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Relevant bibliographies by topics / Pyrrolizidinone

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Academic literature on the topic 'Pyrrolizidinone'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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Journal articles on the topic "Pyrrolizidinone"

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Zhu-Jin, Liu, C. T. Liu, Lu Ren-Rong, and Xu Feng. "A novel approach to the synthesis of 2-benzyl substituted pyrrolizidine and pyrrolizidinone ring systems." Acta Chimica Sinica 6, no. 2 (May 1988): 123–31. http://dx.doi.org/10.1002/cjoc.19880060206.

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Dietrich, Evelyne, and William D. Lubell. "Efficient Synthesis of Enantiopure Pyrrolizidinone Amino Acid." Journal of Organic Chemistry 68, no. 18 (September 2003): 6988–96. http://dx.doi.org/10.1021/jo034739d.

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Cordero, Franca M., Federica Pisaneschi, Karina Meschini Batista, Silvia Valenza, Fabrizio Machetti, and Alberto Brandi. "A New Bicyclic Dipeptide Isostere with Pyrrolizidinone Skeleton." Journal of Organic Chemistry 70, no. 3 (February 2005): 856–67. http://dx.doi.org/10.1021/jo0487653.

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SUGIE, YUTAKA, HIDEO HIRAI, HIROKO KACHI-TONAI, YOON-JEONG KIM, YASUHIRO KOJIMA, YUKIO SHIOMI, AKEMI SUGIURA, et al. "New Pyrrolizidinone Antibiotics CJ-16,264 and CJ-16,367." Journal of Antibiotics 54, no. 11 (2001): 917–25. http://dx.doi.org/10.7164/antibiotics.54.917.

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Escolano, Marcos, Javier Torres Fernández, Fernando Rabasa-Alcañiz, María Sánchez-Roselló, and Carlos del Pozo. "Enantioselective Synthesis of Pyrrolizidinone Scaffolds through Multiple-Relay Catalysis." Organic Letters 22, no. 24 (November 30, 2020): 9433–38. http://dx.doi.org/10.1021/acs.orglett.0c03344.

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Nogawa, Toshihiko, Makoto Kawatani, Masakazu Uramoto, Akiko Okano, Harumi Aono, Yushi Futamura, Hiroyuki Koshino, Shunji Takahashi, and Hiroyuki Osada. "Pyrrolizilactone, a new pyrrolizidinone metabolite produced by a fungus." Journal of Antibiotics 66, no. 10 (May 29, 2013): 621–23. http://dx.doi.org/10.1038/ja.2013.55.

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Salvati, Maria, Franca M. Cordero, Federica Pisaneschi, Francesca Bucelli, and Alberto Brandi. "New developments in the synthesis of pyrrolizidinone-based dipeptide isosteres." Tetrahedron 61, no. 37 (September 2005): 8836–47. http://dx.doi.org/10.1016/j.tet.2005.07.020.

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Sugie, Yutaka, and et al et al. "ChemInform Abstract: New Pyrrolizidinone Antibiotics CJ-16,264 and CJ-16,367." ChemInform 33, no. 21 (May 21, 2010): no. http://dx.doi.org/10.1002/chin.200221182.

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Rao, Mallem H. V. Ramana, Eulàlia Pinyol, and William D. Lubell. "Rigid Dipeptide Mimics: Synthesis of Enantiopure C6-Functionalized Pyrrolizidinone Amino Acids." Journal of Organic Chemistry 72, no. 3 (February 2007): 736–43. http://dx.doi.org/10.1021/jo0616761.

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Chiacchio, Ugo, Antonino Corsaro, Venerando Pistarà, Antonio Rescifina, Giovanni Romeo, and Roberto Romeo. "An asymmetric approach to pyrrolidinone and pyrrolizidinone systems by intramolecular oxime-olefin cycloaddition." Tetrahedron 52, no. 23 (June 1996): 7875–84. http://dx.doi.org/10.1016/0040-4020(96)00358-4.

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Dissertations / Theses on the topic "Pyrrolizidinone"

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Choi, Joong-Kwon. "Synthesis of pyrrolizidine alkaloids /." The Ohio State University, 1985. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487259125219504.

