Investigation of Metabolism-Mediated Toxicity of Pyrrolizidine Alkaloids from Comfrey

Planta Medica ◽  
2011 ◽  
Vol 77 (05) ◽  
Author(s):  
H Tamta ◽  
RS Pawar ◽  
WG Wamer ◽  
E Grundel ◽  
AJ Krynitsky ◽  
...  
Keyword(s):  
Pyrrolizidine Alkaloids

Herbicides compromise biological control of ragwort

2002 ◽  
pp. 147-152
Author(s):  
K. Betteridge ◽  
D. Costall
Keyword(s):  
Biological Control ◽  
Pyrrolizidine Alkaloids ◽  
Animal Health ◽  
Flea Beetle ◽  
Dairy Farm ◽  
Senecio Jacobaea ◽  
Longitarsus Jacobaeae ◽  
High Ester ◽  
Low Levels

In spite of ragwort flea beetle (RFB) being present on a Dannevirke dairy farm, pastures were sprayed each winter to reduce ragwort density and limit the risk of ragwort poisoning of stock. The trial on this farm from June 1999 - October 2001, aimed to determine whether herbicide (H) impacted on RFB and how H and RFB each impacted on ragwort growth and persistence. RFBfree areas were created by spraying with insecticide (I). Effects of ragwort on animal health are also reported. High ester 2,4-D (H) boom-sprayed once only, in June 1999, killed most ragwort plants and reduced RFB larvae densities to low levels before the plants died. Once new ragwort established in treatment H, the plants became infested with RFB larvae. RFB larvae were suppressed by I resulting in ragwort density declining more slowly than in treatments where RFB were not suppressed. Insecticide treatments were stopped after 15 months and, at 24 months, ragwort could not be found within the trial area. Ragwort control was attributed to the cessation of herbicide spraying allowing the RFB population to reach a sufficient density to kill both small and large ragwort plants. Sub-clinical ragwort poisoning was found in livers of culled cows that had grazed on ragwort-dense pastures. Keywords: animal health, biological control, Longitarsus jacobaeae, pyrrolizidine alkaloids, ragwort, ragwort flea beetle, Senecio jacobaea

The Toxicity Effect of Echium Amoenum on the Liver and Kidney of Mice.

2020 ◽  
Vol 17 ◽  
Author(s):  
Mozhgan Ghorbani ◽  
Atefeh Araghi ◽  
Nabi Shariatifar ◽  
Seyed Hooman Mirbaha ◽  
Behrokh Marzban Abbasabadi ◽  
...  
Keyword(s):  
Pyrrolizidine Alkaloids ◽  
Biochemical Analysis ◽  
Liver Enzymes ◽  
Copper Ion ◽  
Control Group ◽  
Dependent Manner ◽  
Toxicity Effect ◽  
Significant Difference ◽  
Liver And Kidney ◽  
Echium Amoenum

Aims: The aim of this study was to investigate the toxic effect of Echium amoenum plants on the liver and kidney of animal model. Background: Echium amoenum is one of the medicinal plants containing pyrrolizidine alkaloids with several properties which has widely consumed among different communities. Objective: The toxic effects of Echium amoenum on the liver and kidney were investigated in this study. Methods: Sixty mice were kept for 28 days under the appropriate laboratory conditions. Echium amoenum extract (25, 12.5, 50 mg / kg, ip.) was administered for 28 days. At the end of experiment, blood samples were drawn and liver and kidneys were removed for evaluating hepatotoxicity and nephrotoxicity of extract. Additionally, experiments were conducted to assay the enzymatic and oxidative activities. Results: There was no significant difference in the levels of copper ion in the liver and kidneys among all groups. There was a significant difference in the levels of lipid peroxidation in the liver of treated groups versus control group. The significant difference was not observed in the levels of glutathione of the liver of all groups. However, the levels of glutathione of the kidney significantly decreased in the treated groups versus control group. There was no significant difference in the liver enzymes including ALP, SGOT, and SGPT between all groups. This indicates that damage increase with enhancing the time and concentrations of extract. Biochemical analysis showed the creatinine and urea levels did not change in the treated groups versus control group. Conclusion: According to the present findings, it is suggested that Echium amoenum causes hepatotoxicity and nephrotoxicity effects in dose and time dependent manner.

Pyrrolizidine alkaloids. XVI. Alkaloids from some plants of the genus Ligularia

1971 ◽  
Vol 36 (6) ◽  
pp. 2205-2215 ◽  
Author(s):  
A. Klásek ◽  
P. Sedmera ◽  
F. Šantavý
Keyword(s):  
Pyrrolizidine Alkaloids

scholarly journals Pyrrolizidine Alkaloids Induce Cell Death in Human HepaRG Cells in a Structure-Dependent Manner

2020 ◽  
Vol 22 (1) ◽  
pp. 202
Author(s):  
Josephin Glück ◽  
Julia Waizenegger ◽  
Albert Braeuning ◽  
Stefanie Hessel-Pras
Keyword(s):  
Cell Death ◽  
Cell Viability ◽  
Pyrrolizidine Alkaloids ◽  
Defense Mechanism ◽  
Hepatoma Cell ◽  
Hepatoma Cell Line ◽  
Dependent Manner ◽  
Human Hepatoma Cell

Pyrrolizidine alkaloids (PAs) are a group of secondary metabolites produced in various plant species as a defense mechanism against herbivores. PAs consist of a necine base, which is esterified with one or two necine acids. Humans are exposed to PAs by consumption of contaminated food. PA intoxication in humans causes acute and chronic hepatotoxicity. It is considered that enzymatic PA toxification in hepatocytes is structure-dependent. In this study, we aimed to elucidate the induction of PA-induced cell death associated with apoptosis activation. Therefore, 22 structurally different PAs were analyzed concerning the disturbance of cell viability in the metabolically competent human hepatoma cell line HepaRG. The chosen PAs represent the main necine base structures and the different esterification types. Open-chained and cyclic heliotridine- and retronecine-type diesters induced strong cytotoxic effects, while treatment of HepaRG with monoesters did not affect cell viability. For more detailed investigation of apoptosis induction, comprising caspase activation and gene expression analysis, 14 PA representatives were selected. The proapoptotic effects were in line with the potency observed in cell viability studies. In vitro data point towards a strong structure–activity relationship whose effectiveness needs to be investigated in vivo and can then be the basis for a structure-associated risk assessment.

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