Sheng Jiangyun, Marquis Robert E
Department of Microbiology & Immunology and Center for Oral Biology, University of Rochester Medical Center, Rochester, NY 14642-8672, USA.
FEMS Microbiol Lett. 2006 Sep;262(1):93-8. doi: 10.1111/j.1574-6968.2006.00374.x.
Caries-causing oral bacteria such as Streptococcus mutans are protected by the actions of F-ATPases against acid damage in dental plaque acidified by glycolytic acid production or ingestion of acids foods and beverages. Catabolites such as glucose and sucrose were found to enhance the protection of S. mutans and also other oral lactic-acid bacteria against acid killing at lethal pH values as low as 2.5. Protection involved glycolysis with the production of lactate and ATP, which is a substrate for F-ATPases. ATP could also be produced by starved cells apparently through synthase activity of the F-ATPase associated with acid decline. Fluoride and the organic weak-acid indomethacin acted to diminish this protection, as did F-ATPase inhibitors such as dicyclohexylcarbodi-imide. Protection against acid killing involving catabolism and synthase activity is likely to be important for plaque cariogenicity.
致龋性口腔细菌，如变形链球菌，通过F - ATP酶的作用，在因糖酵解产酸或摄入酸性食物和饮料而酸化的牙菌斑中免受酸损伤。发现葡萄糖和蔗糖等分解代谢物可增强变形链球菌以及其他口腔乳酸菌在低至2.5的致死pH值下对酸杀伤的保护作用。这种保护作用涉及糖酵解产生乳酸和ATP，而ATP是F - ATP酶的底物。饥饿细胞显然也可以通过与酸减少相关的F - ATP酶的合酶活性产生ATP。氟化物和有机弱酸吲哚美辛以及二环己基碳二亚胺等F - ATP酶抑制剂都能削弱这种保护作用。涉及分解代谢和合酶活性的抗酸杀伤保护作用可能对菌斑致龋性很重要。
