Biology Reference
In-Depth Information
14.4 Discussion
Experimental and clinical data suggest that high concentrations of ROS can cause
nitration and/or oxidation of cellular proteins with alterations in several transcrip-
tion factors that play key roles in both carcinogenesis and drug-induced toxicity
(Portakal et al.
2000
). SOD, GPx, and CAT are considered the main antioxidant
enzymes, being directly involved in the elimination of ROS produced during
normal cellular metabolism or after oxidative insult. The activities of these
enzymes can vary depending on the phenotype of the tumor, being increased in
some and decreased in others. Jung et al. (
1997
) reported decreased or unchanged
activities of these enzymes in prostate cancer. In contrast, Baker et al. (
1997
)
detected lower levels of antioxidant enzymes in malignant prostate epithelial cells
compared to benign prostate epithelial cells. The production of oxygen radicals
increases with tumor progression, implying greater lipid peroxidation, which
induces the degeneration of cell membranes and DNA damage. In our study, levels
of MDA and nitrite in dogs suffering from adenocarcinoma and hemangio-
pericytoma were significantly increased in both plasma and tissue. It has been
demonstrated that superoxide anion and hydroxyl radicals may inactivate the
antioxidant enzymes, particularly catalase, reducing cellular defenses against free
radicals (Mayo et al.
2003
). The decreased activities of antioxidant enzymes and
increased oxidative stress observed in our study agree with the results described by
Peji´ et al. (
2009
) in endometrial adenocarcinoma and may be attributed to a
reduction in antioxidant defenses of the organism. In conclusion, our results
confirm an alteration in oxidative stress in tumor cells, but further studies are
needed to understand whether the observed changes in patients with malignant
tumors are the cause or the consequence of increased oxidative stress.
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