Abstract
Evidence for the participation of active oxygen and organic hydro-peroxides in carcinogenesis has accumulated over the last two decades. The major forms of active oxygen are superoxide (O -2̇ ) and its conjugate acid the hydroperoxyradical (HO -2 ), singlet oxygen (O2), the hydroxyl radical (•OH) and hydrogenperoxide (H2O2). On the basis of epidemiological considerations, Totter (1) has proposed that oxygen-induced cellular damage rather than exposure to industrial pollutants may play a major role in human cancer. The hereditary chromosomal breakage disorders, Ataxia telangiectasia (AT), Fanconi’s Anemia (FA) and Bloom’s Syndrome (BS), are characterized by increased cancer incidence (9). There is evidence for abnormalities in the metabolism of oxygen for all three diseases (10). Cells from patients with these diseases possess increased spontaneous frequencies of chromosomal aberrations and, in the case of BS, also increased frequencies of sister chromatid exchanges (11) (SCE) and spontaneous mutations (12,13). The chromosomal abnormalities in BS fibroblasts can be decreased upon treatment with protease inhibitors (14).
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Cerutti, P.A. (1985). Active Oxygen and Promotion. In: Fischer, S.M., Slaga, T.J. (eds) Arachidonic Acid Metabolism and Tumor Promotion. Prostaglandins, Leukotrienes, and Cancer, vol 3. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2605-2_7
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