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良性前列腺增生症和前列腺癌患者氧化损伤与细胞凋亡之间的可能关系。

Possible relations between oxidative damage and apoptosis in benign prostate hyperplasia and prostate cancer patients.

作者信息

Kosova Funda, Temeltaş Gökhan, Arı Zeki, Lekili Murat

机构信息

Celal Bayar University School of Health, Manisa, Turkey,

出版信息

Tumour Biol. 2014 May;35(5):4295-9. doi: 10.1007/s13277-013-1560-y. Epub 2013 Dec 28.

DOI:10.1007/s13277-013-1560-y
PMID:24375255
Abstract

Cancer has been described as the twentieth century plague, and is a very common health problem. It has been reported that ROS and ROS products play a key role in cancer and that oxidative damage is effective in apoptosis initiation. In this study we aimed to evaluate the relationship between MDA (malondialdehyde), DNA damage (8-hydroxyguanine, 8-OH-dG), and caspase-3 in BHP and prostate cancer patients. Twenty male patients with prostate cancer and 20 male patients with benign prostate hyperplasia were included into this study. The MDA (nanomole), DNA damage (nanograms per millilitre), and caspase-3 (nanograms per millilitre) levels were measured in prostate cancer and benign prostate hyperplasia using Elisa kits (Millipore Corporation, Billerica, MA, USA). In the prostate cancer group, serum MDA (30.96 ± 9.25) and DNA damage (4.42 ± 0.36) levels were significantly raised (p < 0.05) when compared to the benign prostate hyperplasia group (24.05 ± 8.06, 3.99 ± 0.54). However, in the prostate cancer group, serum caspase-3 (2.36 ± 0.82) levels were statistically significantly lowered (p < 0.05) compared with the benign prostate hyperplasia group (3.15 ± 1.04). We observed that altered prooxidant, DNA damage levels may lead to an increase in oxidative damage and may consequently play an important role in prostate carcinogenesis. These findings indicate that, although the triggering of these changes is unknown, changes in the levels of MDA, DNA damage, and caspase-3 in the blood are related to prostatic carcinoma development. In addition, it would be appropriate to conduct new studies with a large number of patients at different stages.

摘要

癌症被描述为二十世纪的瘟疫,是一个非常常见的健康问题。据报道,活性氧(ROS)及其产物在癌症中起关键作用,并且氧化损伤在启动细胞凋亡方面是有效的。在本研究中,我们旨在评估良性前列腺增生(BHP)患者和前列腺癌患者中丙二醛(MDA)、DNA损伤(8-羟基鸟嘌呤,8-OH-dG)和半胱天冬酶-3之间的关系。本研究纳入了20名前列腺癌男性患者和20名良性前列腺增生男性患者。使用酶联免疫吸附测定试剂盒(美国马萨诸塞州比勒里卡的密理博公司)测量前列腺癌和良性前列腺增生患者体内的MDA(纳摩尔)、DNA损伤(每毫升纳克)和半胱天冬酶-3(每毫升纳克)水平。与良性前列腺增生组(24.05±8.06,3.99±0.54)相比,前列腺癌组的血清MDA(30.96±9.25)和DNA损伤(4.42±0.36)水平显著升高(p<0.05)。然而,与良性前列腺增生组(3.15±1.04)相比,前列腺癌组的血清半胱天冬酶-3(2.36±0.82)水平在统计学上显著降低(p<0.05)。我们观察到,促氧化剂和DNA损伤水平的改变可能导致氧化损伤增加,从而可能在前列腺癌发生过程中起重要作用。这些发现表明,尽管这些变化的触发因素尚不清楚,但血液中MDA、DNA损伤和半胱天冬酶-3水平的变化与前列腺癌的发展有关。此外,进行大量不同阶段患者的新研究是合适的。

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