镉离子（Cd++）抑制血清饥饿的NRK - 49F细胞中表皮生长因子（EGF）诱导的DNA合成，但不抑制EGF诱导的myc信使核糖核酸（mRNA）积累。
Cd++ inhibits EGF induced DNA synthesis but not EGF induced myc mRNA accumulation in serum starved NRK-49F cells.
作者信息
Tang N, Clapper J A, Enger M D
机构信息
Department of Zoology, Iowa State University, Ames 50011.
出版信息
Cell Biol Toxicol. 1991 Jan;7(1):35-47. doi: 10.1007/BF00121328.
Cd++ inhibits EGF-induced 3H-thymidine incorporation in serum deprived NRK-49F cells in a dose dependent pattern. The underlying mechanisms for this inhibition are largely unknown. EGF-induced myc mRNA accumulation in NRK-49F cells and the effects of Cd++ on this response were examined under conditions that result in partial or complete inhibition of EGF-induced DNA synthesis. It was found that doses of Cd++ that inhibit EGF-induced DNA synthesis do not inhibit EGF-induced protein synthesis and myc mRNA accumulation. Cd++ doses of 0.5 microM and 1 microM were found actually to increase EGF-induced myc mRNA accumulation and amino acid incorporation. These results show that the effect of Cd++ on EGF-induced DNA synthesis is not due to inhibition of entrance into G1, but rather that Cd++ acts on events subsequent to myc accumulation; that is, events associated with either G1 progression, entry into S or DNA synthesis.
镉离子（Cd++）以剂量依赖的方式抑制血清饥饿的NRK - 49F细胞中表皮生长因子（EGF）诱导的3H - 胸苷掺入。这种抑制作用的潜在机制在很大程度上尚不清楚。在导致EGF诱导的DNA合成部分或完全抑制的条件下，研究了EGF诱导的NRK - 49F细胞中myc mRNA积累以及Cd++对该反应的影响。发现抑制EGF诱导的DNA合成的Cd++剂量并不抑制EGF诱导的蛋白质合成和myc mRNA积累。实际上发现0.5微摩尔和1微摩尔的Cd++剂量会增加EGF诱导的myc mRNA积累和氨基酸掺入。这些结果表明，Cd++对EGF诱导的DNA合成的影响不是由于抑制进入G1期，而是Cd++作用于myc积累之后的事件；也就是说，这些事件与G1期进展、进入S期或DNA合成相关。
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