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Methylguanine DNA methyl transferase activities, glutathione s transferase and nitric oxide in bladder cancer patients.

机译:膀胱癌患者的甲基鸟嘌呤DNA甲基转移酶活性,谷胱甘肽转移酶和一氧化氮。

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摘要

Tumor formation is a multistep process that can be divided in to the stages of tumor initiation, promotion, and progression. DNA repair protein; MGMT is a key suicide enzyme that repairs the mispairing base methylguanine, which is induced in DNA as a minor lesion. The glutathione S transferases (GSTs) are a family of enzymes that are important to protect against alkylating agents. Nitric oxide, contributes to the regulation of tumor angiogenesis. A substantial body of experimental evidence supports the hypothesis that tumor angiogenesis is fundamental for the growth and metastasis of solid tumors. We measured the activities of GST, MGMT, and levels of NO3-/NO2- in the leukocytes from patients with bladder carcinoma and healthy controls and activities of MGMT in the tissue from patients with bladder carcinoma and adjacent normal tissue in bladder. Both GST and tissue MGMT activites were significantly increased in the patient group. There was no significant difference between controls and patients for MGMT activity in peripheral blood leukocytes (PBL). Nitrateitrite levels in PBL, there was no significant difference between controls and patients. Nitrateitrite levels were increased in G2-G3 tumors. In conclusion, we determined high concentrations of nitrite in leukocytes are suspected alkylation damage by induction nitrosamine. Increased DNA alkylation damage may lead the stimulation of MGMT and GST.
机译:肿瘤形成是一个多步骤的过程,可以分为肿瘤开始,促进和发展的阶段。 DNA修复蛋白; MGMT是一种重要的自杀酶,可修复碱基配对的错配碱基甲基鸟嘌呤,该碱基在DNA中被诱导为小损伤。谷胱甘肽S转移酶(GST)是一类重要的酶,可防止烷基化剂的侵害。一氧化氮有助于调节肿瘤血管生成。大量的实验证据支持以下假设:肿瘤血管生成是实体瘤生长和转移的基础。我们测量了膀胱癌和健康对照患者白细胞中GST,MGMT的活性以及NO3- / NO2-的水平,以及膀胱癌和膀胱癌附近正常组织患者组织中MGMT的活性。在患者组中,GST和组织MGMT活性均显着增加。对照组和患者外周血白细胞(PBL)中MGMT活性无显着差异。 PBL中的硝酸盐/亚硝酸盐水平,对照组和患者之间没有显着差异。 G2-G3肿瘤中硝酸盐/亚硝酸盐水平升高。总之,我们确定白细胞中高浓度的亚硝酸盐被怀疑是诱导亚硝胺引起的烷基化破坏。 DNA烷基化损伤的增加可能导致MGMT和GST的刺激。

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