Nishie K
Res Commun Chem Pathol Pharmacol. 1978 Jun;20(3):549-57.
All of the 4 noncarcinogenic nitrosamines (NA) and 4 of 7 carcinogenic nitrosamines examined increased the urinary ascorbic acid output after oral administration to rats. Of the remaining carcinogenic nitrosamines, dimethyl-NA decreased, and diethyl-NA and methyl-n-pentyl-NA only marginally affected ascorbic acid output. All of the carcinogenic nitrosamines, except dipentyl-NA, increased pentobarbital-induced sleeping time (PST), serum glutamic oxalacetic transaminase (SGOT) and produced loss of glycogen and necrosis in the centrologular area of the liver after 1 or 3 oral doses. In contrast, noncarcinogenic nitrosamines and dipentyl-NA shortened PST and had no effect on liver histology (light microscopy) and SGOT. Generally, changes in ascorbic acid output correlated neither with carcinogenicity nor acute hepatotoxicity of known nitrosamines, hence the ascorbic output could not be used to predict the carcinogenicity of unknown or untested nitrosamines.
给大鼠口服后，所检测的4种非致癌性亚硝胺（NA）以及7种致癌性亚硝胺中的4种会增加尿中抗坏血酸的排出量。其余致癌性亚硝胺中，二甲基-NA会使其减少，而二乙基亚硝胺和甲基正戊基亚硝胺对抗坏血酸排出量仅有轻微影响。除二戊基亚硝胺外，所有致癌性亚硝胺在口服1或3次剂量后，都会延长戊巴比妥诱导的睡眠时间（PST）、提高血清谷氨酸草酰乙酸转氨酶（SGOT）水平，并导致肝脏中央小叶区域糖原丢失和坏死。相比之下，非致癌性亚硝胺和二戊基亚硝胺会缩短PST，且对肝脏组织学（光学显微镜检查）和SGOT没有影响。一般来说，抗坏血酸排出量的变化与已知亚硝胺的致癌性和急性肝毒性均无关联，因此抗坏血酸排出量无法用于预测未知或未测试亚硝胺的致癌性。
