Waalkes M P, Wilson M J
Toxicol Lett. 1986 Sep;32(3):289-94. doi: 10.1016/0378-4274(86)90121-9.
Cultured TRL 1215 cells in log phase of growth were exposed first to butyric acid (BA; 0.1-2.0 mM) and then 48 h later, to cadmium (Cd; 10 microM). Metallothionein (MT) concentrations were measured 24 h after Cd addition. Cd alone caused approx. a 10-fold increase in cellular MT levels, while BA alone had no effect. BA pretreatment followed by Cd exposure, however, resulted in MT levels up to 25 times those in control cells. Concurrent exposure to hydroxyurea (HU) eliminated the enhancing effect of BA pretreatment on induction of MT by Cd, indicating that DNA synthesis is required. BA-pretreated cells did not show marked increases in cellular uptake of Cd. BA pretreatment enhances Cd induction of MT synthesis through a mechanism that is dependent on the synthesis of DNA.
处于对数生长期的培养TRL 1215细胞首先暴露于丁酸（BA；0.1 - 2.0 mM），然后在48小时后，暴露于镉（Cd；10 microM）。在添加镉后24小时测量金属硫蛋白（MT）浓度。单独的镉导致细胞MT水平约增加10倍，而单独的BA没有影响。然而，BA预处理后再暴露于镉，导致MT水平高达对照细胞的25倍。同时暴露于羟基脲（HU）消除了BA预处理对镉诱导MT的增强作用，表明DNA合成是必需的。BA预处理的细胞在镉的细胞摄取方面没有显示出明显增加。BA预处理通过一种依赖于DNA合成的机制增强了镉诱导的MT合成。
