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首页> 外文期刊>Archives of Toxicology >Early morphological and functional alterations in canine hepatocytes due to α-amanitin, a major toxin of Amanita phalloides
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Early morphological and functional alterations in canine hepatocytes due to α-amanitin, a major toxin of Amanita phalloides

机译：由于鹅膏伞形毒蕈的主要毒素α-amanitin导致的犬肝细胞的早期形态和功能改变

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The toadstool death cap (Amanita phalloides) and its subspecies, destroying angel (A. virosa) and death angel (A. verna) are responsible for nearly 95% of all fatal mushroom poisonings. High mortality rate in A. phalloides intoxications is principally a result of the acute liver failure following significant hepatocyte damage due to hepatocellular uptake of amanitins, the major toxins of this mushroom. This study evaluated early morphological and functional alterations in hepatocytes exposed to different concentrations of α-amanitin (α-AMA). All experiments were performed on cultured canine hepatocytes since intoxicated with A. phalloides dogs have clinical course and pathological findings similar to those seen in humans. The overall functional integrity and viability of cultured hepatocytes were assessed using the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay and by measurements of lactate dehydrogenase (LDH), total protein, and urea levels. Our results showed that the course of α-AMA toxicity in cultured dog hepatocytes is divided into two phases. The first phase comprises functional cell impairments expressed by significant increase of LDH activity and inhibition of protein and urea synthesis when compared with the control group. This is followed by discrete changes in hepatocyte ultrastructure, including marginalization and condensation of nuclear chromatin, as well as formation of the foamlike cytoplasm. The second stage is lethal and is characterized by ongoing necrosis, and/or apoptosis. This may be related to dose of toxin and time of exposure.
机译：毒菌的死亡帽（伞形毒蕈）及其亚种，破坏性天使（A. virosa）和死亡天使（A. verna）约占所有致命蘑菇中毒的95％。鬼笔环藻中毒的高死亡率主要是由于肝细胞摄取金黄色素（该蘑菇的主要毒素）而导致肝细胞明显受损后急性肝衰竭的结果。这项研究评估了暴露于不同浓度的α-amanitin（α-AMA）的肝细胞的早期形态和功能改变。所有实验均在培养的犬肝细胞上进行，因为用鬼臼曲霉犬中毒后，其临床病程和病理学发现与人类相似。使用MTT [3-（4,5-二甲基噻唑-2-基）-2,5-二苯基四唑鎓溴化物]测定法并通过测量乳酸脱氢酶（LDH），总蛋白，和尿素水平。我们的结果表明，培养的犬肝细胞中α-AMA毒性的过程分为两个阶段。与对照组相比，第一阶段包括功能性细胞损伤，其表现为LDH活性显着增加以及对蛋白质和尿素合成的抑制。随后是肝细胞超微结构的离散变化，包括核染色质的边缘化和凝结，以及泡沫样细胞质的形成。第二阶段是致死性的，其特征在于进行性坏死和/或凋亡。这可能与毒素的剂量和暴露时间有关。

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