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首页> 外文期刊>Toxicologic pathology >Consensus Diagnoses and Mode of Action for the Formation of Gastric Tumors in Rats Treated with the Chloroacetanilide Herbicides Alachlor and Butachlor
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Consensus Diagnoses and Mode of Action for the Formation of Gastric Tumors in Rats Treated with the Chloroacetanilide Herbicides Alachlor and Butachlor

机译：氯乙酰苯胺除草剂甲草胺和丁草胺治疗大鼠胃肿瘤形成的共识性诊断和作用方式

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A panel of pathologists (Panel) was formed to evaluate the pathogenesis and human relevance of tumors that developed in the fundic region of rat stomachs in carcinogenicity and mechanistic studies with alachlor and butachlor. The Panel evaluated stomach sections stained with hematoxylin and eosin, neuron-specific enolase, and chromogranin A to determine the presence and relative proportion of enterochromaffin-like (ECL) cells in the tumors and concluded all tumors were derived from ECL cells. Biochemical and pathological data demonstrated the tumor formation involved a nongenotoxic threshold mode of action (MOA) initially characterized by profound atrophy of the glandular fundic mucosa that affected gastric glands, but not surface epithelium. This resulted in a substantial loss of parietal cells and a compensatory mucosal cell proliferation. The loss of parietal cells caused a marked increase in gastric pH (hypochlorhydria), leading to sustained and profound hypergastrinemia. The mucosal atrophy, together with the increased gastrin, stimulated cell growth in one or more ECL cell populations, resulting in neoplasia. ECL cell autocrine and paracrine effects led to dedifferentiation of ECL cell tumors. The Panel concluded the tumors develop via a threshold-dependent nongenotoxic MOA, under conditions not relevant to humans.
机译：成立了一个病理学家小组（Panel），以评估在大鼠胃底区域发展的肿瘤的发病机理和与人类的相关性，这些研究涉及甲草胺和丁草胺的致癌性和机理研究。专家组评估了用苏木精和曙红，神经元特异性烯醇化酶和嗜铬粒蛋白A染色的胃部切片，以确定肿瘤中肠嗜铬细胞样（ECL）细胞的存在和相对比例，并得出结论，所有肿瘤均来自ECL细胞。生化和病理学数据表明，肿瘤的形成涉及一种非遗传毒性阈值作用模式（MOA），其最初特征是腺胃底粘膜严重萎缩，影响胃腺，但不影响表面上皮。这导致壁细胞大量损失和代偿性粘膜细胞增殖。壁细胞的损失导致胃液pH值明显升高（低氯酸），导致持续性和严重性高胃泌素血症。粘膜萎缩以及胃泌素的增加，刺激了一种或多种ECL细胞群体的细胞生长，从而导致了瘤形成。 ECL细胞的自分泌和旁分泌作用导致ECL细胞肿瘤的去分化。专家组得出结论，在与人类无关的条件下，肿瘤会通过阈值依赖性非遗传毒性MOA发生。

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