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Journal articles on the topic 'Atractyloside'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Kedrov, Alexej, Alex M. Hellawell, Adam Klosin, R. Bill Broadhurst, Edmund R. S. Kunji, and Daniel J. Müller. "Probing the Interactions of Carboxy-atractyloside and Atractyloside with the Yeast Mitochondrial ADP/ATP Carrier." Structure 18, no. 1 (2010): 39–46. http://dx.doi.org/10.1016/j.str.2009.11.009.

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2

Nikles, S., H. Heuberger, E. Hilsdorf, and R. Bauer. "Impact of processing on the content of carboxy-atractyloside and atractyloside in Xanthii fructus (Cang‘erzi)." European Journal of Integrative Medicine 6, no. 1 (2014): 130. http://dx.doi.org/10.1016/j.eujim.2013.12.012.

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3

Bach, P. "Atractyloside (ATR) Cytotoxicity in Renal Cells." Toxicology Letters 78 (August 1995): 63. http://dx.doi.org/10.1016/03784-2749(59)4875h-.

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4

Obatomi, D., and P. H. Bach. "Atractyloside (ATR) cytotoxicity in renal Cells." Toxicology Letters 78 (August 1995): 63. http://dx.doi.org/10.1016/0378-4274(95)94876-i.

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5

Sanchez, Jean-Frédéric, Brice Kauffmann, Axelle Grélard, et al. "Unambiguous structure of atractyloside and carboxyatractyloside." Bioorganic & Medicinal Chemistry Letters 22, no. 8 (2012): 2973–75. http://dx.doi.org/10.1016/j.bmcl.2012.02.040.

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6

Lemoine, Sandrine, Lan Zhu, Gallic Beauchef та ін. "Role of 70-kDa Ribosomal Protein S6 Kinase, Nitric Oxide Synthase, Glycogen Synthase Kinase-3β, and Mitochondrial Permeability Transition Pore in Desflurane-induced Postconditioning in Isolated Human Right Atria". Anesthesiology 112, № 6 (2010): 1355–63. http://dx.doi.org/10.1097/aln.0b013e3181d74f39.

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Background Desflurane during early reperfusion has been shown to postcondition human myocardium. Whether it involves "reperfusion injury salvage kinase" pathway remains incompletely studied. The authors tested the involvement of 70-kDa ribosomal protein S6 kinase, nitric oxide synthase, glycogen synthase kinase (GSK)-3beta, and mitochondrial permeability transition pore in desflurane-induced postconditioning. Methods The authors recorded isometric contraction of human right atrial trabeculae suspended in an oxygenated Tyrode's solution (34 degrees C, stimulation frequency 1 Hz). After a 30-min

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7

Obatomi, D. K., and P. H. Bach. "Biochemistry and Toxicology of the Diterpenoid Glycoside Atractyloside." Food and Chemical Toxicology 36, no. 4 (1998): 335–46. http://dx.doi.org/10.1016/s0278-6915(98)00002-7.

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8

Sanchez, Jean-Frederic, Brice Kauffmann, Axelle Grelard, et al. "ChemInform Abstract: Unambiguous Structure of Atractyloside and Carboxyatractyloside." ChemInform 43, no. 35 (2012): no. http://dx.doi.org/10.1002/chin.201235212.

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9

Stewart, Michael J., and Vanessa Steenkamp. "The Biochemistry and Toxicity of Atractyloside: A Review." Therapeutic Drug Monitoring 22, no. 6 (2000): 641–49. http://dx.doi.org/10.1097/00007691-200012000-00001.

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10

Steenkamp, V., M. J. Stewart, and M. Zuckerman. "Detection of poisoning by Impila (Callilepis laureola) in a mother and child." Human & Experimental Toxicology 18, no. 10 (1999): 594–97. http://dx.doi.org/10.1191/096032799678839428.