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Pereira, Tamara Nishanthi. "Cytotoxic effects of pyrrolizidine alkaloids /." [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18303.pdf.

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Kim, Hea-Young. "Molecular Toxicology of Pyrrolizidine Alkaloids." DigitalCommons@USU, 1994. https://digitalcommons.usu.edu/etd/3910.

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Pyrrolizidine alkaloids are cytotoxic, carcinogenic, and anti-carcinogenic in vivo and in vitro, and they produce many hazardous effects in humans and animals. Pyrrolizidine alkaloids (PAs) also cross-link with DNA and/or protein. However, whether such cross-linking is important to the toxic action of PAs is not known. In addition, the exact mechanism underlying these DNA cross-links or cytotoxicity is also not clear. In three separate studies, I characterized the nature of PA-induced DNA cross-links and the relationships between PA structures and cross-linking potency. In the first study (Chapter II), I found that cross-linking potency of PA congeners coincided with their abilities to cause cytopathologic effects. Macrocyclic a,p-unsaturated diesters PAs and their pyrrolic metabolites were the most potent inhibitors of colony formation, and inducers of cytopathologic changes and megalocyte formation. The macrocyclic α, β-saturated diester PA and open diesters PAs slightly inhibited colony formation, and slightly changed cell morphology. Retronecine and indicine N-oxide were completely inactive. In the next study (Chapter Ill), I found that pyrrolic macrocyclic metabolites were more potent DNA cross-linkers than their parent compounds as determined by alkaline elution. The pyrroles of the macrocyclic diester PAs were potent DNADNA (inter- and/or intra) cross-linkers in BstEll-digested λ-phage DNA or pBR322 plasmid DNA but dehydroretronecine and indicine N-oxide were not. I also examined which DNA sequences were more susceptible to PA-induced cross-links by using a series of restriction endonucleases to determine sequence specificity. The most favorable cross-linking site for PAs appeared to be 5'd(GG) and 5'-d(GA) although other sites, 5'-d(CC) or 5'-d(CG), might be also preferable cross-linking targets. In the next study (Chapter IV), I characterized the nature of DNA-protein interactions induced by PAs, because I found in previous studies that PA-induced cross-links are largely protein associated. In PA or pyrrolic PA exposed cells, cross-linked proteins with molecular weights 40 - 60 kD were detected. Two-dimensional electrophoretic analysis revealed that these proteins were probably acidic in nature. In an in vitro system utilizing pBR322 or Bst Ell-digested λ-phage DNA. dehydrosenecionine induced DNAprotein cross-links with BSA, indicating that such interactions might be related to amino acid composition of protein. These results confirmed that PA-induced DNA cross-links (DNA-DNA, DNA-protein cross-links) are influenced by three structural features: the C1 ,2 unsaturation of pyrrolizidine ring, α, β-unsaturation, and size of the macrocyclic diester ring. The ability to form cross-links was closely related to the known toxic potencies of these PAs. From this research, I also conclude that DNA crosslinking is the most critical event leading to PA-related diseases and that crosslinking is due to pyrrolic metabolites of PAs, not via a common metabolite as was once thought.

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Cooper, Roland Arthur 1963. "Pyrrolizidine alkaloids: Chemical basis of toxicity." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/290581.

