated double bonds are all inert to Al/Hg. ... Protonation of the organotin intermediates thus formed (by sulfinic acid generated in situ) leads to reduced products. Addition ... Total synthesis of (±)-subergorgic acid". Tetrahedron Letters. 31 (38): 5429. doi:10.1016/S0040-4039(00)97864-X. Vedejs, E.; ...
Carboxyatractyloside
... behavior resembles bongkrekic acid while in the mitochondria. Carboxyatractyloside is poisonous to humans ... Carboxylic acids, Plant toxins, Sulfate esters, All stub articles, Organic compound stubs, Biochemistry stubs). ...
Burkholderia gladioli
Subík J, Behún M (April 1974). "Effect of bongkrekic acid on growth and metabolism of filamentous fungi". Archiv für ... B. gladioli is able to more acids than is typical for its genus. B. gladioli has been identified as a plant pathogen in onions ... One pathovariety, growing on coconut pulp, produces the respiratory toxin bongkrek acid which can cause fatal poisoning in ... Contaminated tempe bongkrèk can contain lethal amounts of highly toxic bongkrek acid and toxoflavin.[citation needed] B. ...
Mitochondrial carrier
Another inhibitor, bongkrekic acid, is believed to stabilize a second conformation, with the pit facing the matrix. In this ... Mitochondrial carriers transport amino acids, keto acids, nucleotides, inorganic ions and co-factors through the mitochondrial ... inhibited by bongkrekic acid, in which the substrate binding site is accessible to the mitochondrial matrix, i.e. the fungal ... amino acids, keto acids and cofactors across the membrane. Such proteins include: ADP/ATP carrier protein (ADP-ATP translocase ...
List of food contamination incidents
2020 - In Jixi city, China nine people died after eating homemade fermented corn noodles contaminated with bongkrekic acid. ... 2008 - In Italy, it was discovered that additives included substances like sulfuric acid and hydrochloric acid had been used to ... The first documented bongkrekic acid poisoning in Africa". Clinical Infectious Diseases. 66 (9): 1400-1406. doi:10.1093/cid/ ... Beer served at a funeral in Mozambique was contaminated with bongkrekic acid, resulting in 75 deaths and more than 230 people ...
January 9
17 April 2018). "Description of a Mass Poisoning in a Rural District in Mozambique: The First Documented Bongkrekic Acid ...
Mitochondrial permeability transition pore
... bongkrekic acid and alisporivir (also known as Debio-025). TRO40303 is a newly synthetitised MPT blocker developed by Trophos ... Other factors that increase the likelihood that the MPTP will be induced include the presence of certain fatty acids, and ...
Mozambique funeral beer poisoning
... bongkrekic acid and toxoflavin, in both the beer and the corn flour that was used to help brew it, and concluded that these ... The First Documented Bongkrekic Acid Poisoning in Africa" (PDF). Clinical Infectious Diseases. 66 (9): 1400-1406. doi:10.1093/ ... which had been contaminated with the bacterium Burkholderia gladioli which produced the toxic compound bongkrekic acid. Early ... Nyazema, N. Z. (June 1985). "Crocodile (Crocodylus niloticus) bile acids and arrow poisons". Central African Journal of ...
Adenine nucleotide translocator
In contrast, the second family, which includes bongkrekic acid (BA) and isobongkrekic acid (isoBA), binds the translocase from ... or in the matrix state by the inhibitor bongkrekic acid. Rare but severe diseases such as mitochondrial myopathies are ... or in the matrix state by the inhibitor bongkrekic acid. In 1955, Siekevitz and Potter demonstrated that adenine nucleotides ... Aquila H, Misra D, Eulitz M, Klingenberg M (March 1982). "Complete amino acid sequence of the ADP/ATP carrier from beef heart ...
List of MeSH codes (D02)
2-aminoadipic acid MeSH D02.241.081.337.052.250 - dimethyl adipimidate MeSH D02.241.081.337.075 - bongkrekic acid MeSH D02.241. ... quinic acid MeSH D02.241.511.852 - shikimic acid MeSH D02.241.511.902 - sugar acids MeSH D02.241.511.902.107 - ascorbic acid ... edetic acid MeSH D02.241.081.038.455 - egtazic acid MeSH D02.241.081.038.581 - iodoacetic acid MeSH D02.241.081.038.581.400 - ... hexuronic acids MeSH D02.241.081.844.915.400.500 - iduronic acid MeSH D02.241.081.901.177 - aconitic acid MeSH D02.241.081.901. ...