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Poisoning with impila (Callilepis laureola) is a recurring phenomenon in South Africa. Cases of poisoning with other plants which contain atractyloside also occur in Europe and the Americas. Since poisoning leads to rapid death from renal and/or hepatic failure, it is suspected that many cases are undiagnosed; this is especially so in South Africa, where patients may die without reaching hospital and do not often admit to ingestion of a traditional remedy. We have developed a thin layer chromatographic method for the detection of impila constituents in urine. We describe the clinical symptoms

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11

Feng, Jianhua, Eliana Lucchinetti, Preeti Ahuja, Thomas Pasch, Jean-Claude Perriard та Michael Zaugg. "Isoflurane Postconditioning Prevents Opening of the Mitochondrial Permeability Transition Pore through Inhibition of Glycogen Synthase Kinase 3β". Anesthesiology 103, № 5 (2005): 987–95. http://dx.doi.org/10.1097/00000542-200511000-00013.

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Background Postischemic administration of volatile anesthetics activates reperfusion injury salvage kinases and decreases myocardial damage. However, the mechanisms underlying anesthetic postconditioning are unclear. Methods Isolated perfused rat hearts were exposed to 40 min of ischemia followed by 1 h of reperfusion. Anesthetic postconditioning was induced by 15 min of 2.1 vol% isoflurane (1.5 minimum alveolar concentration) administered at the onset of reperfusion. In some experiments, atractyloside (10 microm), a mitochondrial permeability transition pore (mPTP) opener, and LY294002 (15 mi

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12

Chávez, Edmundo, and Alvaro Osornio. "Temperature dependence of the atractyloside-induced mitochondrial Ca2+ release." International Journal of Biochemistry 20, no. 7 (1988): 731–36. http://dx.doi.org/10.1016/0020-711x(88)90169-3.

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13

Fowlds, D. L., M. T. Smith, and J. van Staden. "Atractyloside and carboxyatractyloside: A study of possible growth regulatory functions." South African Journal of Botany 56, no. 5 (1990): 520–24. http://dx.doi.org/10.1016/s0254-6299(16)31018-3.

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14

Obatomi, David K., and P. H. Bach. "Calpain-I inhibitor protect renal cortical slices exposed to atractyloside." Toxicology Letters 95 (July 1998): 170. http://dx.doi.org/10.1016/s0378-4274(98)80680-2.

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15

Asimakis, G. K., and V. R. Conti. "Phosphate-induced efflux of adenine nucleotides from heart mitochondria." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 5 (1985): H1009—H1016. http://dx.doi.org/10.1152/ajpheart.1985.249.5.h1009.

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Adenine nucleotide efflux from isolated rat heart mitochondria was studied. Inorganic phosphate induced efflux of adenine nucleotides from the mitochondria. This efflux was inhibited by carboxyatractyloside and atractyloside. The rate of efflux showed saturation kinetics with respect to extramitochondrial phosphate (Km, 9.5 mM). Lowering the pH from 7.4 to 6.8 had little or no effect on the rate of efflux. Deenergizing the mitochondria enhanced carboxyatractyloside-insensitive efflux, but it did not affect carboxyatractyloside-sensitive efflux. Extramitochondrial ATP (200 microM) or AMP (200 m

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16

Chen, Liang-Yu, Anren Hu, and Chih-Jui Chang. "The Degradation Mechanism of Toxic Atractyloside in Herbal Medicines by Decoction." Molecules 18, no. 2 (2013): 2018–28. http://dx.doi.org/10.3390/molecules18022018.

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17

Dehrmann, F. M., S. N. Bye, and M. F. Dutton. "The isolation of a storage organelle of atractyloside in Callilepis laureola." Journal of Ethnopharmacology 34, no. 2-3 (1991): 247–51. http://dx.doi.org/10.1016/0378-8741(91)90043-d.

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18

Steenkamp, P. A., N. M. Harding, F. R. van Heerden, and B. E. van Wyk. "Identification of atractyloside by LC–ESI–MS in alleged herbal poisonings." Forensic Science International 163, no. 1-2 (2006): 81–92. http://dx.doi.org/10.1016/j.forsciint.2005.11.010.

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19

Bye, S. N., T. H. T. Coetzer, and M. F. Dutton. "An enzyme immunoassay for atractyloside, the nephrotoxin of Callilepis laureola (Impila)." Toxicon 28, no. 8 (1990): 997–1000. http://dx.doi.org/10.1016/0041-0101(90)90030-b.

