Hepatocellular carcinoma (HCC) is a common malignancy and the main cause of mortality in patients with chronic liver diseases. This study reports the inhibitory effect of boron on HCC induced in rats by administering thioacetamide (TAA) (0.03%) in drinking water for 400days. Boron (4mg/kg body weight) was administered orally after induction of carcinoma. Treatment was continued for 122days, and cell proliferation, histology and biochemistry of treated and control group of rats were studied. Proliferating cell nuclear antigen (PCNA), and [(3)H]-thymidine incorporation, which increased in rats exposed to carcinogen, significantly decreased after boron treatment. PCNA index decreased from 80 in HCC rats to 32 after boron treatment. In the control group, it was 20. Boron caused a dose-dependent decrease in carcinogen-induced [(3)H]-thymidine uptake by the rat hepatocyte. It could partially reverse the activity of selected biochemical indicators of hepatic damage, oxidative stress, selenium and serum retinol, which are depleted in liver cancer, and improved overall health of animal. The study implicates the elevated levels of mammalian molybdenum Fe-S containing flavin hydroxylases, which increase the free radical production and oxidative stress, consequently causing increased hepatic cell proliferation in HCC, and reports boron to ameliorate these changes in liver cancer.

译文

肝细胞癌 (HCC) 是一种常见的恶性肿瘤,是慢性肝病患者死亡的主要原因。这项研究报告了硼通过在饮用水中施用硫代乙酰胺 (TAA) (0.03%) 400天对大鼠诱导的HCC的抑制作用。诱导癌后口服硼 (4mg/kg体重)。持续治疗122天,并研究了治疗组和对照组大鼠的细胞增殖,组织学和生物化学。在暴露于致癌物的大鼠中,增殖细胞核抗原 (PCNA) 和 [(3)H]-胸苷掺入增加,在硼处理后显着减少。硼处理后,PCNA指数从肝癌大鼠的80下降到32。对照组为20。硼导致大鼠肝细胞对致癌物诱导的 [(3)H]-胸苷摄取的剂量依赖性降低。它可以部分逆转肝癌中肝损伤,氧化应激,硒和血清视黄醇的某些生化指标的活性,并改善动物的整体健康状况。该研究暗示了含有黄素羟化酶的哺乳动物钼Fe-S水平升高,这会增加自由基的产生和氧化应激,从而导致HCC中肝细胞增殖增加,并报道硼可以改善肝癌中的这些变化。

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