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In humans, livestock and experimental animals, pyrrolizidine alkaloids (PAs) are toxic as a consequence of their hepatic metabolism to reactive pyrrolic esters, or dehydroalkaloids (DHAs). Despite their similarity in structures, PAs often vary markedly in their lethality (LD₅₀s) and in the organs in which toxicity is expressed. We have examined whether there are differences in the physicochemical properties of certain DHAs which are associated with differences in patterns of metabolism and toxicity produced by the parent PA. Using a potentiometric method to measure hydrolysis, it was determined that the half-lives of the corresponding DHAs of retrorsine, seneciphylline, monocrotaline and trichodesmine were 1.06, 1.60, 3.39 and 5.36 sec, respectively. These values were supported by similar results from experiments measuring reactivity of DHAs toward 4-(p-nitrobenzyl)pyridine. Studies from the isolated rat liver perfused with PAs show that DHA stability is related to patterns of metabolism and toxicity. Perfusion of the primarily hepatotoxic retrorsine and seneciphylline is associated with a greater proportion of metabolite released as non-toxic 7-glutathionyl-6,7-dihydro-1-hydroxymethyl-5H-pyrrolizine (7-GSDHP), a greater proportion alkylating liver macromolecules, and a lower proportion released as DHA into the circulation. Perfusion with monocrotaline and trichodesmine, PAs producing extrahepatic toxicity, produced lower proportions of 7-GSDHP release and liver alkylation, and higher proportions of DHA released into the circulation. Other studies characterizing DHAs included the use of an in vitro enzyme assay in which DHAs were shown to inhibit the phosphotransferase activity of yeast and rat brain hexokinase. Parent PAs, and the hydrolysis product of DHAs, (±)-6,7dihydro-1-hydroxymethyl-5H-pyrrolizine (DHP) did not affect enzyme activity. In vivo studies in rats have established that glutathione and cysteine-conjugated pyrrolic metabolites of PAs likely represent detoxication pathways, providing further support for DHAs as the primary toxic metabolite. We have examined the chemical form of sulfur-bound pyrroles to establish the importance of the 7-ester position in PA toxicity. Additionally, we have developed an efficient technique for the rapid separation and purification of large quantities of PAs using high-speed counter-current chromatography.

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Tang, Minyan. "The asymmetric synthesis of polyhydroxylated pyrrolizidine alkaloids." Department of Chemistry - Faculty of Science, 2004. http://ro.uow.edu.au/theses/233.

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Chapter 1 of this thesis is a review of the literature on the structure, biological activities and synthesis of polyhydroxylated 3-hydroxymethylpyrrolizidine alkaloids. This Chapter also outlines he aims of this project, which were to develop a flexible synthesis of the 1,2,7-trihydroxy-3-hydroxymethylpyrroizidine alkaloid australine, and its epimers. Chapter 2 describes model synthetic chemical studies on the synthesis of the pyrrolizidine core structure. The key synthetic steps, the aminolysis reaction of vinyl expoxides with ally1 amine, the ring-closing metathesis of the resulting diene, syndihydroxylation of the 2,5-dihydropyrrole product and finally ring closure to give the pyrrolizidine nucleus were successfully developed. Chapter 3 describes the application of the chemistry developed in Chapter 2 to the diastereoselective synthesis of the 3-hydroxymethy1-2,3,5,6,7,7 a-hexahydro-1H-pyrrolizine-1,2,7-triol structure, characteristic of several pyrrolizidine natural products. Two unnatural pyrrolizidine alkaloids, (-)-7-espiaustraline and (+)-1,7-diepiaustraline were successfully synthesized. The oxazolidinone group was found to be a useful protecting group in the RCM reaction and, as part of a pyrrolo[1,2-c]oxazol-3-one ring system, functioned as a stereo- and regio-directing group, in a key diastereoselective syn-dihydroxylation reaction and a regioselective nucleophilic ring-opening of a S,S-dioxo-dioxathiole. Chapter 4 describes the asymmetric synthesis of the pyrrolizidine alkaloid, (+)-1-epiaustraline. Attempts to extend this methodology to the synthesis of australine were not successful since the final pyrrolidine ring closure to produce the desired pyrrolizine was not productive.

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Wild, Stacie Lynn. "Pyrrolizidine alkaloids: Hepatic metabolism and extrahepatic toxicity." Diss., The University of Arizona, 1994. http://hdl.handle.net/10150/186599.

