Portakal O, Ozkaya O, Erden Inal M, Bozan B, Koşan M, Sayek I
Department of Biochemistry, The Medical School of Osmangazi University, Eskişehir, Turkey.
Clin Biochem. 2000 Jun;33(4):279-84. doi: 10.1016/s0009-9120(00)00067-9.
An increasing amount of experimental and epidemiological evidence implicates the involvement of oxygen derived radicals in the pathogenesis of cancer development. Oxygen derived radicals are able to cause damage to membranes, mitochondria, and macromolecules including proteins, lipids and DNA. Accumulation of DNA damages has been suggested to contribute to carcinogenesis. It would, therefore, be advantageous to pinpoint the effects of oxygen derived radicals in cancer development.
In the present study, we investigated the relationship between oxidative stress and breast cancer development in tissue level. Breast cancer is the most common malignant disease in Western women. Twenty-one breast cancer patients, who underwent radical mastectomy and diagnosed with infiltrative ductal carcinoma, were used in the study. We determined coenzyme Q10 (Q) concentrations, antioxidant enzyme activities (mitochondrial and total superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase), and malondialdehyde (MDA) levels in tumor and surrounding tumor-free tissues.
Q concentrations in tumor tissues significantly decreased as compared to the surrounding normal tissues (p < 0.001). Higher MDA levels were observed in tumor tissues than noncancerous tissues (p < 0.001). The activities of MnSOD, total SOD, GSH-Px and catalase in tumor tissues significantly increased (p < 0.001) compared to the controls.
These findings may support that reactive oxygen species increased in malignant cells, and may cause overexpression of antioxidant enzymes and the consumption of coenzyme Q10. Increased antioxidant enzyme activities may be related with the susceptibility of cells to carcinogenic agents and the response of tumor cells to the chemotherapeutic agents. Administration of coenzyme Q10 by nutrition may induce the protective effect of coenzyme Q10 on breast tissue.
越来越多的实验和流行病学证据表明，氧衍生自由基参与癌症发生的病理过程。氧衍生自由基能够对细胞膜、线粒体以及包括蛋白质、脂质和DNA在内的大分子造成损伤。DNA损伤的积累被认为与致癌作用有关。因此，明确氧衍生自由基在癌症发生中的作用将是有益的。
在本研究中，我们在组织水平上研究了氧化应激与乳腺癌发生之间的关系。乳腺癌是西方女性中最常见的恶性疾病。本研究使用了21例接受根治性乳房切除术并被诊断为浸润性导管癌的乳腺癌患者。我们测定了肿瘤组织和肿瘤周围无瘤组织中辅酶Q10（Q）的浓度、抗氧化酶活性（线粒体和总超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶）以及丙二醛（MDA）水平。
与周围正常组织相比，肿瘤组织中的Q浓度显著降低（p<0.001）。肿瘤组织中的MDA水平高于非癌组织（p<0.001）。与对照组相比，肿瘤组织中锰超氧化物歧化酶、总超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶的活性显著增加（p<0.001）。
这些发现可能支持恶性细胞中活性氧增加，并可能导致抗氧化酶的过度表达和辅酶Q10的消耗。抗氧化酶活性增加可能与细胞对致癌剂的易感性以及肿瘤细胞对化疗药物的反应有关。通过营养方式给予辅酶Q10可能诱导辅酶Q10对乳腺组织的保护作用。
