目的　研究正常食管上皮和食管癌组织中致癌性丙二醛 DNA加合物 (M1 dG)含量 ,探讨DNA氧化损伤与食管癌发生和发展的关系。方法　所有组织标本均来自食管癌高发区河南林县 ,32例正常食管上皮标本来源于组织活检 ,30例食管癌组织标本来源于外科手术切除的食管癌。DNA中M1 dG加合物含量以32 P 后标记方法测定。结果　在全部正常食管上皮和癌组织DNA中均检测到M1 dG加合物 ,但其含量 (中位数 )在正常食管上皮中为 3 .4/ 10 8核苷酸 (范围为 1.7/ 10 8～ 5 5 .4/ 10 8核苷酸 ) ,远低于食管癌组织的 14.1/ 10 8核苷酸 (范围为 1.4/ 10 8～ 5 9.0 / 10 8核苷酸 ) ,差异有极显著性(P <0 .0 0 0 1)。该加合物水平与受试者的性别、年龄、吸烟状态以及涉及酒精氧化产生自由基的细胞色素p45 0 2E1基因多态性无明显相关。结论　脂质过氧化产生的丙二醛对DNA的损伤可在食管上皮中累积 ,在癌组织中达相当高的水平 ,提示M1 dG加合物可能是导致食管癌发生和发展的重要因素。 Objective To study the carcinogenicity of malondialdehyde DNA adduct (M1 dG) in normal esophageal epithelial and esophageal cancer tissues and to explore the relationship between DNA oxidative damage and the occurrence and development of esophageal cancer. Methods All tissue samples were from Linxian County, Henan Province, a high-risk area of ​​esophageal cancer. 32 normal esophageal epithelial specimens were derived from biopsy, and 30 specimens of esophageal cancer were derived from surgically resected esophageal cancer. The content of M1 dG adduct in DNA was determined by the 32 P post-labeling method. Results The M1 dG adduct was detected in all normal esophageal epithelium and cancer tissue DNA, but its content (median) was 3.4/10 8 nucleotides in the normal esophageal epithelium (range 1.7/10 8 ~ 5 5 .4/10 8 nucleotides, much lower than the 14.1/108 nucleotides of esophageal cancer tissues (range 1.4/108 ~ 59.0/108 nucleotides), the difference is extremely significant (P < 0 0 0 0 1). The adduct levels were not significantly correlated with the subject’s sex, age, smoking status, and the polymorphism of the cytochrome p45 02E1 gene involved in the production of free radicals by alcohol oxidation. Conclusion DNA damage induced by malondialdehyde caused by lipid peroxidation can accumulate in esophageal epithelium and reach a very high level in cancer tissues, suggesting that M1 dG adduct may be an important factor leading to the occurrence and development of esophageal cancer.