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Pyrrolizidine alkaloids are proposed to be metabolized in the liver to reactive pyrrole species, or dehydroalkaloids. These reactive pyrroles are hypothesized to be responsible for pyrrolizidine alkaloid toxicity. This dissertation research has established that dehydroalkaloids are, in fact, metabolites of pyrrolizidine alkaloids. It was first determined that dehydromonocrotaline is produced during hepatic microsomal metabolism of monocrotaline and that it has the ability to bind in vitro with a synthetic thiol-containing resin, Thiopropyl Sepharose 6B. Similarly, synthetic dehydromonocrotaline binds to this resin. Dehydromonocrotaline was identified as a pyrrolizidine alkaloid metabolite based upon its resin cleavage products. When resin-bound pyrrole, synthetic or microsomally generated, was cleaved in a buffered, ethanolic silver nitrate solution, O⁷-ethyl dehydroretronecine was the major product, supporting the suggestion that the pyrrole generated by hepatic microsomes is dehydromonocrotaline. This system was then used to determine the formation of dehydroalkaloids from other pyrrolizidine alkaloids. These other alkaloids--trichodesmine, retrorsine, senecionine and heliotrine--cause toxicity to the liver as well as to extrahepatic organs. Their metabolism in this system reveals that alkaloids which produce extrahepatic toxicity have an increased percentage of reactive metabolites formed by phenobarbital-induced hepatic microsomes. Therefore, this system in vitro can be a good predictor of alkaloids which may produce extrahepatic toxicity in vivo. Trichodesmine is a pyrrolizidine alkaloid that is unique in its neurotoxicity. It is structurally similar to monocrotaline, yet it varies widely in its toxicity. It was determined that trichodesmine is more toxic in the rat than monocrotaline as indexed by LD₅₀ values. The distribution of pyrrolic metabolites reveals that trichodesmine treatment results in brain pyrrole levels 4 times higher than monocrotaline, retrorsine, or control. Histopathologic investigation of trichodesmine-treated animals reveals severe neuronal death in the cerebral cortex. These results suggest that neurotoxicity observed with trichodesmine is a result of pyrrole metabolites reaching the brain, thus providing further evidence for the involvement of pyrrole metabolites in pyrrolizidine alkaloid-induced extrahepatic toxicity.

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Mitchell, Douglas. "Synthetic studies towards pyrrolizidine and indolizidine alkaloids." Thesis, Sheffield Hallam University, 1992. http://shura.shu.ac.uk/20067/.

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This project was concerned with the synthesis of the pyrrolizidine alkaloids supinidine, trachelanthamidine and isoretronecanol and also synthetic studies towards the indolizidine alkaloid 251D. In all cases, the synthesis began from a cheap, readily-available, simple amino acid, in this case glutamic acid, and proceeded to a suitable monocyclic intermediate which could then undergo an intramolecular Horner-Wittig cyclisation reaction to form the required bicyclic core structure. Subsequent modification reactions then led in the pyrrolizidine series to penultimate precursors of the target alkaloids supinidine, trachelanthamidine and isoretronecanol, and in the indolizidine series to a bicyclic intermediate in the synthesis towards the toxin 251D. The intramolecular Horner-Wittig cyclisation reaction was found to proceed with retention of chirality, thus leading to the enantiospecific synthesis of the pyrrolizidine alkaloids. The use of alternative monocyclic intermediates in the intramolecular Horner-Wittig cyclisation reaction, thus leading to other pyrrolizidine alkaloids is also discussed. One of the major problems encountered in this project was the solubility of the unprotected monocyclic amide intermediates, and this was overcome by the use of N-benzyl and N- carbobenzyloxy protecting groups; in the indolizidine synthesis where the unprotected monocyclic amides were necessary, the reaction work-up for these intermediates usually required continuous solvent extraction. Another major problem was the instability of the bicyclic amide intermediates and some of the monocyclic intermediates,As well as covering a comprehensive background of each class of alkaloid, this report also contains an in-depth discussion of the key intramolecular Horner-Wittig cyclisation reaction and suggestions for its use in the possible synthesis of other classes of alkaloids.

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Drew, Gail L. "DNA-Protein Cross-Linking by Pyrrolizidine Alkaloids." DigitalCommons@USU, 1997. https://digitalcommons.usu.edu/etd/3919.