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20

Qi, Lu, Fuyao Song, Yue Han, Ying Zhang, and Yanqing Ding. "Atractyloside targets cancer-associated fibroblasts and inhibits the metastasis of colon cancer." Annals of Translational Medicine 8, no. 21 (2020): 1443. http://dx.doi.org/10.21037/atm-20-1531.

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21

Vancompernolle, Katia, Franky Van Herreweghe, Gwenda Pynaert, et al. "Atractyloside-induced release of cathepsin B, a protease with caspase-processing activity." FEBS Letters 438, no. 3 (1998): 150–58. http://dx.doi.org/10.1016/s0014-5793(98)01275-7.

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22

Obatomi, David K., N. T. K. Thanh, and T. H. Bach. "Differences in atractyloside-induced lipid changes in precision-cut rat renal slices." Toxicology Letters 95 (July 1998): 170. http://dx.doi.org/10.1016/s0378-4274(98)80679-6.

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23

Kephalas, T., F. Alikaridis, K. Pantelia, and D. Papadakis. "Production of carboxyatractyloside and atractyloside by cell suspension cultures of Atractylis gummifera." Phytochemistry 51, no. 1 (1999): 53–54. http://dx.doi.org/10.1016/s0031-9422(98)00710-9.

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24

Song, Rui, Huining Bian, Xuliang Huang, and Ke-seng Zhao. "Atractyloside induces low contractile reaction of arteriolar smooth muscle through mitochondrial damage." Journal of Applied Toxicology 32, no. 6 (2011): 402–8. http://dx.doi.org/10.1002/jat.1688.

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25

Song, Rui, Huining Bian, Xuliang Huang, and Ke-seng Zhao. "Atractyloside induces low contractile reaction of arteriolar smooth muscle through mitochondrial damage." Journal of Applied Toxicology 33, no. 10 (2013): 1192. http://dx.doi.org/10.1002/jat.2915.

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26

THANH, NGUYÊÑ T. K., DAVID K. OBATOMI, and PETER H. BACH. "Lipid profiling in renal and hepatic tissue slices following exposure to atractyloside." Biochemical Society Transactions 25, no. 1 (1997): 35S. http://dx.doi.org/10.1042/bst025035s.

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27

Strasberg, Paula. "Cerebrosides and psychosine disrupt mitochondrial functions." Biochemistry and Cell Biology 64, no. 5 (1986): 485–89. http://dx.doi.org/10.1139/o86-067.

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Glucocerebroside and galactocerebroside increased the respiratory rate of liver and brain mitochondria by 33–400% and produced an average 30% decrease in oxidative phosphorylation. Psychosine stimulated mitochondrial respiration 66–700%. At concentrations over 100 μg/mg mitochondrial protein, oxidative phosphorylation was completely inhibited. Atractyloside did not prevent the rspiratory stimulation. Ca2+ transport was blocked and addition of ATP could not overcome this inhibition. The possible deleterious effect of glycosphingolipids on the conformation of the mitochondrial membrane and cellu

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28

Xu, Shizhao, Xiaojie Qi, Yuqiang Liu, et al. "UPLC-MS/MS of Atractylenolide I, Atractylenolide II, Atractylenolide III, and Atractyloside A in Rat Plasma after Oral Administration of Raw and Wheat Bran-Processed Atractylodis Rhizoma." Molecules 23, no. 12 (2018): 3234. http://dx.doi.org/10.3390/molecules23123234.

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Atractylodis Rhizoma is the dried rhizome of Atractylodes lancea (Thunb.) DC. or Atractylodes chinensis (DC.) Koidz and is often processed by stir-frying with wheat bran to reduce its dryness and increase its spleen tonifying activity. However, the mechanism by which the processing has this effect remains unknown. To explain the mechanism based on the pharmacokinetics of the active compounds, a rapid, sensitive ultra-performance liquid chromatography-tandem mass spectrometry method was developed to analyze atractylenolides I, II, and III, and atractyloside A simultaneously in rat plasma after

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29

McKee, Edward E., Alice T. Bentley, Ronald M. Smith, Jonathan R. Kraas, and Christina E. Ciaccio. "Guanine nucleotide transport by atractyloside-sensitive and -insensitive carriers in isolated heart mitochondria." American Journal of Physiology-Cell Physiology 279, no. 6 (2000): C1870—C1879. http://dx.doi.org/10.1152/ajpcell.2000.279.6.c1870.

