Cariogenic Streptococcus mutans encounters a variety of host defense factors produced in oral cavity. Nitric oxide (NO) and NO-mediated reactive nitrogen species are potential antimicrobials of innate immunity that can threaten the fitness of S. mutans in their ecological niches. Streptococcal strategies to detoxify cytotoxic NO, which allow S. mutans to persist in caries or other environments of the oral cavity, remain unknown. In this study, we directly measured NO consumption rates of S. mutans isolated in Korea. Surprisingly, all S. mutans strains were unable to consume exogenous NO efficiently, while an intracellular parasite Salmonella enterica serovar Typhimurium expressing the NO-metabolizing enzyme flavohemoglobin consumed most of the NO. This result suggested that S. mutans has alternative detoxification systems for tolerating NO-induced nitrosative stresses.

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.