Baer-Dubowska W, Gnojkowski J, Fenrych W
Department of Pharmaceutical Biochemistry, K. Marcinkowski University Medical School, Poznan, Poland.
Nutr Cancer. 1997;29(1):42-7. doi: 10.1080/01635589709514600.
Tannic acid, a naturally occurring plant phenol, was shown to inhibit the mutagenicity and/or tumorigenicity of several polycyclic aromatic hydrocarbons in mouse skin. In this study the effect of topical application of tannic acid on epidermal aryl hydrocarbon hydroxylase, glutathione S-transferase, and binding of benzo[a]pyrene (B[a]P) to epidermal DNA was compared with the activity of synthetic gallic acid esters. Single topical application of 8 mumol octyl and dodecyl gallate had no effect on the induction of aryl hydrocarbon hydroxylase, whereas propyl gallate and tannic acid increased the enzyme activity by nearly 200%. Application of the phenolics one hour before 0.2 mumol of B[a]P enhanced the enzyme activity, but the observed differences were not significant in comparison with a B[a]P-treated group of mice. Application of dodecyl and octyl gallates to mouse skin resulted in three- and twofold increases, respectively, in the activity of glutathione S-transferase. Combined treatment with dodecyl gallate and B[a]P also resulted in significant enhancement of this enzyme activity. Application of the same dose of tannic acid to mouse skin one hour before the application of 0.2 or 1 mumol of B[a]P afforded 60% inhibition of covalent benzo[a]pyrene-diol-epoxide binding to epidermal DNA. Gallic acid esters with the exception of dodecyl gallate were less effective inhibitors of benzo[a]pyrene-diol-epoxide binding, especially when the higher dose of B[a]P was used. These results indicate that the antitumorigenic activity of tannic acid involves the interaction of the ultimate carcinogen with DNA rather than an altered metabolism. The linkage between gallic acid and glucose in natural plant phenols is also more effective at inhibiting B[a]P binding to epidermal DNA than the linkage with the alkyl group in synthetic gallates.
单宁酸是一种天然存在的植物酚，已被证明能抑制小鼠皮肤中几种多环芳烃的致突变性和/或致癌性。在本研究中，将单宁酸局部应用于表皮芳烃羟化酶、谷胱甘肽S-转移酶以及苯并[a]芘（B[a]P）与表皮DNA结合的影响，与合成没食子酸酯的活性进行了比较。单次局部应用8 μmol的辛酯和十二烷基酯对芳烃羟化酶的诱导没有影响，而没食子酸丙酯和单宁酸使该酶活性增加了近200%。在给予0.2 μmol B[a]P前1小时应用酚类物质可增强该酶活性，但与B[a]P处理的小鼠组相比，观察到的差异不显著。将十二烷基酯和辛酯应用于小鼠皮肤，分别使谷胱甘肽S-转移酶活性增加了三倍和两倍。十二烷基酯与B[a]P联合处理也显著增强了该酶活性。在给予0.2或1 μmol B[a]P前1小时，将相同剂量的单宁酸应用于小鼠皮肤，可使共价苯并[a]芘-二醇-环氧化物与表皮DNA的结合受到60%的抑制。除十二烷基酯外，没食子酸酯对苯并[a]芘-二醇-环氧化物结合的抑制作用较小，尤其是在使用较高剂量的B[a]P时。这些结果表明，单宁酸的抗肿瘤活性涉及最终致癌物与DNA的相互作用，而非代谢改变。天然植物酚中没食子酸与葡萄糖的连接，在抑制B[a]P与表皮DNA结合方面，也比合成没食子酸酯中与烷基的连接更有效。
