Humans are daily exposed to 7,12-dimethylbenz(a)anthracene (DMBA), a well known polycyclic aromatic hydrocarbons (PAH). This study investigated the role of dietary intake of Vitamin K (VK), a polyphenolic compound, with potential antioxidative properties, against DMBA-induced hepatotoxicity. Sixty experimental animals (120-150 g) were divided into six groups (A-F): Control, DMBA (80 mg/kg bw) only, VK (0.00 g/10 kg) diet only, VK (7.5 g/10 kg) diet only, DMBA + VK (0.0 g/10 kg) diet and DMBA + VK (7.5 g/10 kg) diet. Single oral administration of DMBA (80 mg/kg body weight) to Wistar rats resulted in hepatic damage after 16 weeks. DMBA significantly (P < .05) decreased the activities of catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST) and glutathione peroxidase (GPx). Levels of reduced glutathione (GSH) and Vitamin C were significantly decreased with increase in malondialdehyde (MDA) and nitric oxide (NO) levels in serum and liver. Aspartate aminotransaminase (AST), alanine aminotransaminase (ALT), γ-glutamyltransferase (GGT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) activities were significantly (P < .05) elevated in the serum but reduced in the liver of DMBA-administered group. Ingestion of 7.5 g/10 kg VK diet prevented the up regulations in inflammatory biomarkers (granulocyte macrophage colony stimulating factor (GM-CSF) and interleukin 17A (IL-17A)) which elicited liver damaged in the DMBA-treated group. DMBA induced hepatic alterations in DMBA-treated group but was restored to near normal in VK (7.5 g/10 kg) diet group. These findings suggest the protective potential of increased dietary intake of vitamin K against DMBA-induced hepatic dysfunction.

中文翻译：

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维生素 K 可防止 7,12-二甲基苯（A）蒽诱导的 Wistar 大鼠肝毒性

人类每天都会接触到 7,12-二甲基苯并 (a) 蒽 (DMBA)，这是一种众所周知的多环芳烃 (PAH)。本研究调查了膳食摄入维生素 K (VK) 的作用，维生素 K (VK) 是一种多酚化合物，具有潜在的抗氧化特性，对 DMBA 诱导的肝毒性的作用。60 只实验动物（120-150 克）分为六组（AF）：对照组、仅 DMBA（80 毫克/千克体重）、仅 VK（0.00 克/10 千克）饮食、VK（7.5 克/10 千克）饮食仅，DMBA + VK (0.0 g/10 kg) 饮食和 DMBA + VK (7.5 g/10 kg) 饮食。对 Wistar 大鼠单次口服 DMBA（80 毫克/千克体重）导致 16 周后肝损伤。DMBA 显着 (P < .05) 降低过氧化氢酶 (CAT)、超氧化物歧化酶 (SOD)、谷胱甘肽-S-转移酶 (GST) 和谷胱甘肽过氧化物酶 (GPx) 的活性。随着血清和肝脏中丙二醛 (MDA) 和一氧化氮 (NO) 水平的增加，还原型谷胱甘肽 (GSH) 和维生素 C 的水平显着降低。天冬氨酸转氨酶 (AST)、丙氨酸转氨酶 (ALT)、γ-谷氨酰转移酶 (GGT)、碱性磷酸酶 (ALP) 和乳酸脱氢酶 (LDH) 活性在血清中显着升高（P < .05），但在肝脏中降低DMBA 管理组。摄入 7.5 g/10 kg V​​K 饮食阻止了炎症生物标志物（粒细胞巨噬细胞集落刺激因子 (GM-CSF) 和白介素 17A (IL-17A)）的上调，这在 DMBA 治疗组中引起了肝脏损伤。DMBA 诱导 DMBA 治疗组的肝脏改变，但在 VK (7.5 g/10 kg) 饮食组中恢复到接近正常。