Nimi S, Yamaguchi T, Hayakawa T
Division of Biological Chemistry and Biologicals, National Institute of Health Sciences, Tokyo, Japan.
Biol Pharm Bull. 1998 Oct;21(10):1009-12. doi: 10.1248/bpb.21.1009.
The effect of dexamethasone (Dex) pretreatment on the Dex-dependent induction of tyrosine aminotransferase (TAT) activity was studied in primary cultured rat hepatocytes. The extent of the Dex-dependent induction of TAT activity decreased during culture in untreated cells. Dex pretreatment prevented this decrease. A Scatchard plot analysis of the results of a [3H]Dex binding assay showed that hepatocytes cultured for 2.5 h possessed both high and low affinity binding sites in their cytosols. The number of both high and low affinity binding sites decreased during culture for a further 24 h in untreated cells. Dex pretreatment partly prevented the decrease in low affinity binding sites but had no effect on the decrease in high affinity binding sites. These results show that Dex pretreatment counteracts the usual decrease in the inducibility of TAT activity, and suggest that this action of Dex may be due to the maintenance of low affinity binding sites. These results also suggest that low affinity binding sites could possibly mediate the biological response to Dex.
在地鼠原代培养肝细胞中，研究了地塞米松（Dex）预处理对Dex依赖性酪氨酸转氨酶（TAT）活性诱导的影响。在未处理的细胞培养过程中，Dex依赖性TAT活性诱导程度降低。Dex预处理可防止这种降低。对[3H]Dex结合试验结果进行Scatchard作图分析表明，培养2.5小时的肝细胞胞浆中同时存在高亲和力和低亲和力结合位点。在未处理的细胞中，再培养24小时期间，高亲和力和低亲和力结合位点的数量均减少。Dex预处理部分防止了低亲和力结合位点的减少，但对高亲和力结合位点的减少没有影响。这些结果表明，Dex预处理可抵消TAT活性诱导性通常的降低，并提示Dex的这种作用可能是由于低亲和力结合位点的维持。这些结果还提示，低亲和力结合位点可能介导对Dex的生物学反应。
