Althoff J, Eagen M, Grandjean C
J Natl Cancer Inst. 1975 Nov;55(5):1209-11. doi: 10.1093/jnci/55.5.1209.
Oxidation at the beta carbon occurred in metabolism of di-n-propylnitrosamine (DPN), previously shown to be carcinogenic for animals. When 2,2'-dimethyldipropylnitrosamine (DMDPN) was injected sc once a week for life into male and female Syrian hamsters at levels of 500, 250, 125, and 62.5 mg/kg body weight, it induced neoplasms in the nasal cavities, larynx, trachea, and stem bronchi. Since the presence of a methyl group on the beta carbon suggested that DMDPN could not undergo beta oxidation, the carcinogenicity of DPN for these portions of the respiratory tract was probably unrelated to beta oxidation, though earlier experiments had indicated the possibility of this mechanism. Because DMDPN failed to induce neoplasms in other organs, the carcinogenicity of DPN or its beta metabolites for the lungs, liver, pancreas, and kidneys was not explained by this experiment.
β-碳位的氧化发生在二正丙基亚硝胺(DPN)的代谢过程中,此前已证明DPN对动物具有致癌性。当以500、250、125和62.5mg/kg体重的剂量,每周一次皮下注射2,2'-二甲基二正丙基亚硝胺(DMDPN)至成年叙利亚仓鼠体内时,它会诱发鼻腔、喉、气管和主支气管的肿瘤。由于β-碳位上存在一个甲基,这表明DMDPN无法进行β-氧化,因此DPN对呼吸道这些部位的致癌性可能与β-氧化无关,尽管早期实验表明存在这种机制的可能性。由于DMDPN未能在其他器官中诱发肿瘤,因此该实验无法解释DPN或其β-代谢产物对肺、肝、胰腺和肾脏的致癌性。