CAS 23109-05-9 α-Amanitin - Analytical Products / Alfa Chemistry

CAT	AP23109059
CAS	23109-05-9
Structure
MDL Number	MFCD00215842
Molecular Weight	918.97
EC Number	245-432-2
InChI Key	CIORWBWIBBPXCG-UHFFFAOYSA-N
REAXYS Number	1071138

Description	from Amanita phalloides, ≥90% (HPLC), powder
Solubility	H2O: 1.0 mg/mL
Assay	≥90% (HPLC)
Color	white to light yellow
Form	powder
MP	254-255 °C (lit.)
Size	1MG, 100MG
Storage Conditions	−20°C

An Effective Antidotal Combination of Polymyxin B and Methylprednisolone for α-amanitin Intoxication

Juliana Garcia, Vera Marisa Costa, Antonio Bovolini, José Alberto Duarte, Daniela Ferreira Rodrigues, Maria de Lourdes Bastos, Félix Carvalho

Arch Toxicol. 2019 May;93(5):1449-1463.

PMID: 30891624

Prolonged α-amanitin Treatment of Cells for Studying Mutated Polymerases Causes Degradation of DSIF160 and Other Proteins

David C Tsao, Noh Jin Park, Anita Nag, Harold G Martinson

RNA. 2012 Feb;18(2):222-9.

PMID: 22194310

Selective Fluorescent Sensing of α-amanitin in Serum Using Carbon Quantum Dots-Embedded Specificity Determinant Imprinted Polymers

Liming Feng, Lei Tan, He Li, Zhiguang Xu, Guixian Shen, Youwen Tang

Biosens Bioelectron. 2015 Jul 15;69:265-71.

PMID: 25770458

Synthesis of the Death-Cap Mushroom Toxin α-Amanitin

Kaveh Matinkhoo, Alla Pryyma, Mihajlo Todorovic, Brian O Patrick, David M Perrin

J Am Chem Soc. 2018 May 30;140(21):6513-6517.

PMID: 29561592

TP53 Loss Creates Therapeutic Vulnerability in Colorectal Cancer

Yunhua Liu, Xinna Zhang, Cecil Han, Guohui Wan, Xingxu Huang, Cristina Ivan, Dahai Jiang, Cristian Rodriguez-Aguayo, Gabriel Lopez-Berestein, Pulivarthi H Rao, Dipen M Maru, Andreas Pahl, Xiaoming He, Anil K Sood, etc.

Nature. 2015 Apr 30;520(7549):697-701.

PMID: 25901683

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Case Study

α-Amanitin Induces Hepatocyte Autophagy

Xu, Yue, et al. Toxicology Letters 383 (2023): 89-97.

Amanitin poisoning is one of the most life-threatening types of mushroom poisoning. α-Amanitin plays a key role in amanita toxicity and has a toxic effect on the liver.
Establishment of α-Amanitin-Induced Liver Injury Animal Model: SD rats were intraperitoneally injected with different concentrations of α-amantin (0, 0.01, 0.05, 0.1, and 0.8 mg/kg) for 24 hours. The liver injury caused by α-amantin was assessed by measuring the changes in ALT and AST levels in serum and observing morphological changes in the liver using H&E staining. As shown in Figure 1-A, compared to the saline group, the ALT and AST levels in rats significantly increased after 24 hours of exposure to different concentrations of α-amantin (*P < 0.05, **P < 0.01, ***P < 0.001 vs. control). Figure 1-B illustrates that with increasing concentrations of α-amantin, significant morphological changes occurred in liver tissue, including edema of hepatocytes around the central vein and mild swelling and degeneration of hepatocytes with inflammatory cell infiltration, indicating the successful establishment of an α-amantin-induced liver injury model in rats.

α-Amanitin Induces Inflammatory Response in Human Hepatocellular Carcinoma HepG2 Cells

Zhao, Zhiyong, et al. Chemosphere 364 (2024): 143157.

α-Amanitin (AMA) is a hepatotoxic mushroom toxin responsible for over 90% of mushroom poisoning fatalities worldwide, posing a severe threat to human life and health. There is limited evidence indicating that AMA induces inflammatory responses and inflammatory infiltration both in vitro and in vivo; however, the molecular mechanisms remain unknown.
In this study, human hepatocellular carcinoma cells (HepG2) were exposed to various concentrations of AMA for a short duration. The results showed that AMA increased the production of reactive oxygen species (ROS) and elevated the release of malondialdehyde (MDA) and lactate dehydrogenase (LDH), leading to oxidative damage in HepG2 cells. Furthermore, AMA exposure significantly increased the secretion levels of inflammatory cytokines and activated the NLRP3 inflammasome. The NLRP3 inhibitor MCC950 and the NF-κB inhibitor Bay11-7082 were able to reverse the inflammatory response. Additionally, N-acetylcysteine (NAC) blocked the upregulation of the NF-κB/NLRP3 signaling pathway and significantly alleviated the inflammatory response. These results suggest that AMA can induce inflammation by activating the NLRP3 inflammasome triggered by the ROS/NF-κB signaling pathway. Our study provides new insights into the molecular mechanisms of AMA-induced inflammatory injury and may contribute to the establishment of new preventive strategies against AMA hepatotoxicity.