Objectives: An increasing amount of experimental and epidemiological eviden
ce implicates the involvement of oxygen derived radicals in the pathogenesi
s of cancer development. Oxygen derived radicals are able to cause damage t
o membranes, mitochondria, and macromolecules including proteins, lipids an
d DNA. Accumulation of DNA damages has been suggested to contribute to carc
inogenesis. It would, therefore, be advantageous to pinpoint the effects of
oxygen derived radicals in cancer development.
Design and methods: In the present study, we investigated the relationship
between oxidative stress and breast cancer development in tissue level. Bre
ast cancer is the most common malignant disease in Western women. Twenty-on
e breast cancer patients, who underwent radical mastectomy acid diagnosed w
ith infiltrative ductal carcinoma, were used in the study. We determined co
enzyme Q10 (Q) concentrations. antioxidant enzyme activities (mitochondrial
and total superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), cat
alase), and malondialdehyde (MDA) levels in tumor and surrounding tumor-fre
e tissues.
Results: Q concentrations in tumor tissues significantly decreased as compa
red to the surrounding normal tissues (p < 0.001). Higher MDA levels were o
bserved in tumor tissues than noncancerous tissues (p < 0.001). The activit
ies of MnSOD, total SOD, GSH-Px and catalase in tumor tissues significantly
increased (p < 0.001) compared to the controls.
Conclusions: These Findings may support that reactive oxygen species increa
sed in malignant cells, and may cause overexpression of antioxidant enzymes
and the consumption of coenzyme Q10. Increased antioxidant enzyme activiti
es may be related with the susceptibility of cells to carcinogenic agents a
nd the response of tumor cells to the chemotherapeutic agents. Administrati
on of coenzyme Q10 by nutrition may induce the protective effect of coenzym
e Q10 on breast tissue. Copyright (C) 2000 The Canadian Society of Clinical
Chemists.