Oxidative Stress and Carcinogenesis - Theoretical Introduction
Authors:
Richard Salzman 1; J. Tomandl 2; L. Pácal 3; K. Kaňková 3; Z. Horáková 1; R. Kostřica 1
Authors‘ workplace:
Klinika otorinolaryngologie a chirurgie hlavy a krku LF MU a FN u sv. Anny, Brno
; přednosta prof. MUDr. R. Kostřica, CSc.
1; Biochemický ústav LF MU, Brno
2; Ústav experimentální patofyziologie LF MU, Brno
3
Published in:
Otorinolaryngol Foniatr, 56, 2007, No. 1, pp. 39-44.
Category:
Comprehensive Reports
Overview
Potentially causal relationship between oxidative stress and cancer attracted much attention over the past several years since balance between pro-oxidant and antioxidant capacities is supposed to play an important role in cancer development.
Reactive oxygen species (ROS) is a term usually reserved to describe group of highly reactive forms of oxygen carrying one or more unpaired electrons. They include superoxide anion, hydrogen peroxide, hydroxyl radical, singlet oxygen, etc. Surplus electrons, unused for generation of proton gradient, can interact with oxygen to produce superoxide. If not neutralized rapidly enough by the action of antioxidative enzymes and non-enzymatic antioxidants, the intracellular structures are damaged by oxidation.
Source of ROS evoking oxidative stress is either exogenous or endogenous. The most important exogenous oxidants are ozone and cigarette smoke. Endogenously, numerous inflammatory cells, e.g. eosinophils, alveolar macrophages, etc., release ROS. However, mitochondria, more precisely protein complexes of the mitochondrial respiratory chain, are a dominant source of endogenous ROS. Pro-oxidant and antioxidant capacities in a healthy cell are kept in dynamic equilibrium by neutralizing overproduction of ROS and rebuilding of damaged intracellular structures.
Clinical and experimental studies have provided sufficient background supporting an important role of oxidative stress in cancer development. Oxidative stress is related to cancer in multiple ways. First, oxidative stress can mediate oxidative damage to DNA and thereby initially promote carcinogenesis. Second, many malignant cells have an abnormal ability to cope with oxidative stress due to alterations in their antioxidant properties. One of the cancers with strongest link to oxidative damage and oxidative stress is head and neck squamous cell carcinoma since tobacco and alcohol as sources of massive quantities of ROS are clearly identified as etiologic factors of these malignancies.
The authors present theoretical background of genesis and effect of oxidative stress in head and neck cancer. Furthermore, hypotheses of its impact on carcinogenesis are discussed.
Key words:
oxidative stress, antioxidative enzymes, head and neck cancer, carcinogenesis, reactive oxygen species, oxygen free radicals.
Sources
1. Agosti, J. M., Altman, L. C., Ayars, G. H. et al.: The injurious effect of eosinophil peroxidase, hydrogen peroxidase and habides on pneumocytes in vitro. Journal of Allergy and Clinical Immunology, 79, 1987, s. 496-504.
2. Ayars, G. H., Altman, L. C., McManus, M. M. et al.: The injurious effect of eosinophil peroxidase-halide system and major basic protein in human nasal epithelium in vitro. American Review of Respiratory Disease, 140, 1989, s. 125-131.
3. Barnes, P. J.: Reactive oxygen species and airway inflammation. Free Radical Biology&Medicine, 9, 1990, s. 235-243.
4. Bohn, S. K., Smeland, S., Sakhi, A. K.: Post-radiotherapy plasma total glutathione is associated to outcome in patients with head and neck squamous cell carcinoma. Cancer Letters. 18, 2, s. 240-247
5. Bhuvarahamurthy, V., Balasubramanian, N., Govindasamy, S.: Effect of radiotherapy and chemoradiotherapy on circulating antioxidant system of human uterine cervical carcinoma. Molecular and Cellular Biochemistry, 158, 1996, 1, s. 17-23.
6. Comhair, S., Thomassen, M. J., Erzurum, S. C.: Differential induction of extracellular glutathione peroxidase and nitric oxidesynthase 2 in airways of healthy individuals exposed to 100% oxygen or cigarette smoke. American Journal of Respiratory Cell and Molecular Biology, 23, 2000, s. 350-354.
7. Curtin, J. F., Donovan, M., Cotter, T. G.: Regulation and measurement of oxidative stress in apoptosis. Journal of Immunological Methods, 265, 2002, s. 49-72.
8. Dreher, D., Junod, A. F.: Role of oxygen free radicals in cancer development. European Journal of Cancer, 32, 1, 1996, s. 30-38.
9. Forsberg, L., de Faire, U., Morgenstern, R.: Oxidative stress, human genetic variation, and disease. Archives of Biochemistry and Biophysics, 389, 1, 2001, s. 84-93.
10. Forsberg, L., Lyrenas, L., de Faire, U., Morgenstern, R.: A common functional C-T substitution polymorphism in the promoter region of the human catalase gene influences transcription factor binding, reporter gene transcription and is correlated to blood catalase levels. Free radical biology&medicine, 30, 5, 2001, s. 500-505.
11. Fu, Y., Cheng, W. H., Porres, J. M., Ves, D. A., Lei, X. G.: Knock-out of cellular glutathione peroxidase gene renders mice susceptible to diquat-induced oxidative stress. Free radical Biology&Medicine, 27, 1999, 5-6, s. 605-611.
12. Genkinger, J. M., Platz, E. A., Hoffman, S. C.: C47T polymorhism in manganese superoxide dismutase, antioxidant intake and survival. Mechanisms of Ageing and Development, 127, 2006, 4, s. 371-377.
