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Effect of NADH dehydrogenase-2 Deficiency to the Bacterial Resistance against Reactive Oxygen/Nitrogen Species

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¹ÚÈñÁ¤ ( Park Hee-Jeong ) - Á¶¼±´ëÇб³ Ä¡°ú´ëÇÐ ±¸°­¹Ì»ý¹°ÇÐ ¹× ¸é¿ªÇб³½Ç
ä±Ç¼® ( Chae Kwon-Seok ) - °æºÏ´ëÇб³ »ç¹ü´ëÇÐ °úÇб³À°ÇкÎ
¹æÀϼö ( Bang Iel-Soo ) - Á¶¼±´ëÇб³ Ä¡°ú´ëÇÐ ±¸°­¹Ì»ý¹°ÇÐ ¹× ¸é¿ªÇб³½Ç

Abstract


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 proton across membrane, generating a proton gradient which leads ATP synthesis by F0F1ATPase. Bacterial ETC initiates with oxidation of NADH by NADH dehydrogenase complex (complex ¥°). Therefore, damage of complex ¥° 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 ¥° 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.

Å°¿öµå

Electron transport chain; NADH dehydrogenase-2; Salmonella; Reactive oxygen/nitrogen species

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