C28H38O7
The molecular formula C28H38O7 (molar mass: 486.60 g/mol, exact mass: 486.2618 u) may refer to: Bongkrek acid, or bongkrekic ... acid Andrastin A This set index page lists chemical structure articles associated with the same molecular formula. If an ...
Bongkrekic Acid-a Review of a Lesser-Known Mitochondrial Toxin - PubMed
Bongkrekic acid is a mitochondrial ANT toxin and is reported primarily in outbreaks of food-borne poisoning involving coconut ... Bongkrekic acid is a heat-stable, highly unsaturated tricarboxylic fatty acid with a molecular weight of 486 kDa. Outbreaks ... Bongkrekic Acid-a Review of a Lesser-Known Mitochondrial Toxin Mehruba Anwar 1 , Amelia Kasper 2 , Alaina R Steck 3 , Joshua G ... Bongkrekic Acid-a Review of a Lesser-Known Mitochondrial Toxin Mehruba Anwar et al. J Med Toxicol. 2017 Jun. ...
Fatal 3-Nitropropionic Acid Poisoning after Consuming Coconut Water - Volume 27, Number 1-January 2021 - Emerging Infectious...
... which has developed a method for the detection of bongkrekic acid (5,6). However, neither bongkrekic acid nor the isomer ... Bongkrekic acid-a review of a lesser-known mitochondrial toxin. J Med Toxicol. 2017;13:173-9. DOIPubMedGoogle Scholar ... The symptoms of 3-NPA toxicity in humans are similar to those for bongkrekic acid, as described regarding sugar cane poisoning ... Identification of the potent toxin bongkrekic acid in a traditional African beverage linked to a fatal outbreak. Forensic Sci ...
Science Clips - Volume 9, Issue 48, December 5, 2017
Toxic levels of bongkrekic acid (BA) were detected in the suspect pombe but not in the control pombe. Burkholderia gladioli ... Description of a mass poisoning in a rural district in Mozambique: The first documented bongkrekic acid poisoning in Africa ... and nucleic acid-based carbapenemase detection tests that identify carbapenemase activity directly or their associated ...
Biomarkers Search
MeSH Browser
Bongkrekic Acid Preferred Term Term UI T005356. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1975). ... Carboxylic Acids [D02.241] * Acids, Acyclic [D02.241.081] * Dicarboxylic Acids [D02.241.081.337] * Adipates [D02.241.081.337. ... Bongkrekic Acid Preferred Concept UI. M0002799. Registry Number. 11076-19-0. Scope Note. An antibiotic produced by Pseudomonas ... Bongkrekic Acid. Tree Number(s). D02.241.081.337.075. Unique ID. D001865. RDF Unique Identifier. http://id.nlm.nih.gov/mesh/ ...
MeSH Browser
Bongkrekic Acid Preferred Term Term UI T005356. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1975). ... Carboxylic Acids [D02.241] * Acids, Acyclic [D02.241.081] * Dicarboxylic Acids [D02.241.081.337] * Adipates [D02.241.081.337. ... Bongkrekic Acid Preferred Concept UI. M0002799. Registry Number. 11076-19-0. Scope Note. An antibiotic produced by Pseudomonas ... Bongkrekic Acid. Tree Number(s). D02.241.081.337.075. Unique ID. D001865. RDF Unique Identifier. http://id.nlm.nih.gov/mesh/ ...
Fatal 3-Nitropropionic Acid Poisoning after Consuming Coconut Water - Volume 27, Number 1-January 2021 - Emerging Infectious...
... which has developed a method for the detection of bongkrekic acid (5,6). However, neither bongkrekic acid nor the isomer ... Bongkrekic acid-a review of a lesser-known mitochondrial toxin. J Med Toxicol. 2017;13:173-9. DOIPubMedGoogle Scholar ... The symptoms of 3-NPA toxicity in humans are similar to those for bongkrekic acid, as described regarding sugar cane poisoning ... Identification of the potent toxin bongkrekic acid in a traditional African beverage linked to a fatal outbreak. Forensic Sci ...