13. Hrizostov, D., Gadjeva, V., Vlaykova, T., Dimitrov, G.: Evaluation of oxidative stress in patients with cancer. Archives of Physiology and Biochemistry, 109, 2001, 4, s. 331-336.
14. Hunt, C. R., Sim, J. E., Sullivan, S. J. et al.: Genomic instability and catalase gene amplification induced by chronic exposure to oxidative stress. Cancer Research, 58, 2003, s 3986-3992.
15. Chistyakov, D. A:, Savostanov, K. V., Zotova, E. V., Nosikov ,V. V.: Polymorphisms in the Mn-SOD and EC-SOD genes and their relationship to diabetic neuropathy in type I diabetes mellitus. BMC Medical Genetics, 2, 2000, s. 4-10.
16. Jaloszynski, P., Jaruga, O., Olinski, R., Biczysko, W., Szyfter, W., Nagy, E. et al.: Oxidative DNA base modifications and polycyclic aromatic hydrocarbon DNA adducts in squamous cell carcinoma of larynx. Free Radicals Research, 37, 2003, 3, s. 231-240.
17. Kaynar, H., Meral, M., Turhan, H., Keles, M., Celik, G., Akcay, F.: Glutathione peroxidase, glutathione-S-transferase, catalase, xanthine oxidase, Cu-Zn superoxide dismutase activities, total glutathione, nitric oxide and malondialdehyde levels in erythrocytes of patients with small cell and non-small cell lung cancer. Cancer Letters, 227, 2005, 2, s. 133-139.
18. Korotkina, R N., Matskevitch, G. N., Devlikano, A. S., Vishnevskii, A. A., Kunitsyn, A. G., Karelin, A. A.: Activity of glutathione metabolizing and antioxidant enzymes in malignant and benign tumors of human lungs. Bulletin of experimental Biology and Medicine, 133, 2002, 6, s. 606-608.
19. Nadif, R.: Effect of TNF and LTA polymorphisms on biological markers of response to oxidative stimuli in coal miners. Journal of Medical Genetics, 40, 2003, s. 96-103.
20. Otto-Knapp, R., Jurgovski, K., Schierhorn, K. et al.: Antioxidative enzymes in human nasal mucosa after exposure to ozone. Possible role of GSTM1 deficiency. Inflammation Research, 52, 2003, s. 51-55.
21. Racek, J.: Oxidační stres a možnosti jeho ovlivnění. Praha, Galen, 2003, s. 90.
22. Ratnasinghe, D., Tangrea, J. A., Andersen, M. R. et al.: glutathione peroxidase codon 198 polymorphism variant increases lung cancer risk. Cancer Research, 60, 2000, s. 6381-6383.
23. Sabitha, K. E., Shyamaladevi, C. S.: Oxidant and antioxidant activity changes in patients with oral cancer and treated with radiotherapy. Oral Oncology, 35, 1999, s. 273-277.
24. Samir, M., el Kholy, N. M.: Thiobarbituric acid reactive substances in patients with laryngeal cancer. Clinical Otolaryngology and Allied Science, 24, 1999, 3, s. 232-234.
25. Sandstrom, J., Karlsson, K., Edlund, T., Marklund, S. L.: Heparin-affinity patterns and composition of extracellular superoxide dismutase in human plasma and tissues. Biochemical Journal, 294, 1993, s. 853-857.
26. Seven, A., Civelek, S., Inci E., Inci, F., Korkut, N., Burcak, G.: Evaluation of oxidative stress parameters in blood of patients with laryngeal carcinoma. Clinical Biochemistry. 32, 5, 1999, s. 369-373.
27. Subapriya, R., Kumaraguruparan, R., Nagini, S., Thangavelu, A.: Oxidant-antioxidant status in oral precancer and oral cancer patients. Toxicology Mechanisms and Methods, 13, 2003, s. 77-81.
28. Szalagatys, A., Korzon, M.: The role of oxidative stress in pathogenesis of asthma. Medical Science Monitor, 9, 2003, 4, s. 89-93.
29. Szuster-Ciesielska, A., Hryciuk-Umer, E., Stepulak, A., Kupisz, K., Kandefer-, M.: Reactive oxygen species production by blood neutrophils of patients with laryngeal carcinoma and antioxidative enzyme activity in their blood. Acta Oncologica. 43, 2004, 3, s. 252-258.
30. Štípek, S., Borovanský, J., Čejková, J. et al.: Antioxidanty a volné radikály ve zdraví a nemoci. Praha, Grada Publishing, 2000, s. 320.
31. Taysi, S., Uslu, C., Akcay, F., Sutbeyaz, M. Y.: Malondiadehyde and nitric oxide levels in the plasma of patients with advanced laryngeal cancer. Surgery Today, 33, 2003, 9, s. 651-654.
32. Tomblyn, M., Kasarskis, E. J., Xu, Y. St. Clair, D. K.: Distribution of MnSOD polymorphisms in sporadic ALS patients. Journal of Molecular Neuroscience, 10, 1998, s. 65-66.
33. Yigitbasi, O G., Guney, E., Haghighi, N., Dogan, P., Saraymen, R., Balkanli, S.: Oxidant and antioxidant status in larynx squamous cell carcinomas. Journal of Experimental and Clinical Cancer Research, 19, 2000, 4, s. 447-451.
Labels
Audiology Paediatric ENT ENT (Otorhinolaryngology)Article was published in
Otorhinolaryngology and Phoniatrics
2007 Issue 1
Most read in this issue
- Quality of Life in Patients with Tracheostomy
- Results of Therapy in Early Stages of Glottic Larynx Cancer Summary
- Chylous Fistulas
- Complex Re-education of Voice in AFC