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乙醇,其对豚鼠胃黏膜蛋白质合成的影响。

Ethanol, its effect on the synthesis of proteins by guinea-pig gastric mucosa.

作者信息

Spohn M, McColl I

出版信息

Biochem Pharmacol. 1986 Jun 1;35(11):1909-14. doi: 10.1016/0006-2952(86)90311-4.

Abstract

Incorporation of L-[U-14C]leucine into proteins is taken to indicate the synthesis of proteins by guinea pig gastric mucosa. Ethanol reduced the synthesis of proteins in vitro by homogenized mucosa, by isolated gastric epithelial cell preparations and by intact tissue. Intact stomach wall incubated without ethanol in phosphate buffered saline showed progressively increasing incorporation of the precursor into tissue proteins and into proteins which were secreted into the mucosal incubation media. On isopycnic CsCl gradient fractionation radioactive tissue proteins were found at the top of the gradient (fraction L1, sp.gr.1.11-1.20) while radioactive secreted proteins sedimented to the bottom of the gradient as the carbohydrate rich high density gastric mucosal glycoprotein fraction L3 (sp.gr.1.29-1.33). Ethanol significantly but reversibly reduced the incorporation of radioactive leucine by intact mucosa into both the tissue proteins and the secreted proteins. Uptake of the precursor into the intracellular acid soluble pool was not impaired by ethanol and no significant differences were detected in the specific activities of free intracellular leucine between the ethanol treated samples and the corresponding controls. It is suggested that the ulcerogenic nature of ethanol may be associated with inhibition of the synthesis of proteins within mucosal epithelium leading to reduction in the output of mucosal secretory glycoproteins with subsequent impairment of the cytoprotective properties of the dynamic mucous barrier.

摘要

采用L-[U-¹⁴C]亮氨酸掺入蛋白质的方法来指示豚鼠胃黏膜中蛋白质的合成。乙醇降低了匀浆黏膜、分离的胃上皮细胞制剂以及完整组织在体外的蛋白质合成。在磷酸盐缓冲盐溶液中不添加乙醇孵育的完整胃壁,其前体掺入组织蛋白质和分泌到黏膜孵育培养基中的蛋白质的量逐渐增加。在等密度氯化铯梯度分级分离中,放射性组织蛋白出现在梯度顶部(L1组分,比重1.11 - 1.20),而放射性分泌蛋白则作为富含碳水化合物的高密度胃黏膜糖蛋白组分L3(比重1.29 - 1.33)沉淀到梯度底部。乙醇显著但可逆地降低了完整黏膜将放射性亮氨酸掺入组织蛋白和分泌蛋白中的量。乙醇并未损害前体进入细胞内酸溶性池的过程,并且在乙醇处理样品和相应对照之间,细胞内游离亮氨酸的比活性未检测到显著差异。有人提出,乙醇的致溃疡性质可能与抑制黏膜上皮内蛋白质合成有关,导致黏膜分泌糖蛋白输出减少,进而损害动态黏液屏障的细胞保护特性。

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