PEROXIDASE IN SALIVA AND PREVENTION OF ORAL DISEASE

乳过氧化物酶（LP）、过氧化氢（H2 O2）和硫氰酸根离子（SCN-） 在人类唾液中形成抑菌系统。 口服“乳酸 细菌释放H2 O2作为碳水化合物代谢的副产品。 唾液腺、口腔粘膜和唾液中受刺激的白细胞可能 也产生H2 O2和分泌过氧化物酶。 过氧化物酶催化 SCN-被H2 O2氧化生成次硫代硫酸根离子（OSCN-）， 次硫氰酸（HOSCN）的酸碱平衡。 HOSCN氧化 细菌酶和转运系统的必需巯基， 导致代谢和生长的抑制。 某些细菌，如 作为S.由于它们的能力，变异人对抑制具有有限的抵抗力， 以将某些二硫化物化合物快速还原成巯基形式。 这些巯基化合物通过以下方式保护必需的蛋白质巯基： 与抑制剂反应并将其还原为SCN-。 这些研究将建立一种测定LP抗菌活性的方法 在唾液中对存在于唾液样品中的细菌的活性。 使用这种方法，可以增加LP抗菌剂的作用， 将被审查。 这些试剂增加了过氧化物的供应， 以产生更有效抑制剂，或抑制 细菌的酶参与抵抗。 其他研究将 确定机制并检查针对S的活性特异性。变异体， 其他口腔链球菌和细菌，通常不定植 嘴里 白细胞对SCN-依赖性抗菌药物的贡献 将通过刺激唾液中白细胞H2 O2的产生来研究活性 以及测量白细胞过氧化物酶。 这些研究将提供关于 过氧化物酶系统与细菌，可以生存和生长在 这种抗菌系统的存在。 这些研究还应提供 评价LP系统在自然界中重要性的基础 抵抗口腔疾病，（1）通过开发测量Lp的方法 可用于临床环境的抗微生物活性，以及 (2)通过鉴定可以增加药物的功效或选择性的药剂， 对口腔病原体的抗菌作用。 这样的代理人可以 用于比较LP系统在正常人群中的效果， 在接受该药剂的人群中的效果。

Lactoperoxidase (LP), hydrogen peroxide (H2O2) and thiocyanate ion (SCN-) form a bacteriostatic system in human saliva. The oral "lactic-acid bacteria" release H2O2 as a by-product of carbohydrate metabolism. Stimulated leukocytes in the salivary glands, oral mucosa, and saliva may also produce H2O2 and secrete peroxidase enzymes. Peroxidases catalyze the oxidation of SCN- by H2O2 to yield hypothiocyanine ion (OSCN-), which is in acid-base equilibrium with hypothiocyanous acid (HOSCN). HOSCN oxydizes essential sulfhydryl groups of bacterial enzymes and transport systems, resulting in inhibition of metabolism and growth. Certain bacteria such as S. mutans have a limited resistance to inhibition, due to their ability to rapidly reduce certain disulfide compounds to the sulfhydryl forms. These sulfhydryl compounds protect essential protein sulfhydryls by reacting with the inhibitor and reducing it back to SCN-. These studies will establish a method for measuring LP antibacterial activity in saliva against the bacteria present in the saliva sample. Using this method, the effects of agents that may increase LP antibacterial will be examined. These agents increase the supply of peroxides, change the LP system so as to produce a more potent inhibitor, or inhibit bacterial enzymes involved in resistance. Additional studies will determine mechanisms and examine specificity of activity against S. mutans, other oral streptococci, and bacterial that usually do not colonize the mouth. The contribution of leukocytes to SCN--dependent antimicrobial activity will be studied by stimulating leukocyte H2O2 production in saliva and measuring leukocyte peroxidase enzymes. These studies will provide information about the interaction of the peroxidase system with the bacteria that can survive and grow in the presence of this antimicrobial system. The studies should also provide a basis for evaluating the significance of the LP system in natural resistance to oral disease, (1) by developing methods to measure Lp antimicrobial activity that could be used in the clinical environment, and (2) by identifying agents that can increase the efficacy or selectivity of antimicrobial action against oral pathogens. Such agents could then be used to compare the effect of the LP system in the normal population with the effect in a population receiving the agent.