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通过在饮食中添加鲍曼-伯克蛋白酶抑制剂抑制二甲基肼诱导的小鼠致癌作用。

Suppression of dimethylhydrazine-induced carcinogenesis in mice by dietary addition of the Bowman-Birk protease inhibitor.

作者信息

St Clair W H, Billings P C, Carew J A, Keller-McGandy C, Newberne P, Kennedy A R

机构信息

Department of Cancer Biology, Harvard School of Public Health, Boston, Massachusetts 02115.

出版信息

Cancer Res. 1990 Feb 1;50(3):580-6.

PMID:2297699
Abstract

In the present study the effect of feeding the soybean-derived Bowman-Birk protease inhibitor (BBI) on dimethylhydrazine (DHM)-induced gastrointestinal tract and liver carcinogenesis in mice was examined. In this investigation we found the addition of 0.5 or 0.1% semipurified BBI or 0.1% purified BBI to the diet of DMH-treated mice resulted in a statistically significant suppression of angiosarcomas and nodular hyperplasia of the liver and adenomatous tumors of the gastrointestinal tract. Autoclaved BBI or BBI which had its trypsin inhibitory domain specifically inactivated was found to be ineffective in suppressing the induction of these liver and gastrointestinal tract lesions. The results of this study also indicate that BBI, included as 0.5% of the diet or less, has the ability to suppress carcinogenesis with no observed adverse effects on the health of the mice.

摘要

在本研究中,检测了喂食大豆来源的鲍曼-伯克蛋白酶抑制剂(BBI)对二甲基肼(DMH)诱导的小鼠胃肠道和肝癌变的影响。在这项研究中,我们发现在经DMH处理的小鼠饮食中添加0.5%或0.1%的半纯化BBI或0.1%的纯化BBI,可在统计学上显著抑制肝血管肉瘤、肝结节性增生以及胃肠道腺瘤性肿瘤。发现经高压灭菌的BBI或其胰蛋白酶抑制结构域被特异性灭活的BBI在抑制这些肝脏和胃肠道病变的诱导方面无效。本研究结果还表明,饮食中BBI含量为0.5%或更低时,具有抑制癌变的能力,且未观察到对小鼠健康有不良影响。

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