Journal of The Korean Society of Clinical Toxicology

The Protective Effect of Green Tea Extract on Alpha-amanitin Induced Hepatotoxicity: Su Hwan An, Kyung Hoon Sun, Ran Hong, Byoung Rai Lee, Yongjin Park; J Korean Soc Clin Toxicol. 2019;17(2):58-65. Published online December 31, 2019; DOI: https://doi.org/10.22537/jksct.2019.17.2.58

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Purpose: Alpha-amanitin induces potent oxidative stress and apoptosis, and may play a significant role in the pathogenesis of hepatotoxicity. This study examined the mechanisms of α-amanitin-induced apoptosis in vitro, and whether green tea extract (GTE) offers protection against hepatic damage caused by α-amanitin (AMA) induced apoptosis in vivo. Methods: The effects of GTE and SIL on the cell viability of cultured murine hepatocytes induced by AMA were evaluated using an MTT assay. Apoptosis was assessed by an analysis of DNA fragmentation and caspase-3. In the in vivo protocol, mice were divided into the following four groups: control group (0.9% saline injection), AMA group (α-amanitin 0.6 mg/kg), AMA+SIL group (α-amanitin and silibinin 50 mg/kg), and AMA+GTE group (α-amanitin and green tea extract 25 mg/kg). After 48 hours of treatment, the hepatic aminotransferase and the extent of hepatonecrosis of each subject was evaluated. Results: In the hepatocytes exposed to AMA and the tested antidotes, the cell viability was significantly lower than the AMA only group. An analysis of DNA fragmentation showed distinctive cleavage of hepatocyte nuclear DNA in the cells exposed to AMA. In addition, the AMA and GTE or SIL groups showed more relief of the cleavage of the nuclear DNA ladder. Similarly, values of caspase-3 in the AMA+GTE and AMA+SIL groups were significantly lower than in the AMA group. The serum AST and ALT levels were significantly higher in the AMA group than in the control and significantly lower in the AMA+GTE group. In addition, AMA+GTE induced a significant decrease in hepatonecrosis compared to the controls when a histologic grading scale was used. Conclusion: GTE is effective against AMA-induced hepatotoxicity with its apoptosis regulatory properties under in vitro and in vivo conditions.

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Effects of herbal and mushroom formulations used in Traditional Chinese Medicine on in vitro human cancer cell lines at the preclinical level: An empirical review of the cell killing mechanisms
Qiulan Wu, Tingting Dai, Jie Song, Xiaorong Liu, Shaomin Song, Lili Li, Jingbing Liu, Arivalagan Pugazhendhi, Joe Antony Jacob
Process Biochemistry.2020; 94: 136. CrossRef

Severe Liver Toxicity Caused by Amatoxin (Case Series): Joo-Hyun Suh, Sung-Jin Kim, Young-Kuk Chung, Woong-Gil Choi, Young-Se Kwon, Hyung-Keun Roh; J Korean Soc Clin Toxicol. 2006;4(1):73-77. Published online June 30, 2006

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Abstract PDF: Poisoning with mushroom containing amatoxin may be a real medical emergency and is characterized by long incubation time lag, gastrointestinal symptoms, hepatotoxic phase and sometimes death. We report a family of parents and two children who ingested wild mushroom and recovered from varying degrees of hepatotoxicity. After eating cooked wild mushroom and its soup, they all developed abdominal pain, vomiting and diarrhea 11 hours later, Their liver enzymes reached peak level between 48 and 72 hours after the ingestion. Among the family members, 5-year-old girl showed the most severe hepatic toxicity of AST/ALT 14,099/13,176 IU/L. They were all treated with supportive measures including repeated activated charcoal and penicillin G and recovered from the hepatotoxicity between 7 and 28 days after the ingestion. Being based on the shape and a typical course of the amatoxin poisoning, we presume that this wild mushroom belongs to Amanita virosa.

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