Horn W, Maier H, Born A J
Medizinische Klinik III, Universität Giessen.
Klin Wochenschr. 1988;66 Suppl 11:105-7.
Superoxide radicals and other reactive oxygen products are likely to play a role in the development of mouth cancer since they are able to convert penultimate carcinogens present in cigarette smoke into ultimate carcinogens. Those radicals can be generated, e.g., by phagocytes infiltrating inflamed mucosa or by semiquinone radicals present in cigarette tar. We therefore measured the ability of oral mucosa of patients with oropharyngeal tumors to reduce cytochrome c. All patients were heavy smokers and drinkers. It was found that patient mucosa had by far more reducing power than control mucosa. Within the control group, smokers' mucosa was most active. When tested, the cytochrome c reduction was not inhibitable by superoxide dismutase or copper(II)3,5-diisopropylsalicylate. We hypothesize that reduction of cytochrome c by oral mucosa of smokers and patients with mouth cancer is primarily due to residues of cigarette tar containing conjugated quinones of mixed oxidative states which are strong reductants as well as producers of oxygen-centered radicals.
超氧自由基和其他活性氧产物可能在口腔癌的发展中起作用，因为它们能够将香烟烟雾中存在的前致癌物转化为终致癌物。这些自由基可以例如由浸润发炎黏膜的吞噬细胞或香烟焦油中存在的半醌自由基产生。因此，我们测量了口咽肿瘤患者口腔黏膜还原细胞色素c的能力。所有患者均为重度吸烟者和饮酒者。结果发现，患者的黏膜还原能力远高于对照黏膜。在对照组中，吸烟者的黏膜活性最高。经测试，细胞色素c的还原不受超氧化物歧化酶或铜（II）3,5 - 二异丙基水杨酸盐的抑制。我们推测，吸烟者和口腔癌患者的口腔黏膜对细胞色素c的还原主要是由于香烟焦油中的残留物，这些残留物含有混合氧化态的共轭醌，它们既是强还原剂又是以氧为中心的自由基的产生者。