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In previous work (McKee EE, Bentley AT, Smith RM Jr, and Ciaccio CE, Biochem Biophys Res Commun 257: 466–472, 1999), the transport of guanine nucleotides into the matrix of intact isolated heart mitochondria was demonstrated. In this study, the time course and mechanisms of guanine nucleotide transport are characterized. Two distinct mechanisms of transport were found to be capable of moving guanine nucleotides across the inner membrane. The first carrier was saturable, displayed temperature dependence, preferred GDP to GTP, and did not transport GMP or IMP. When incubated in the absence of ex

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30

Brucoli, Federico, Maria T. Borrello, Paul Stapleton, Gary N. Parkinson, and Simon Gibbons. "Structural Characterization and Antimicrobial Evaluation of Atractyloside, Atractyligenin, and 15-Didehydroatractyligenin Methyl Ester." Journal of Natural Products 75, no. 6 (2012): 1070–75. http://dx.doi.org/10.1021/np300080w.

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31

Warnette-Hammond, M. E., and H. A. Lardy. "Catecholamine and vasopressin stimulation of gluconeogenesis from dihydroxyacetone in the presence of atractyloside." Journal of Biological Chemistry 260, no. 23 (1985): 12647–52. http://dx.doi.org/10.1016/s0021-9258(17)38920-2.

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32

Kunji, Edmund R. S., and Marilyn Harding. "Projection Structure of the Atractyloside-inhibited Mitochondrial ADP/ATP Carrier of Saccharomyces cerevisiae." Journal of Biological Chemistry 278, no. 39 (2003): 36985–88. http://dx.doi.org/10.1074/jbc.c300304200.

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33

Calmes, M., F. Crespin, C. Maillard, E. Ollivier, and G. Balansard. "High-performance liquid chromatographic determination of atractyloside and carboxyatractyloside from Atractylis gummifera L." Journal of Chromatography A 663, no. 1 (1994): 119–22. http://dx.doi.org/10.1016/0021-9673(94)80503-2.

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34

Malekova, Lubica, Viera Kominkova, Miroslav Ferko, et al. "Bongkrekic acid and atractyloside inhibits chloride channels from mitochondrial membranes of rat heart." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1767, no. 1 (2007): 31–44. http://dx.doi.org/10.1016/j.bbabio.2006.10.004.

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35

Jang, Youngho, Jinkun Xi, Huihua Wang, Robert A. Mueller, Edward A. Norfleet та Zhelong Xu. "Postconditioning Prevents Reperfusion Injury by Activating δ-Opioid Receptors". Anesthesiology 108, № 2 (2008): 243–50. http://dx.doi.org/10.1097/01.anes.0000299437.93898.4a.

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Background While postconditioning has been proposed to protect the heart by targeting the mitochondrial permeability transition pore (mPTP), the detailed mechanism underlying this action is unknown. The authors hypothesized that postconditioning stimulates opioid receptors, which in turn protect the heart from reperfusion injury by targeting the mPTP. Methods Rat hearts (both in vivo and in vitro) were subjected to 30 min of ischemia and 2 h of reperfusion. Postconditioning was elicited by six cycles of 10-s reperfusion and 10-s ischemia. To measure nitric oxide concentration, cardiomyocytes l

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36

McAllister, Sandra E., Homa Ashrafpour, Neil Cahoon, et al. "Postconditioning for salvage of ischemic skeletal muscle from reperfusion injury: efficacy and mechanism." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 2 (2008): R681—R689. http://dx.doi.org/10.1152/ajpregu.90303.2008.

