Hvattum E, Sollie E, Sørensen H N
Institute of Medical Biochemistry, University of Oslo, Norway.
Biochem Pharmacol. 1993 Oct 5;46(7):1307-10. doi: 10.1016/0006-2952(93)90482-c.
Morris 7800 C1 hepatoma cells were grown in the presence of 80 microM tetradecylthioacetic acid (TTA), a peroxisome proliferator, for 1 year (long-term-treated cells). The growth of the Morris 7800 C1 hepatoma cells was inhibited in cells treated with TTA for up to 8 days. Treatment of the cells with TTA for 1 year did not reduce growth further. The growth inhibition was easily reversed by insulin (0.4 microM). Peroxisomal acyl-CoA oxidase (ACO) (EC 1.3.99.3) activity was increased 5.5 times in cells treated with TTA for 3 days. In the cells treated with TTA for 1 year the ACO activity was increased only two times. A similar ACO mRNA half-life (two times the control) was found in cells treated with TTA for 1 year and for 3 days. This implies a loss of effect of TTA on the transcription rate of the ACO gene in long-term-treated cells.
将Morris 7800 C1肝癌细胞在80微摩尔十四烷基硫代乙酸(TTA,一种过氧化物酶体增殖剂)存在的情况下培养1年(长期处理的细胞)。用TTA处理长达8天的Morris 7800 C1肝癌细胞的生长受到抑制。用TTA处理细胞1年并未进一步降低其生长。胰岛素(0.4微摩尔)可轻易逆转生长抑制。在用TTA处理3天的细胞中,过氧化物酶体酰基辅酶A氧化酶(ACO)(EC 1.3.99.3)活性增加了5.5倍。在用TTA处理1年的细胞中,ACO活性仅增加了两倍。在用TTA处理1年和3天的细胞中发现了相似的ACO mRNA半衰期(为对照的两倍)。这意味着在长期处理的细胞中,TTA对ACO基因转录速率的影响丧失。