Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura 35516, Egypt.
Arch Toxicol. 2010 May;84(5):389-96. doi: 10.1007/s00204-010-0511-2. Epub 2010 Jan 30.
Aflatoxin B(1) is a potent hepatotoxic and hepatocarcinogenic mycotoxin. Lipid peroxidation and oxidative DNA damage are the principal manifestations of aflatoxin B(1)-induced toxicity that could be counteracted by antioxidants. Many plant constituents have been reported to prevent liver damage associated with lipid peroxidation. In this study, curcumin (polyphenolic antioxidant purified from turmeric) and resveratrol (polyphenol obtained from grapes) were evaluated for possible protection against liver injury induced by aflatoxin B(1) in rats. Adult male Fischer rats were divided into six groups including untreated control, curcumin control (200 mg/kg BW), resveratrol control (10 mg/kg BW) and aflatoxin B(1) (25 microg/kg BW). Other two groups were administered either curcumin or resveratrol along with aflatoxin B(1). The study was carried out for 90 days. At the end of the experiment period, blood and tissue samples were collected from the animals before they were killed. Livers were collected for histopathologic studies and fixed in 10% buffered formalin solution. Serum was used for estimation of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and gamma-glutamyl transferase (gamma-GT) enzymes. The lipid peroxidation, reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were estimated in liver homogenates. The results revealed that aflatoxin B(1) administration caused liver damage as indicated by statistically significant (P < 0.05) increase in serum ALT, AST and gamma-GT levels. In addition, there were general statistically significant reductions in the activities of GSH, SOD, CAT, GSH-Px, and an increase in lipid peroxidation in the liver of aflatoxin B(1)-treated group compared to the untreated control group. Curcumin showed a significant hepatoprotective activity by lowering the levels of serum marker enzymes, lipid peroxidation and elevating the levels of GSH, SOD, CAT and GSH-Px. However, resveratrol failed to protect from the aflatoxin B(1)-induced liver injury. These findings suggest that curcumin but not resveratrol has a hepatoprotective effect against aflatoxin B(1)-induced liver injury.
黄曲霉毒素 B(1) 是一种具有强烈肝毒性和致癌性的真菌毒素。脂质过氧化和氧化 DNA 损伤是黄曲霉毒素 B(1) 诱导毒性的主要表现形式,抗氧化剂可以对抗这种毒性。许多植物成分已被报道可预防与脂质过氧化相关的肝损伤。在这项研究中,姜黄素(从姜黄中提取的多酚抗氧化剂)和白藜芦醇(从葡萄中提取的多酚)被评估是否可能预防黄曲霉毒素 B(1) 诱导的大鼠肝损伤。成年雄性 Fischer 大鼠分为六组,包括未处理对照组、姜黄素对照组(200mg/kg BW)、白藜芦醇对照组(10mg/kg BW)和黄曲霉毒素 B(1)(25μg/kg BW)。另外两组同时给予姜黄素或白藜芦醇和黄曲霉毒素 B(1)。研究进行了 90 天。在实验期结束时,在处死动物之前从动物身上采集血液和组织样本。收集肝脏进行组织病理学研究,并固定在 10%缓冲福尔马林溶液中。血清用于估计丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)和γ-谷氨酰转移酶(γ-GT)酶。肝匀浆中估计脂质过氧化、还原型谷胱甘肽(GSH)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)。结果表明,黄曲霉毒素 B(1) 给药导致肝损伤,血清 ALT、AST 和 γ-GT 水平显著升高(P <0.05)。此外,与未处理对照组相比,黄曲霉毒素 B(1) 处理组肝脏中 GSH、SOD、CAT、GSH-Px 的活性普遍显著降低,脂质过氧化增加。姜黄素通过降低血清标记酶、脂质过氧化水平和提高 GSH、SOD、CAT 和 GSH-Px 水平表现出显著的保肝活性。然而,白藜芦醇未能防止黄曲霉毒素 B(1) 引起的肝损伤。这些发现表明,姜黄素而不是白藜芦醇对黄曲霉毒素 B(1) 诱导的肝损伤具有保护作用。