In order to disclose the relationship between mutations of mitochondrial DNA (mtDNA) and gastric car-cinogenesis, we screened the entire mtDNA sequence in 30 cases of human gastric cancer and matched normal tissues by using denaturing high-performance liquid chromatogra-phy (DHPLC) and DNA sequencing. Our data showed that high frequency (66.7%, 20/30) of mitochondrial genome mutation occurred in gastric cancer. Among these variants, 17 cases (56.7%, 17/30) were identified to be somatic mutation. High level mutant frequency was found in ND4, ND5 coding genes and D-loop control region, which was 36.7%, 26.7% and 30% respectively. Comparing with complexes Ⅲ, Ⅳ and V of the electron transport chain, we found that variants appeared to be more frequent in the subunit genes of complex I. Most of mutations were base substitutions (85.4%, 41/48). Our results suggested that mutations of subunit genes encoding complex I, especially MM, ND4 and ND5 genes, might contribute to human gastric carcinogenesis. In order to disclose the relationship between mutations of mitochondrial DNA (mtDNA) and gastric car-cinogenesis, we screened the entire mtDNA sequence in 30 cases of human gastric cancer and matched normal tissues by using heterogeneous high-performance liquid chromatogra-phy (DHPLC) Our data showed that high frequency (66.7%, 20/30) of mitochondrial mutations in gastric cancer. Among these variants, 17 cases (56.7%, 17/30) were identified to be somatic mutation. High level Mutation frequency was found in ND4, ND5 coding genes and D-loop control region, which was 36.7%, 26.7% and 30% respectively. Comparing with complexes III, IV and V of the electron transport chain, we found that variants more frequent in the subunit genes of complex I. Most of mutations were base substitutions (85.4%, 41/48). Our results suggesting that mutations of subunit genes encoding complex I, especially MM, ND4 and ND5 genes, might contribute to human gastric carc inogenesis.