The electron transport chain (ETC) delivers electrons from many substrates to reduce molecular oxygen to water. ETC accomplishes the stepwise transfer of electrons through series of protein complexes conferring oxidation‐reduction reactions with concomitant transport of p roton across membrane, g enerating a proton g radient which leads ATP s ynthesis b y F0F1ATPase. Bacterial ETC initiates with oxidation of NADH by NADH dehydrogenase complex (complex I). Therefore, damage of complex I leads to insufficient function of ETC and accumulation of NADH inside the cell. Contribution of ETC activity and its consequent changes of NADH levels to bacterial damage response against reactive oxygen and nitrogen species (ROS/RNS) has been poorly understood. In this study, by constructing ndh mutant Salmonella lacking complex I NADH dehydrogenase 2, we evaluated the effect of ETC deficiency to bacterial resistance against ROS and RNS. The growth of ndh mutant Salmonella is impaired in the culture media containing hydrogen peroxide, but rather accelerates in the media containing nitric oxide donors. Data suggest that redox potential of NADH accumulated inside the cell by ETC blockage may affect inversely to bacterial resistance against reactive oxygen species and reactive nitrogen species.

I. 서론
 II. 연구재료 및 방법
  1. 사용균주 및 배지
  2. ndh 돌연변이 S. Typhimurium 제조
  3. 활성산소종과 활성질소종에 대한 세균의 민감도 분석
 III. 결과 및 고찰
 IV. 참고문헌

• 박희정(조선대학교 치과대학 구강미생물학 및 면역학교실) | Hee Jeong Park
• 채권석(경북대학교 사범대학 과학교육학부) | Kwon Seok Chae
• 방일수(조선대학교 치과대학 구강미생물학 및 면역학교실) | Iel Soo Bang correspondence