Kerkvliet N I, Koller L D, Baecher L G, Brauner J A
J Natl Cancer Inst. 1979 Aug;63(2):479-83.
In vivo MSB tumor growth and cell-mediated cytotoxicity (CMC) to MSB tumor cells in vitro were studied in male C57BL/6 mice exposed to 0, 3, 30, or 300 ppm Cd as CdCl2 in their drinking water for 21 weeks prior to and during tumor growth. CMC was assessed on days 5, 12, and 19 post injection with the use of both a 51Cr release assay and a 51Cr post-label assay. Cd exposure significantly inhibited the growth of MSB tumors in vivo and enhanced the levels of CMC in the tumor-bearing hosts. Peak levels of CMC on day 12 post tumor injection were significantly increased in Cd-exposed animals. However, whereas the inhibition of tumor growth was directly dependent on the dose of Cd, the enhancement of CMC was inversely related to dosage. These data suggested that other mechanisms in addition to increased CMC were involved in tumor growth inhibition. Possible factors such as direct inhibition of tumor growth by Cd and decreased serum blocking levels in Cd-exposed animals are discussed.
在雄性C57BL/6小鼠体内研究了MSB肿瘤的生长以及在肿瘤生长之前和期间，给小鼠饮用含0、3、30或300 ppm氯化镉（CdCl₂）的水21周后，其对MSB肿瘤细胞的细胞介导细胞毒性（CMC）。在注射后第5、12和19天，使用⁵¹Cr释放试验和⁵¹Cr后标记试验评估CMC。镉暴露显著抑制了体内MSB肿瘤的生长，并提高了荷瘤宿主的CMC水平。在肿瘤注射后第12天，镉暴露动物的CMC峰值水平显著增加。然而，虽然肿瘤生长的抑制直接取决于镉的剂量，但CMC的增强与剂量呈负相关。这些数据表明，除了增加CMC外，其他机制也参与了肿瘤生长的抑制。文中讨论了可能的因素，如镉对肿瘤生长的直接抑制以及镉暴露动物血清阻断水平的降低。
