OXIDATIVE STRESS IN ORAL STEPTOCOCCI

口腔链球菌的氧化应激

• 批准号: 6615754
• 负责人: ROBERT E MARQUIS
• 金额: $ 30.5万
• 依托单位: UNIVERSITY OF ROCHESTER
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-09-15 至 2005-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6615754
• 关键词: NAD(P)H oxidoreductase; Streptococcus; antibacterial agents; bacterial genetics; biofilm; chelating agents; dental agent; dental plaque; fluoride ion; free radical oxygen; gene mutation; glutathione reductase; hydrogen peroxide; oral bacteria; oxidative stress; peroxidases; superoxide dismutase; NAD(P)H oxidoreductase; Streptococcus; antibacterial agents; bacterial genetics; biofilm; chelating agents; dental agent; dental plaque; fluoride ion; free radical oxygen; gene mutation; glutathione reductase; hydrogen peroxide; oral bacteria; oxidative stress; peroxidases; superoxide dismutase

Oxygen metabolism and resultant oxidative damage caused by metabolically generated reactive oxygen species (ROS) are key processes affecting the activities of plaque bacteria. The organisms have developed multiple mechanisms to protect themselves against oxidative damage, including superoxide dismutase, peroxidases, sulfhydryl reductases and DNA repair enzymes. The major source of O2 for supragingival plaque is air in the mouth, while that for subgingival plaque is crevicular fluid. Since plaque is a thin biofilm, O2 moves readily into the film to be metabolized, and plaque generally has been found to have residual O2 levels about 10% that of air-saturated water. However, the important O2 is the metabolized portion, which then is the source of ROS. In addition, many oral healthcare products contain hydrogen peroxide, which can be radicalized through Fenton reactions to cause oxidative damage. The objectives of this application are to develop a clearer picture of oxidative damage to plaque bacteria, primarily oral streptococci, and to identify through use of genetic mutants the major protective mechanisms. Part of the project has a very practical aim of devising better ways to control oral infectious diseases with an emphasis on caries and use of peroxides. The specific aims are: 1. Determine the roles played by NADH-linked oxidases, peroxidases and glutathione reductase in protection of oral streptococci against hydrogen peroxide and other oxidatively damaging agents, 2. Define the roles that superoxide and superoxide dismutase play in oxidative damage and protection against damage, 3. Elucidate the interactions of transition-metal cations, chelators and fluoride in oxidative damage, including interactions with oxygen- metabolizing and protective enzymes.

由代谢产生的活性氧（ROS）引起的氧代谢和产生的氧化损伤是影响斑块细菌活性的关键过程。 这些生物已经开发了多种机制来保护自己免受氧化损伤，包括超氧化物歧化酶，过氧化物酶，硫酰基还原酶和DNA修复酶。 上牙菌斑的O2的主要来源是空气中的空气，而subgingival斑块的空气是缝隙液。由于斑块是一种薄的生物膜，因此O2很容易移入膜以进行代谢，并且通常发现斑块的剩余O2水平约为空气饱和水的10％。 但是，重要的O2是代谢部分，然后是ROS的来源。 此外，许多口腔保健产品含有过氧化氢，可以通过芬顿反应激进，从而导致氧化损伤。 该应用的目的是制定对斑块细菌（主要是口服链球菌）的氧化损害的更清晰图像，并通过使用遗传突变体的主要保护机制来识别。 该项目的一部分具有非常实际的目的，即设计更好的方法来控制口腔传染病，重点是龋齿和使用过氧化物。 具体目的是：1。确定NADH连接的氧化酶，过氧化物酶和谷胱甘肽还原酶在保护口腔链球菌针对过氧化氢和其他氧化损伤剂的保护方面所起的作用，2。定义在超级氧化物和上氧化物中的损害和保护损伤中扮演的氧化物和超级氧化物爆发的作用。氧化损伤，包括与氧代谢和保护酶的相互作用。