Choline Deficiency, Partial Hepatectomy, and Liver Tumors in Rats and Mice.
Choline Deficiency, Partial Hepatectomy, and Liver Tumors in Rats and Mice.
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DOI：
10.1177/019262338201000212
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发表时间：
1982-02-01
影响因子：
1.5
通讯作者：
Clark, Anthony J
中科院分区：
文献类型：
--
作者：
Newberne, Paul M;Camargo, Joao Lauro V de;Clark, Anthony J
胆碱缺乏（CD）可增加大鼠肝脏对多种结构和效力多样的肝细胞致癌物的耐受性。虽然严重的CD导致小结节性肝硬化和增强的肿瘤诱导，但即使是轻度缺乏，没有肝硬化也足以导致致癌反应增加。CD的作用部分是通过调节微粒体和（可能）负责致癌物激活/失活的细胞溶质酶介导的。B6 C3 F1杂交小鼠对许多物质或条件引发/促进肝肿瘤非常敏感。胆碱缺乏或部分肝切除术单独或共同作用，在没有任何已知致癌物的情况下，显著增强肝肿瘤诱导。这些数据表明，该品系小鼠的肝脏在出生时或出生后不久就“启动”，并且可以通过非致癌物质或条件促进。
Choline deficiency (CD) increases susceptability of (he rat liver to a number of hepatocellular carcinogens with a wide diversity of structure and potency. While severe CD results in micronodular cirrhosis and enhanced tumor induction, even a mild deficiency, without cirrhosis is sufficient to result in the increased carcinogenic response. The effects of CD are in part mediated via modulation of microsomal and, possibly, cytosolic enzymes responsible for activation/deactivation of carcinogens. The B6C3F1 hybrid mouse is remarkably sensitive to initiation/promotion of liver tumors by many substances or conditions. Choline deficiency or partial hepatectomy alone, or in concert, markedly enhances liver tumor induction in the absence of any known carcinogen. These data indicate that the liver of this strain of mouse is "initiated" at or shortly after birth and can be promoted by non-carcinogenic substances or conditions.