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Pyrrolizidine alkaloids (PAs) are natural plant compounds found in hundreds of plant species worldwide and are reported to have cytotoxic, carcinogenic, antimitotic, and gentotoxic activity. PAs are metabolized by the cytochrome P450 (CYP) sytem to the pyrrole or the N-oxide form. They pyrroles are bifunctional electrophillic alkylators that bind cellular nucleophiles such as DNA and proteins and disrupt normal cell processes, including DNA replication and gene transcription, and can cause megalocytosis. The pyrroles dehyrosenecionine (DHSN) and dehydromoncrotaline (DHMO) are among the most potent PA cross-linkers and inducers of megalocytosis. DHSN and DHMO-induced cross-links in cultured normal (MDBK) and neoplastic (MCF7) cells were nalyzed by SDS-PAGE and Western blot and both were found to contain the protein actin. Actin is crucial to DNA replication and is known to be involved in cross-links induced by cis-dichlorodiammine platinum II (cistplatin), a well known cross-linking drug used for the treatment of cancer. Actin cross-linking may explain the antimitotic, megalocytotic, and anticarcinogenic effects of PAs. Since protein cross-linking is an important mode of action for PAs, we were interested in what characteristics of the protein might make it a good nucleophilic target. Thus, further research was undertaken based on the hypothesis that cysteine residues, and specifically free sulfhydryl groups, are attractive targets for the bifunctional electrophilic alkylators DHSN and DHMO. Nucleophiles were selected for their abundance in the cell, their cysteine content, and their relationship to the documented side effects of PAs. Actin, glutathione (GSH), metallothionein, topoisomerase II, and cysteine were all found to cross-link with DHSN and DHMO in vitro while methionine, with no free sulfhydryl groups, did not cross-link. Our results support the hypothesis that cysteine residues are a key characteristic of proteins that are cross-linked by PAs. The cross-links could have negative effects to the cell as in the case of binding actin or topoisomerase II to alter normal DNA processes and replication, or beneficial effects such as binding to electrophillic scavengers like GSH or metallothionine as a detoxifying mechanism. the nucleophiles we tested in vitro and found to form cross-links with DHSN and DHMO may help to explain the antimitotic carcinogenic, and anticarcinogenic effects of PAs.

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Pink, Jennifer Helen. "Synthesis of fused lactams via N-acyliminium ions." Thesis, University of Sheffield, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242373.

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Hagan, Desmond Bernard. "Biosynthesis and synthesis of pyrrolizidine alkaloids and analogues." Thesis, University of Glasgow, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.284533.

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Books on the topic "Pyrrolizidinone"

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Chemistry and toxicology of pyrrolizidine alkaloids. London: Academic Press, 1986.

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Hol, Wilhelmina Hermina Geertruida. The role of pyrrolizidine alkaloids from Senecio jacobaea in the defence against fungi. [Leiden: Universiteit Leiden, 2003.

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Máčel, Mirka. On the evolution of the diversity of pyrrolizidine alkaloids: The role of insects as selective forces. [Leiden: Universiteit Leiden, 2003.

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World Health Organization (WHO). Pyrrolizidine Alkaloids. World Health Organization, 1988.

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Pyrrolizidine alkaloids. Geneva: World Health Organization, 1988.

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M, Rizk A., ed. Naturally occurring pyrrolizidine alkaloids. Boca Raton, Fla: CRC Press, 1991.

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Pyrrolizidine Alkaloids Health and Safety Guide. World Health Organization, 1989.

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Hovermale, Jeannette Talbot. Metabolism of pyrrolizidine alkaloids by ruminal microbes. 1998.

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Lee, Nadine Chauyi. Synthetic studies on necic acids of pyrrolizidine alkaloids. 1998.

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Deyo, James A. Immunotoxicity of the pyrrolizidine alkaloid monocrotaline in C57B1/6 mice. 1991.

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Book chapters on the topic "Pyrrolizidinone"

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Liu, Dongyou. "Pyrrolizidine Alkaloids." In Handbook of Foodborne Diseases, 1109–14. Boca Raton : Taylor & Francis, [2019] | Series: Food microbiology series | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2018. http://dx.doi.org/10.1201/b22030-104.

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Mroczek, T., and K. Glowniak. "Pyrrolizidine Alkaloids." In Natural Products in the New Millennium: Prospects and Industrial Application, 1–46. Dordrecht: Springer Netherlands, 2002. http://dx.doi.org/10.1007/978-94-015-9876-7_1.

