Paulsen J E
Virchows Arch B Cell Pathol Incl Mol Pathol. 1984;46(3):199-204. doi: 10.1007/BF02890309.
Pretreatment (at 1 h) with retinoic acid (RA) inhibited both the 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced wave of epidermal putrescine accumulation (which peaked at 8 h) and the first wave of epidermal DNA synthesis (which peaked at 16 h), but failed to depress the second wave of DNA synthesis (which peaked at 32 h) even with a second application of RA at 16 h. The inhibitory action of RA pretreatment on the DNA synthesis peak at 16 h was dosedependent. Thus, there may be an association between the putrescine accumulation at 8 h and the wave of DNA synthesis at 16 h. When TPA-stimulated epidermis was pretreated with RA, exogenous putrescine (given i.p.) affected neither the reduced putrescine accumulation nor the reduced first wave of DNA synthesis. However, exogenous putrescine potentiated stimulated DNA synthesis, both at 16 h after TPA and at 32 h after RA plus TPA.
用视黄酸(RA)预处理(1小时)可抑制12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)诱导的表皮腐胺积累波(在8小时达到峰值)和第一波表皮DNA合成(在16小时达到峰值),但即使在16小时再次应用RA,也未能抑制第二波DNA合成(在32小时达到峰值)。RA预处理对16小时DNA合成峰值的抑制作用呈剂量依赖性。因此,8小时腐胺积累与16小时DNA合成波之间可能存在关联。当用RA预处理TPA刺激的表皮时,外源性腐胺(腹腔注射)既不影响腐胺积累的减少,也不影响第一波DNA合成的减少。然而,外源性腐胺增强了TPA后16小时以及RA加TPA后32小时的刺激DNA合成。