Iron-induced tissue damage and cancer: The role of reactive oxygen species-free radicals

被引:153
作者
Okada, S
机构
[1] First Department of Pathology, Okayama University Medical School, Okayama
[2] First Department of Pathology, Okayama University Medical School, Okayama 700
关键词
acute tubular necrosis; animal models; free radicals; iron; nitrilotriacetate; reactive oxygen species; renal cell carcinoma;
D O I
10.1111/j.1440-1827.1996.tb03617.x
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Oxygen is poisonous, but we cannot live without it. The high oxidizing potential of oxygen molecules (dioxygen) is a valuable source of energy for the organism and its reactivity is low; that is, spin forbidden. However, the dioxygen itself is a 'free radical' and, especially in the presence of transition metals, it is a major promoter of radical reactions in the cell. Humans survive only by virtue of their elaborate defense mechanisms against oxygen toxicity. Iron is the most abundant transition metal in the human body. Because iron shows wide variation in redox potential with different co-ordination ligands, it may be used as a redox intermediate in many biological mechanisms. However, it is precisely this redox activeness that makes iron a key participant in free radical production. The current research on the relationship between iron and cancer is briefly reviewed. Research results are reported here which indicate that iron, when bound to certain ligands, can cause free-radical mediated tissue damage and become carcinogenic. The present study also suggests that iron may also have a significant role in spontaneous human cancer.
引用
收藏
页码:311 / 332
页数:22
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