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我们研究了以硫氧还蛋白还原酶为靶点的创新抗肿瘤药物—乙烷硒啉在不同剂量下,对小鼠H22肝癌肿瘤组织中的氧化还原状态的影响。主要考察了小分子抗氧化物质谷胱甘肽(GSH),脂质过氧化产物丙二醛(MDA)含量及重要的抗氧化物酶活性以反映H22肿瘤组织中的氧还状态。我们发现,GSH含量,硫氧还蛋白还原酶和超氧化物歧化酶的活性的降低,以及丙二醛含量的升高,都和肿瘤生长抑制及乙烷硒啉的剂量密切相关。而谷胱甘肽还原酶以及谷胱甘肽过氧化物酶在一些药物剂量下,有代偿性的活性上升趋势。过氧化氢酶几乎不受影响。最后,我们研究了肿瘤生长抑制率与这些肿瘤氧还因子的关系。我们的研究显示:乙烷硒啉可能是通过诱导氧化应激水平抑制小鼠体内H22肿瘤细胞的生长。
We investigated the effects of ethane selenide, an innovative antitumor drug targeting thioredoxin reductase, on the redox status of mouse H22 hepatoma tumor tissue at various doses. The main contents of glutathione (GSH), malondialdehyde (MDA), and antioxidant enzyme activities of small molecule antioxidants were investigated to reflect the oxygen status in H22 tumor tissues. We found that the reduction of GSH content, the activity of thioredoxin reductase and superoxide dismutase, and the increase of malondialdehyde content are closely related to the tumor growth inhibition and dose of ethaselen. And glutathione reductase and glutathione peroxidase in some drug doses, compensatory activity upward trend. Catalase is almost unaffected. Finally, we examined the relationship between tumor growth inhibition and these tumor oxygens. Our study shows that ethaselen may inhibit the growth of H22 tumor cells in mice by inducing oxidative stress.