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We tested our hypothesis that postischemic conditioning (PostC) is effective in salvage of ischemic skeletal muscle from reperfusion injury and the mechanism involves inhibition of opening of the mitochondrial permeability transition pore (mPTP). In bilateral 8 × 13 cm pig latissimus dorsi muscle flaps subjected to 4 h ischemia, muscle infarction increased from 22 ± 4 to 41 ± 1% between 2 and 24 h reperfusion and remained unchanged at 48 (38 ± 6%) and 72 (40 ± 1%) h reperfusion ( P < 0.05; n = 4 pigs). PostC induced by four cycles of 30-s reperfusion/reocclusion at the onset of reperfusion

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37

Penna, Claudia, Fabio Settanni, Francesca Tullio, et al. "GH-Releasing Hormone Induces Cardioprotection in Isolated Male Rat Heart via Activation of RISK and SAFE Pathways." Endocrinology 154, no. 4 (2013): 1624–35. http://dx.doi.org/10.1210/en.2012-2064.

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Abstract GHRH stimulates GH synthesis and release from the pituitary and exerts direct effects in extrapituitary tissues. We have previously shown that pretreatment with GHRH reduces cardiomyocyte apoptosis and improves heart function in isolated rat hearts subjected to ischemia/reperfusion (I/R). Here, we determined whether GHRH given at reperfusion reduces myocardial reperfusion injury and investigated the molecular mechanisms involved in GHRH effects. Isolated rat hearts subjected to I/R were treated at the onset of reperfusion with: 1) GHRH; 2) GHRH+GHRH antagonist JV-1-36; 3) GHRH+mitocho

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38

Zhang, Shi-zhong, Ning-fu Wang, Jian Xu та ін. "κ-Opioid Receptors Mediate Cardioprotection by Remote Preconditioning". Anesthesiology 105, № 3 (2006): 550–56. http://dx.doi.org/10.1097/00000542-200609000-00019.

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Background Remote preconditioning is known to be cardioprotective, but the exact mechanism has not been fully elucidated. The objective of the current study was to investigate the role of kappa-opioid receptors in cardioprotection by remote preconditioning and reveal possible underlying mechanisms. Methods Remote preconditioning was induced in anesthetized male Sprague-Dawley rats by three cycles of 5 min of right femoral artery occlusion followed by 5 min of reperfusion. Myocardial ischemia-reperfusion was achieved by ligation of the left anterior descending coronary artery for 30 min and the

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39

Lemoine, Sandrine, Stéphane Allouche, Laurent Coulbault, et al. "Mechanisms Involved in Cardioprotective Effects of Pravastatin Administered during Reoxygenation in Human Myocardium In Vitro." Anesthesiology 116, no. 4 (2012): 824–33. http://dx.doi.org/10.1097/aln.0b013e31824be77c.

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Background The authors investigated the effect of pravastatin during reoxygenation after myocardial hypoxia and examined the involvement of nitric oxide synthase, mitochondrial permeability transition pore, and expression of markers of apoptosis in human myocardium in vitro. Methods Human atrial trabeculae were exposed to hypoxia for 30 min and reoxygenation for 60 min (control group; n = 10). Pravastatin (5, 10, 50, 75 μM; n = 6 in each group) was administered throughout the reoxygenation. In separate groups (n = 6 in each group), pravastatin 50 μM was administered in the presence of 200 μM L

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40

Laurens, J. B., L. C. Bekker, V. Steenkamp, and M. J. Stewart. "Gas chromatographic–mass spectrometric confirmation of atractyloside in a patient poisoned with Callilepis laureola." Journal of Chromatography B: Biomedical Sciences and Applications 765, no. 2 (2001): 127–33. http://dx.doi.org/10.1016/s0378-4347(01)00410-8.

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41

Gao, Qin, Hong-Yang Pan, Shuang Qiu, et al. "Atractyloside and 5-hydroxydecanoate block the protective effect of puerarin in isolated rat heart." Life Sciences 79, no. 3 (2006): 217–24. http://dx.doi.org/10.1016/j.lfs.2005.12.040.

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42

Obatomi, David K., Stephen Brant, Vethanayagam Anthonypillai, and Peter H. Bach. "Toxicity of Atractyloside in Precision-Cut Rat and Porcine Renal and Hepatic Tissue Slices." Toxicology and Applied Pharmacology 148, no. 1 (1998): 35–45. http://dx.doi.org/10.1006/taap.1997.8316.

