Related Experiment Video
Updated: Jul 19, 2026
An Improved Method for Rapid Intubation of the Trachea in Mice
Published on: February 22, 2016
Pathological effects of the mushroom toxin alpha-amanitin on BALB/c mice
Jian Zhao1, Mei Cao, Jie Zhang
1Division of Cancer Biotherapy, State Key Laboratory of Biotherapy, West China Medical School, Sichuan University, Chengdu 610064, PR China.
Abstract:
The pathological effects of alpha-amanitin on BALB/c mice after receiving intravenous injection were evaluated by RP-HPLC and mouse genome oligonucleotide microarray. The content of alpha-amanitin in Amanita virosa was about 2833.8 microg/g dry fruiting body. The liver and kidneys showed critical pathological changes after alpha-amanitin poisoning, and sera BUN, Crea, ALT, AST, TBIL and DBIL were the sensitive markers. The compound alpha-amanitin was detected in liver and kidney tissue homogenates by RP-HPLC after 48 h. The results of mouse genome oligonucleotide microarray showed 146 genes' expression changed, which formed the alternant network. The expression of 66 genes decreased, while 80 ones increased with more than two-fold differential expression after 48 h. The compound alpha-amanitin influenced not only RNA polymerase II, but also the expression of its associated genes. The application of mouse oligo chip provided valuable data for further understanding the biological properties and molecular pathogenesis of alpha-amanitin, also might be helpful for screening the curative drug for alpha-amanitin intoxication.
Insights
Alpha-amanitin from Amanita virosa causes severe liver and kidney damage in mice, identified by sensitive serum markers. Gene expression analysis revealed significant changes, impacting RNA polymerase II and related pathways.
Area of Science:
- Toxicology
- Molecular Biology
- Genomics
Background:
- Alpha-amanitin is a potent toxin found in Amanita virosa mushrooms.
- Mushroom poisoning can lead to severe organ damage, particularly in the liver and kidneys.
- Understanding the molecular mechanisms of alpha-amanitin toxicity is crucial for developing treatments.
Purpose of the Study:
- To evaluate the pathological effects of alpha-amanitin in BALB/c mice.
- To investigate the molecular changes induced by alpha-amanitin using gene expression profiling.
- To identify potential biomarkers and therapeutic targets for alpha-amanitin intoxication.
Main Methods:
- Intravenous injection of alpha-amanitin into BALB/c mice.
- Analysis of pathological changes in liver and kidneys.
- Quantification of alpha-amanitin in tissues using RP-HPLC.
- Genome-wide gene expression analysis using mouse oligonucleotide microarrays.
Main Results:
- Significant pathological changes observed in the liver and kidneys.
- Elevated serum levels of BUN, Crea, ALT, AST, TBIL, and DBIL indicated organ damage.
- Alpha-amanitin was detected in liver and kidney tissues 48 hours post-injection.
- Mouse genome oligonucleotide microarray identified 146 differentially expressed genes (66 decreased, 80 increased) after 48 hours.
- Affected genes included those related to RNA polymerase II, suggesting a disruption of transcription.
Conclusions:
- Alpha-amanitin induces critical pathological changes in mouse liver and kidneys.
- Serum markers effectively indicate alpha-amanitin poisoning.
- Gene expression profiling reveals molecular pathways affected by alpha-amanitin, including RNA polymerase II.
- This study provides data for understanding alpha-amanitin pathogenesis and aids in screening for antidote drugs.
