Arffmann E J, Rasmussen K S, Hansen F N
J Natl Cancer Inst. 1981 Nov;67(5):1071-5.
Methyl linoleate hydroperoxide (MLHP) and native methyl linoleate (ML) were tested for carcinogenicity toward the gastrointestinal (GI) tract in male specific-pathogen-free outbred Wistar rats. N-Methyl-N-nitro-N-nitrosoguanidine (MNNG) was given in the drinking water in a dose of 20 mg/liter when cocarcinogenic properties of the test substances were to be tested. MLHP and ML were fed by stomach tube and had no effect as complete carcinogens. Given concomitantly with MNNG, ML did not enhance carcinogenesis. MLHP in conjunction with MNNG was the only treatment which, as treatment with MNNG in a dose of 83 mg/liter, led to an increase of GI cancers in animals that died before day 354. Cumulative results after a maximum of 612 days showed a distribution of GI cancers in favor of the glandular stomach only after MLHP was given with MNNG.
在雄性无特定病原体的远交系Wistar大鼠中，对亚油酸甲酯氢过氧化物（MLHP）和天然亚油酸甲酯（ML）进行了胃肠道致癌性测试。当要测试受试物质的促癌特性时，在饮用水中给予剂量为20毫克/升的N-甲基-N-硝基-N-亚硝基胍（MNNG）。通过胃管给MLHP和ML喂食，它们作为完全致癌物没有效果。与MNNG同时给予时，ML不会增强致癌作用。与MNNG联合使用的MLHP是唯一一种治疗方法，与以83毫克/升的剂量使用MNNG一样，导致在第354天前死亡的动物中胃肠道癌症增加。在最长612天的累积结果显示，只有在MLHP与MNNG一起给予后，胃肠道癌症才在腺胃中出现分布优势。
