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暴露于乙酸甲基氧化偶氮甲醇的青鳉肝脏的连续组织学变化。

Sequential histological changes in the liver of medaka exposed to methylazoxymethaol acetate.

作者信息

Hoshikawa Yumiko, Furukawa Satoshi, Irie Kota, Kimura Masayuki, Takeuchi Kazuya, Sugiyama Akihiko

机构信息

Biological Research Laboratories, Nissan Chemical Corporation, 1470 Shiraoka, Shiraoka-shi, Saitama 349-0294, Japan.

Veterinary Clinical Pathology, Faculty of Veterinary Medicine, Okayama University of Science, 1-3 Ikoinooka, Imabari, Ehime 794-8555, Japan.

出版信息

J Toxicol Pathol. 2020 Oct;33(4):219-226. doi: 10.1293/tox.2020-0033. Epub 2020 Jul 25.

Abstract

We performed a medaka bioassay for the carcinogenicity of methylazoxymethaol acetate (MAM-Ac) to examine the sequential histological changes in the liver from 3 days after exposure until tumor development. The medaka were exposed to MAM-Ac at a concentration of 2 ppm for 24 hours, and were necropsied at 3, 7, 10, 14, 21, 28, 35, 42, 49, 60, and 91 days after exposure. MAM-Ac induced four cases of hepatocellular adenoma and one case of hepatocellular carcinoma in 8 fish after 60 or 91 days of exposure. Histological changes in the liver until tumor development were divided into three phases. In the cytotoxic phase (1-10 days), MAM-Ac-exposed hepatocytes showed vacuolar degeneration and underwent necrosis and apoptosis, resulting in multiple foci of hepatocyte loss. In the repopulation phase (14-35 days), the areas of hepatocyte loss were filled with hepatic cysts and the remaining hepatocytes were surrounded by hepatic stellate-like cells (or spindle cells) and gradually disappeared. In the proliferation phase (42-91 days), the original hepatic parenchyma was regenerated and progressively replaced by regenerative hyperplastic nodules and/or liver neoplasms. The medaka retained a strong hepatocyte regenerative ability in response to liver injury. It is considered that this ability promotes the proliferation of initiated hepatocytes in multistep carcinogenesis and influences the development of liver tumor over a short period in medaka.

摘要

我们进行了一项关于乙酸甲基偶氮甲醇(MAM-Ac)致癌性的青鳉生物测定,以检查从暴露后3天直至肿瘤形成期间肝脏的组织学变化顺序。将青鳉暴露于浓度为2 ppm的MAM-Ac中24小时,并在暴露后3、7、10、14、21、28、35、42、49、60和91天进行尸检。暴露60或91天后,MAM-Ac在8条鱼中诱导出4例肝细胞腺瘤和1例肝细胞癌。在肿瘤形成之前肝脏的组织学变化分为三个阶段。在细胞毒性阶段(1-10天),暴露于MAM-Ac的肝细胞出现空泡变性,随后发生坏死和凋亡,导致多个肝细胞缺失灶。在再生阶段(14-35天),肝细胞缺失区域充满肝囊肿,剩余的肝细胞被肝星状样细胞(或梭形细胞)包围并逐渐消失。在增殖阶段(42-91天),原始肝实质再生,并逐渐被再生性增生结节和/或肝脏肿瘤取代。青鳉对肝损伤具有很强的肝细胞再生能力。据认为,这种能力促进了多步骤致癌过程中起始肝细胞的增殖,并在短期内影响青鳉肝脏肿瘤的发展。

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