van Rijn H, Bevers M M, van Wijk R, Wicks W D
J Cell Biol. 1974 Jan;60(1):181-91. doi: 10.1083/jcb.60.1.181.
The ability of N(6), O(2)'-dibutyryl cyclic AMP (DBcAMP) to regulate a number of metabolic events in four lines of cultured rat hepatomas has been examined. Although dexamethasone induces tyrosine transaminase in all four lines, DBcAMP induces this enzyme normally only in H35 cells. A slight increase in transaminase activity was seen with MH(1)C(1) cells and HTC cells, but no effect was detectable in RLC cells. In contrast, phosphoenolpyruvate carboxykinase activity is increased by both agents in H35 and MH(1)C(1) cells, but neither had any effect in HTC or RLC cells. DBcAMP caused a rapid inhibition of the growth rate and DNA synthesis and an increase in protein content in both H35 and MH(1)C(1) cells but not in HTC or RLC cells. The effect of DBcAMP on DNA synthesis in MH(1)C(1) cells could be reversed by deoxycytidine as is also the case with H35 cells. The resistance of HTC and RLC cells to DBcAMP was not due to reduced uptake or deacylation as judged by studies with [(3)H]DBcAMP. The cyclic nucleotide appears to enter the cells by passive diffusion as the intracellular concentration approaches that in the medium within 30-60 min. Possible explanations for the differential responses observed are discussed.
已研究了N(6),O(2)'-二丁酰环磷酸腺苷(DBcAMP)对四株培养的大鼠肝癌细胞系中若干代谢事件的调节能力。虽然地塞米松在所有四株细胞系中均可诱导酪氨酸转氨酶，但DBcAMP通常仅在H35细胞中正常诱导该酶。在MH(1)C(1)细胞和HTC细胞中观察到转氨酶活性略有增加，但在RLC细胞中未检测到任何影响。相反，在H35和MH(1)C(1)细胞中，两种药物均可增加磷酸烯醇丙酮酸羧激酶活性，但在HTC或RLC细胞中均无任何作用。DBcAMP导致H35和MH(1)C(1)细胞的生长速率和DNA合成迅速受到抑制，蛋白质含量增加，但在HTC或RLC细胞中则不然。与H35细胞一样，脱氧胞苷可逆转DBcAMP对MH(1)C(1)细胞中DNA合成的影响。通过对[(3)H]DBcAMP的研究判断，HTC和RLC细胞对DBcAMP的抗性并非由于摄取减少或去酰化。随着细胞内浓度在30 - 60分钟内接近培养基中的浓度，环核苷酸似乎通过被动扩散进入细胞。讨论了观察到的差异反应的可能解释。
