Jackson J H
Department of Immunology, Scripps Research Institute, La Jolla, California 92037.
Environ Health Perspect. 1994 Dec;102 Suppl 10(Suppl 10):155-7. doi: 10.1289/ehp.94102s10155.
Chronic exposure to oxidants is associated with an increased incidence of malignancy; however, the mechanism(s) by which oxidants contribute to carcinogenesis is unknown. Since oncogene activation plays an important role in carcinogenesis, we hypothesized that hydroxyl radical-induced DNA damage might contribute to carcinogenesis by causing oncogene activation. The studies reported herein demonstrate that hydroxyl radical-induced DNA damage can activate the K-ras 4B and C-Raf-l oncogenes by causing point mutations and deletions, respectively. In addition, our results indicate that a) hydroxyl radical-induced DNA damage causes selective base substitutions; b) the four DNA bases have different susceptibilities to hydroxyl radical-induced mutations; and c) hydroxyl radical-induced mutations are not randomly distributed among oncogene codons. Our studies suggest that oncogene activation could be one potential mechanism by which oxidants contribute to carcinogenesis.
长期暴露于氧化剂与恶性肿瘤发病率增加有关;然而,氧化剂促成致癌作用的机制尚不清楚。由于癌基因激活在致癌过程中起重要作用,我们推测羟基自由基诱导的DNA损伤可能通过引起癌基因激活而促成致癌作用。本文报道的研究表明,羟基自由基诱导的DNA损伤可分别通过引起点突变和缺失来激活K-ras 4B和C-Raf-1癌基因。此外,我们的结果表明:a)羟基自由基诱导的DNA损伤导致选择性碱基置换;b)四种DNA碱基对羟基自由基诱导的突变具有不同的敏感性;c)羟基自由基诱导的突变并非随机分布在癌基因密码子中。我们的研究表明,癌基因激活可能是氧化剂促成致癌作用的一种潜在机制。