Reactive oxygen metabolites, antioxidants and head and neck cancer

This manuscript will review the probable role of reactive oxygen metabolite s (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 trigge rs. Certain etiologies are characteristic of HNC and include infectious age nts 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. R OM species are formed in the process of cellular respiration, specifically during oxidative phosphorylation. These ubiquitous molecules are highly tox ic in the cellular environment. Of the many effects of ROM, especially impo rtant are their effect on DNA. Specifically, ROM cause a variety of DNA dam age, including insertions, point mutations, and deletions. Thus, it is hypo thesized that ROM may be critically involved in the etiology of malignant d isease 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 mech anisms are overwhelmed, uncontrolled cellular proliferation may follow, pot entially 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 vi tamins (A, C, and E), nutrient trace elements (selenium), enzymes (superoxi de dismutase, glutathione peroxidase, and catalase), hormones (melatonin), and a host of natural and synthetic compounds (lazaroids, allopurinol, ging ko extract). Thus, this paper will also review the possible benefit derived from the use of such scavengers/blockers in the prevention of HNC. (C) 199 9 John Wiley & Sons, Inc.