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首页> 外文期刊>Archives of Toxicology >Epigenetic properties of the diarrhetic marine toxin okadaic acid: inhibition of the gap junctional intercellular communication in a human intestine epithelial cell line.
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Epigenetic properties of the diarrhetic marine toxin okadaic acid: inhibition of the gap junctional intercellular communication in a human intestine epithelial cell line.

机译：腹泻性海洋毒素冈田酸的表观遗传特性：抑制人肠上皮细胞系中间隙连接的细胞间通讯。

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Okadaic acid (OA) is produced by several types of dinoflagellates (marine plankton) and has been implicated as the causative agent of diarrhetic shellfish syndrome. Previous studies have shown that okadaic acid is a tumor promoter and a specific potent inhibitor of protein phosphatases and protein synthesis. These effects in turn affect intracellular processes such as metabolism, contractility, gene transcription, and the maintenance of cytoskeletal structure. Gap junctional intercellular communication (GJIC) is a means of maintaining cellular homeostasis in organs, the disruption of which favors tumor cell growth. The GJIC involves the transfer of small water-soluble molecules through intercellular channels (gap junctions), composed of proteins called connexins. OA disrupts cellular homeostasis in Caco-2 cells through several mechanisms including protein synthesis inhibition, apoptosis, and clastogenic effects. The aim of this study was then to evaluate the expression of the connexin 43 (Cx 43) mRNA in relation with the cytotoxicity induced by OA (3.75-60 ng/ml) in a human colonic epithelial cell line in culture (Caco-2 cells). OA produced a dose-dependent inhibition of GJIC in Caco-2 cells, along with a parallel decrease in the expression of Cx 43 as shown by immunohistochemistry using anti-Cx 43 antibody. Since Cx 43 is implicated in the suppression of tumors and OA is a tumor promoter, the inhibition of GJIC may play an important role in its carcinogenesis. These data are discussed in relation to the toxicity of OA, total RNA synthesis, and possible specificity of Cx 43 inhibition in the GJIC.
机译：冈田酸（OA）由多种类型的鞭毛藻（海洋浮游生物）产生，并已被认为是腹泻性贝类综合症的病原体。先前的研究表明，冈田酸是一种肿瘤促进剂，是蛋白质磷酸酶和蛋白质合成的特定有效抑制剂。这些作用反过来会影响细胞内过程，例如代谢，收缩力，基因转录和细胞骨架结构的维持。间隙连接细胞间通讯（GJIC）是维持器官中细胞稳态的一种手段，这种破坏有利于肿瘤细胞的生长。 GJIC涉及水溶性小分子通过细胞间通道（间隙连接）的转移，该通道由称为连接蛋白的蛋白质组成。 OA通过多种机制破坏Caco-2细胞中的细胞稳态，这些机制包括蛋白质合成抑制，细胞凋亡和裂解作用。然后，本研究的目的是评估培养物中人结肠上皮细胞系（Caco-2细胞）中连接蛋白43（Cx 43）mRNA的表达与OA（3.75-60 ng / ml）诱导的细胞毒性的相关性。 ）。 OA在Caco-2细胞中产生了剂量依赖性的GJIC抑制作用，同时Cx 43的表达也平行下降，如使用抗Cx 43抗体的免疫组织化学所示。由于Cx 43与肿瘤的抑制有关，而OA是肿瘤的启动子，因此抑制GJIC可能在其致癌作用中起重要作用。讨论了有关OA毒性，总RNA合成以及GJIC中Cx 43抑制作用可能的特异性的这些数据。

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