Tsuda H, Okamoto H
Carcinogenesis. 1986 Nov;7(11):1805-7. doi: 10.1093/carcin/7.11.1805.
The effect of glycyrrhetinic acid (GA) on the metabolic cooperation between 6-thioguanine-resistant (6TGR) and sensitive (6TGS) Chinese hamster V79 H3 cells, was investigated. Because GA has been reported to inhibit strongly tumor formation in mouse skin induced by 7,12-dimethylbenz[a]anthracene (DMBA) plus teleocidin or DMBA plus 12-O-tetradecanoylphorbol-13-acetate (TPA), we expected that GA might restore the metabolic cooperation inhibited by TPA. The results were contrary to our expectations. GA (20-50 microM) acted cumulatively with TPA to inhibit metabolic cooperation even more, and GA (20-75 microM), by itself, was found to be a strong inhibitor of metabolic cooperation. GA was not mutagenic at the concentrations examined (0-100 microM).
研究了甘草次酸（GA）对6-硫鸟嘌呤抗性（6TGR）和敏感（6TGS）中国仓鼠V79 H3细胞之间代谢合作的影响。由于据报道GA能强烈抑制由7,12-二甲基苯并[a]蒽（DMBA）加远藤菌素或DMBA加12-O-十四烷酰佛波醇-13-乙酸酯（TPA）诱导的小鼠皮肤肿瘤形成，我们预期GA可能恢复被TPA抑制的代谢合作。结果与我们的预期相反。GA（20 - 50微摩尔）与TPA累积作用，甚至更强烈地抑制代谢合作，并且发现GA（20 - 75微摩尔）自身就是代谢合作的强抑制剂。在所检测的浓度（0 - 100微摩尔）下，GA没有致突变性。
