## Background: The importance of hypoxia in limiting the sensitivity of tumor cells to ionizing radiation has long been known. ## Methods: We evaluated the tissue oxygenation status with a polarographic needle electrode system in 37 patients with malignancies of the head and neck and correlated t
Reactive oxygen metabolites, antioxidants and head and neck cancer
โ Scribed by Michael D. Seidman; Wayne S. Quirk; Najeeb A. Shirwany
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 107 KB
- Volume
- 21
- Category
- Article
- ISSN
- 1043-3074
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โฆ Synopsis
This manuscript will review the probable role of reactive oxygen metabolites (ROM) in the etiopathogenesis of head and neck cancer (HNC). Cancer is a heterogeneous disorder with multiple etiologies including somatic and germ-line mutations, cellular homeostatic disturbances, and environmental triggers. Certain etiologies are characteristic of HNC and include infectious agents such as the Epstein-Barr virus, the use of tobacco, and consumption of alcohol.
A large body of evidence implicates ROM in tumor formation and promotion. ROM species are formed in the process of cellular respiration, specifically during oxidative phosphorylation. These ubiquitous molecules are highly toxic in the cellular environment. Of the many effects of ROM, especially important are their effect on DNA. Specifically, ROM cause a variety of DNA damage, including insertions, point mutations, and deletions. Thus, it is hypothesized that ROM may be critically involved in the etiology of malignant disease through their possible impact on protooncogenes and tumor suppressor genes. Additionally, empirical evidence suggests that ROM may also affect the balance between apoptosis and cellular proliferation. If apoptotic mechanisms are overwhelmed, uncontrolled cellular proliferation may follow, potentially leading to tumor formation. Thus, this manuscript will critically review the evidence that supports the role of ROM in tumorigenesis.
ROM scavengers and blockers have shown both in vivo and in vitro effects of attenuating the toxicity of ROM. Such compounds include the antioxidant vitamins (A, C, and E), nutrient trace elements (selenium), enzymes (superoxide dismutase, glutathione peroxidase, and catalase), hormones (melatonin), and a host of natural and synthetic compounds (lazaroids, allopurinol, gingko extract). Thus, this paper will also review the possible benefit derived from the use of such scavengers/blockers in the prevention of HNC.
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