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43

Yang, Liu, Lulu Chen, Shunjun Xu, Xing Zeng, Yi Feng, and Peishan Xie. "RRLC-MS/MS method for the quantitation of atractyloside in Fructus Xanthii (Xanthium sibiricum)." Analytical Methods 5, no. 8 (2013): 2093. http://dx.doi.org/10.1039/c3ay26610a.

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44

Stewart, M. J., V. Steenkamp, S. Van der merwe, M. Zuckerman, and N. J. Crowther. "The cytotoxic effects of a traditional Zulu remedy, impila (Callilepis laureola)." Human & Experimental Toxicology 21, no. 12 (2002): 643–47. http://dx.doi.org/10.1191/0960327102ht309oa.

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The traditional Zulu remedy impila (Callilepis laureola) can cause acute fatal hepatocellular necrosis, especially in children. We investigated the mechanism(s) of toxicity using HuH-7 hepatocytes. Impila tubers were extracted with boiling water and the aqueous extract was used at different concentrations to study the effects on the morphology of the cells. Flow cytometry and labelling with fluorescent antibodies to tubulin were also used. At high concentrations, necrosis occurred; however, at lower concentrations, the extracts gave rise to a variety of changes including hypercondensation of c

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45

Obatomi, David K., and Peter H. Bach. "Inhibition of mitochondrial respiration and oxygen uptake in isolated rat renal tubular fragments by atractyloside." Toxicology Letters 89, no. 2 (1996): 155–61. http://dx.doi.org/10.1016/s0378-4274(96)03799-x.

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46

Larabi, Islam Amine, Mohamed Azzouz, Rania Abtroun, Mohamed Reggabi, and Bachra Alamir. "Déterminations des teneurs en atractyloside dans les racines d’Atractylis gummifera L.provenant de six régions d’Algérie." Annales de Toxicologie Analytique 24, no. 2 (2012): 81–86. http://dx.doi.org/10.1051/ata/2012009.

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47

Roux, Pierre, Agnès Le Saux, Christelle Fiore, et al. "Fluorometric Titration of the Mitochondrial ADP/ATP Carrier Protein in Muscle Homogenate with Atractyloside Derivatives." Analytical Biochemistry 234, no. 1 (1996): 31–37. http://dx.doi.org/10.1006/abio.1996.0046.

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48

Lemoine, Sandrine, Lan Zhu, Damien Legallois, Massimo Massetti, Alain Manrique та Jean-Luc Hanouz. "Atorvastatin-induced Cardioprotection of Human Myocardium Is Mediated by the Inhibition of Mitochondrial Permeability Transition Pore Opening via Tumor Necrosis Factor-α and Janus Kinase/Signal Transducers and Activators of Transcription Pathway". Anesthesiology 118, № 6 (2013): 1373–84. http://dx.doi.org/10.1097/aln.0b013e31828a7039.

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Abstract Background: The role of tumor necrosis factor-α (TNF-α), Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, and mitochondrial Permeability Transition Pore in atorvastatin-induced cardioprotection were examined in human myocardium, in vitro. Methods: Isometric force of contraction of human right atrial trabeculae was recorded during 30-min hypoxia and 60-min reoxygenation (control) and in the presence of atorvastatin (0.1 µm, 1 µm, 10 µm). In early reoxygenation, the TNF-α inhibitor, AG490 (inhibitor of JAK/STAT), or atractyloside (mitochondrial Permeab

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49

Obatomi, David K., Nguyen T. K. Thanh, Stephen Brant, and Peter H. Bach. "The toxic mechanism and metabolic effects of atractyloside in precision-cut pig kidney and liver slices." Archives of Toxicology 72, no. 8 (1998): 524–30. http://dx.doi.org/10.1007/s002040050537.

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50

Koechel, Daniel A., and Mark E. Krejci. "Extrarenal and direct renal actions of atractyloside contribute to its acute nephrotoxicity in pentobarbital-anesthetized dogs." Toxicology 79, no. 1 (1993): 45–66. http://dx.doi.org/10.1016/0300-483x(93)90205-7.

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