Lipman T O, Diamond A, Mellow M H, Patterson K Y
J Am Coll Nutr. 1987 Feb;6(1):41-6. doi: 10.1080/07315724.1987.10720164.
Zinc and vitamin A are known to interact, and deficiencies have been associated with carcinogenesis in experimental animals and humans. Since we previously have demonstrated decreased plasma zinc and vitamin A levels in patients with esophageal cancer, we wished to examine endoscopically obtained epithelial tissue for vitamin A and zinc content. This was not feasible for vitamin A, but using newly developed techniques for zinc analysis of small tissue samples, we measured esophageal epithelial zinc as well as plasma zinc and plasma vitamin A in 21 patients with esophageal cancer, 17 patients with esophagitis, and 12 normals. Mean plasma zinc in the esophageal cancer group (56 +/- 3 micrograms/dl) (mean +/- SEM) was significantly less than in the esophagitis group (72 +/- 5 micrograms/dl) and the normals (78 +/- 5 micrograms/dl). Mean plasma vitamin A in the esophageal cancer group (32 +/- 3 micrograms/dl) was significantly less than the esophagitis group (57 +/- 4 micrograms/dl) or the normals (58 +/- 5 micrograms/dl). There was no significant difference in tissue zinc content (measured as micrograms zinc/g wet weight of tissue, mean +/- SEM) among cancerous tissue (57 +/- 5 micrograms/g) and adjacent normal tissue (61 +/- 4 micrograms/g), esophagitis tissue (66 +/- 6 micrograms/g) and adjacent normal tissue (61 +/- 6 micrograms/g), or normal esophageal tissue (59 +/- 6 micrograms/g). We conclude that deficiencies of zinc or vitamin A may be cofactors in the induction of human esophageal cancer, but a mechanism cannot be accounted for by differences in epithelial zinc content.
锌和维生素A已知会相互作用,并且在实验动物和人类中,它们的缺乏与致癌作用有关。由于我们之前已证明食管癌患者血浆锌和维生素A水平降低,因此我们希望通过内镜检查获取上皮组织,检测其中维生素A和锌的含量。对于维生素A来说,这不可行,但我们使用新开发的技术分析小组织样本中的锌含量,测定了21例食管癌患者、17例食管炎患者和12例正常人的食管上皮锌以及血浆锌和血浆维生素A的含量。食管癌组的平均血浆锌含量(56±3微克/分升)(平均值±标准误)显著低于食管炎组(72±5微克/分升)和正常组(78±5微克/分升)。食管癌组的平均血浆维生素A含量(32±3微克/分升)显著低于食管炎组(57±4微克/分升)或正常组(58±5微克/分升)。癌组织(57±5微克/克)与相邻正常组织(61±4微克/克)、食管炎组织(66±6微克/克)与相邻正常组织(61±6微克/克)或正常食管组织(59±6微克/克)之间的组织锌含量(以每克组织湿重中锌的微克数计,平均值±标准误)无显著差异。我们得出结论,锌或维生素A缺乏可能是人类食管癌诱发过程中的辅助因素,但上皮锌含量的差异无法解释其机制。