Mathur A, Wallenius K, Abdulla M
Acta Odontol Scand. 1979;37(5):277-84. doi: 10.3109/00016357909004697.
Three-week-old female rats were fed 0.09 (zinc-deficient), 0.77 (zinc-adequate) or 3.98 (zinc-supplemented) mmol zinc/kg diet in three experimental groups and the palatal mucosa was painted with the water-soluble carcinogen 4-nitroquinoline N-oxide (4NQO) three times a week for 20 weeks. The zinc-supplemented diet seemed to retard the induction of carcinogenesis, whereas a low-zinc diet had the opposite effect. Once initial cellular changes had been induced the supplementary zinc seemed to accelerate their further advancement. Zinc-deficiency in animals fed a copper/zinc low-zinc diet was reflected in the plasma and liver zinc levels as well as in the copper/zinc ratio. The development of cancer was accompanied by a decrease in plasma zinc and an increase in the plasma copper/zinc ratio as well as in the liver zinc. These changes were most remarkable in the zinc-supplemented group.
将三周龄雌性大鼠分为三个实验组,分别喂食含0.09(缺锌)、0.77(锌充足)或3.98(补锌)毫摩尔锌/千克饮食,每周三次用水溶性致癌物4-硝基喹啉N-氧化物(4NQO)涂抹腭黏膜,持续20周。补锌饮食似乎延缓了致癌作用的诱导,而低锌饮食则有相反的效果。一旦诱导出初始细胞变化,补充锌似乎会加速其进一步发展。喂食铜/锌低锌饮食的动物体内缺锌反映在血浆和肝脏锌水平以及铜/锌比值上。癌症的发展伴随着血浆锌的降低、血浆铜/锌比值以及肝脏锌的增加。这些变化在补锌组最为显著。