Pesquisa | Portal Regional da BVS
Foodborne bongkrekic acid (BA) poisoning is a fatal foodborne disease in China. From 2010-2020, a total of 19 BA poisoning ... Epidemiology of foodborne bongkrekic acid poisoning outbreaks in China, 2010 to 2020. ... The prohibition of traditional processed homemade fermented corn flour products and improvement in bongkrekic acid poisoning ...
ABORTIFACIENT AGENTS ABORTIFACIENT AGENTS
ANTI-INFECTIVE AGENTS BONGKREKIC ACID ANTI-INFECTIVE AGENTS BREFELDIN A ANTI-INFECTIVE AGENTS BROMODEOXYURIDINE ANTI-INFECTIVE ... EXCITATORY AMINO ACID AGENTS IBOGAINE EXCITATORY AMINO ACID AGENTS IBOTENIC ACID EXCITATORY AMINO ACID AGENTS KAINIC ACID ... EXCITATORY AMINO ACID AGONISTS IBOTENIC ACID EXCITATORY AMINO ACID AGONISTS KAINIC ACID EXCITATORY AMINO ACID AGONISTS N- ... FOLIC ACID ANTAGONISTS DAPSONE FOLIC ACID ANTAGONISTS FOLIC ACID ANTAGONISTS FOLIC ACID ANTAGONISTS METHOTREXATE FOLIC ACID ...
Uncouplers of oxidative phosphorylation. | Environmental Health Perspectives | Vol. 87, No.
Synthesis and evaluation of simplified functionalized bongkrekic acid analogs, Tetrahedron, 10.1016/j.tet.2018.01.018, 74:9, ( ... Bongkrekic Acid Analogue, Lacking One of the Carboxylic Groups of its Parent Compound, Shows Moderate but pH-insensitive ... Chen S, Dobrovolsky V, Liu F, Wu Y, Zhang Z, Mei N and Guo L (2014) The Role of Autophagy in Usnic Acid-Induced Toxicity in ... Gupta R, Hemansi , Gautam S, Shukla R and Kuhad R (2017) Study of charcoal detoxification of acid hydrolysate from corncob and ...
DeCS
Bongkrekic Acid [D02.241.081.337.075] Bongkrekic Acid * Fumarates [D02.241.081.337.302] Fumarates ... Derivatives of malonic acid (the structural formula CH2(COOH)2), including its salts and esters. ... Derivatives of malonic acid (the structural formula CH2(COOH)2), including its salts and esters.. ...
DeCS
Bongkrekic Acid [D02.241.081.337.075] Bongkrekic Acid * Fumarates [D02.241.081.337.302] Fumarates ... Derivatives of adipic acid. Included under this heading are a broad variety of acid forms, salts, esters, and amides that ... Derivatives of adipic acid. Included under this heading are a broad variety of acid forms, salts, esters, and amides that ... Acids, Adipic. Acids, Hexanedioic. Adipic Acids. Hexanedioic Acids. Tree number(s):. D02.241.081.337.052. ...
µ
... bone tuberculosis bone wax bone wire bone wires bonfire bonfires bong bongkrekate bongkrekates bongkrekic acid bongkrekic acids ... acid radical acid radicals acid reaction acid reactions acid-resistance acid-resistant acidrine acids acid salt acid salts acid ... acid-base equilibria acid-base equilibrium acid bath acid baths acidbinding acid binding acid-binding acid cell acid cells acid ... acid fast acid-fast acid fast bacilli acid-fast bacilli acid fast bacillus acid-fast bacillus acidfastness acid fastness acid- ...
NDF-RT Code NDF-RT Name
Bongkrekic Acid N0000010078 borage oil N0000166854 Boranes N0000007027 Borates N0000007157 boric acid N0000008066 Boric Acids ... Neutral N0000006806 Amino Acids N0000011372 Amino Acids, Acidic N0000011248 Amino Acids, Aromatic N0000011332 Amino Acids, ... Acyclic N0000008269 Acids, Aldehydic N0000007628 Acids, Carbocyclic N0000007629 Acids, Heterocyclic N0000007630 Acids, ... Amino Acid Isomerases N0000167825 Amino Acid Oxidoreductases N0000169801 Amino Acid Transport System A N0000169803 Amino Acid ...
Esters1
- Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain a 1,6-carboxy terminated aliphatic structure. (bvsalud.org)
Salts2
- Derivatives of malonic acid (the structural formula CH2(COOH)2), including its salts and esters. (bvsalud.org)
- Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain a 1,6-carboxy terminated aliphatic structure. (bvsalud.org)