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Westendorf, J. "Pyrrolizidine Alkaloids — General Discussion." In Adverse Effects of Herbal Drugs, 193–205. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-49340-9_16.

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Westendorf, J. "Pyrrolizidine Alkaloids — Cynoglossum officinale." In Adverse Effects of Herbal Drugs, 207–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-49340-9_17.

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Westendorf, J. "Pyrrolizidine Alkaloids — Petasites Species." In Adverse Effects of Herbal Drugs, 211–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-49340-9_18.

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Westendorf, J. "Pyrrolizidine Alkaloids — Senecio Species." In Adverse Effects of Herbal Drugs, 215–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-49340-9_19.

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Westendorf, J. "Pyrrolizidine Alkaloids — Symphytum Species." In Adverse Effects of Herbal Drugs, 219–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-49340-9_20.

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Westendorf, J. "Pyrrolizidine Alkaloids — Tussilago farfara." In Adverse Effects of Herbal Drugs, 223–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-49340-9_21.

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Seigler, David S. "Pyrrolizidine, Quinolizidine, and Indolizidine Alkaloids." In Plant Secondary Metabolism, 546–67. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4913-0_30.

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Wiedenfeld, Helmut. "Alkaloids Derived From Ornithine: Pyrrolizidine Alkaloids." In Natural Products, 359–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-22144-6_9.

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Conference papers on the topic "Pyrrolizidinone"

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Schrenk, D. "Provisional relative potency factors for pyrrolizidine alkaloids – scientifically justified?" In Phytotherapiekongress 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1697263.

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Ober, Dietrich. "Repeated evolution of insect adaptations to toxic pyrrolizidine alkaloids of plants." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.94260.

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Rutz, L., L. Gao, and D. Schrenk. "Structure-dependent cytotoxicity of different pyrrolizidine alkaloids in primary rat hepatocytes." In Phytotherapiekongress 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1697293.

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Scaramal, João P. S., Kristerson R. Luna-Freire, and and Fernando Coelho. "Substrate-controlled Asymmetric Morita-Baylis-Hillman Reaction: an Approach to the Synthesis of Pyrrolizidinones and Pyrrolizidines." In 15th Brazilian Meeting on Organic Synthesis. São Paulo: Editora Edgard Blücher, 2013. http://dx.doi.org/10.5151/chempro-15bmos-bmos2013_20131014152540.

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Hadi, NSA, EE Bankoglu, O. Kelber, H. Sievers, and H. Stopper. "Studies on mechanism of genotoxicity of selected pyrrolizidine alkaloids in HepG2 cells in vitro." In Jubiläumskongress Phytotherapie 2021 Leib und Magen – Arzneipflanzen in der Gastroenterologie 50 Jahre Gesellschaft für Phytotherapie. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1731499.

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Haas, M., K. Wirachowski, JH Küpper, D. Schrenk, and J. Fahrer. "Structure-dependent genotoxicity and cytotoxicity of eleven pyrrolizidine alkaloids in CYP3A4-proficient human liver cells." In Jubiläumskongress Phytotherapie 2021 Leib und Magen – Arzneipflanzen in der Gastroenterologie 50 Jahre Gesellschaft für Phytotherapie. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1731472.

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Schenk, A., B. Siewert, S. Toff, and J. Drewe. "Determination of 34 pyrrolizidine alkaloids (PA) as contaminants in various plant extracts using UHPLC-ToF-HRMS." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608497.

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Forsch, K., B. Siewert, L. Disch, M. Unger, and J. Drewe. "In vitro screening of acute hepatic cytotoxicity of pyrrolizidine alkaloids in human and rodent hepatic cell lines." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608451.

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Reports on the topic "Pyrrolizidinone"

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Pereboom, D. P. K. H., M. de Nijs, J. G. J. Mol, and P. P. J. Mulder. Research study for pyrrolizidine alkaloids in alfalfa and herbal tea : EURLPT-MP02 (2019). Wageningen: Wageningen Food Safety Research, 2021. http://dx.doi.org/10.18174/545714.

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