Sehrawat Anuradha, Sharma Sonia, Sultana Sarwat
Section of Chemoprevention and Nutrition Toxicology, Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard, Hamdard University, New Delhi, India.
Redox Rep. 2006;11(2):85-95. doi: 10.1179/135100006X101066.
Tannic acid, present in almost every food derived from plants, has been widely investigated as a chemopreventive agent because, apart from its use as a food additive, pharmacological studies have demonstrated its many health-promoting properties. In this study, we show the modulatory effect of tannic acid on 2-acetylaminofluorene (2-AAF)-mediated hepatic oxidative stress and cell proliferation in rats. 2-AAF (50 mg/kg body weight) caused reduction in hepatic glutathione content and the activities of hepatic anti-oxidant enzymes and phase-II metabolizing enzymes with an enhancement of xanthine oxidase activity, lipid peroxidation and hydrogen peroxide content. 2-AAF treatment also induced serum oxaloacetate and pyruvate transaminase, lactate dehydrogenase and gamma-glutamyl transpeptidase. Treatment of rats orally with tannic acid (125 and 250 mg/kg body weight) resulted in significant recovery of hepatic glutathione content, antioxidant and phase-II metabolizing enzymes. Also, significant decreases in lipid peroxidation, xanthine oxidase, hydrogen peroxide generation and liver damage marker enzymes were observed. The antiproliferative efficacy of the tannic acid was also evaluated. The promotion parameters induced (ornithine decarboxylase activity and DNA synthesis) by 2-AAF administration in the diet with partial hepatectomy (PH) were also significantly suppressed, dose dependently, by tannic acid. Hence, we propose that tannic acid might suppress the promotion stage via inhibition of oxidative stress and polyamine biosynthetic pathway.
几乎每种植物性食物中都含有的单宁酸，作为一种化学预防剂已得到广泛研究，因为除了用作食品添加剂外，药理学研究已证实其具有多种促进健康的特性。在本研究中，我们展示了单宁酸对2-乙酰氨基芴（2-AAF）介导的大鼠肝脏氧化应激和细胞增殖的调节作用。2-AAF（50毫克/千克体重）导致肝脏谷胱甘肽含量降低、肝脏抗氧化酶和II相代谢酶活性降低，同时黄嘌呤氧化酶活性、脂质过氧化和过氧化氢含量增加。2-AAF处理还诱导了血清草酰乙酸和丙酮酸转氨酶、乳酸脱氢酶和γ-谷氨酰转肽酶。给大鼠口服单宁酸（125和250毫克/千克体重）后，肝脏谷胱甘肽含量、抗氧化酶和II相代谢酶显著恢复。此外，脂质过氧化、黄嘌呤氧化酶、过氧化氢生成和肝损伤标志物酶也显著降低。还评估了单宁酸的抗增殖功效。在部分肝切除（PH）的饮食中，2-AAF给药诱导的促进参数（鸟氨酸脱羧酶活性和DNA合成）也被单宁酸剂量依赖性地显著抑制。因此，我们提出单宁酸可能通过抑制氧化应激和多胺生物合成途径来抑制促进阶段。
