PEROXIDASE IN SALIVA AND PREVENTION OF ORAL DISEASE

乳过氧化物酶(LP)、过氧化氢(H_2O_2)和硫氰酸盐离子(SCN-) 在人类唾液中形成抑菌系统。口服“乳酸片” 细菌“释放过氧化氢，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 还会产生过氧化氢并分泌过氧化物酶。过氧化物酶催化 用过氧化氢氧化SCN-生成次硫菁离子(OSCN-)，它在 次硫氰酸(HOSCN)的酸碱平衡。HOSCN氧化剂 细菌酶和运输系统的基本巯基， 从而抑制新陈代谢和生长。某些细菌，如 因为变形链球菌对抑制的抵抗力有限，因为他们的能力 使某些二硫化物迅速还原为巯基形式。 这些硫基化合物通过以下方式保护必需的蛋白质硫基 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抗菌剂的方法 唾液中对唾液样本中存在的细菌的活性。 利用这种方法，可以增加LP抗菌药物的效果 将会被检查。这些制剂增加了过氧化氢的供应，改变了 从而产生更有效抑制物，或抑制 参与抗药性的细菌酶。更多的研究将 确定机制并检查抗变形链球菌活性的特异性， 其他口腔链球菌，以及通常不定植于 嘴。白细胞在SCN依赖抗菌药物中的作用 活性将通过刺激唾液中白细胞过氧化氢的产生来研究。 以及测定白细胞过氧化物酶。 这些研究将提供关于两国之间相互作用的信息。 过氧化物酶系统中的细菌可以在 这个抗菌系统的存在。这些研究还应该提供一个 评价LP制度在自然界中意义的依据 对口腔疾病的抵抗力，(1)通过发展测量LP的方法 可以在临床环境中使用的抗菌活性，以及 (2)通过确定可以提高药物有效性或选择性的药物 对口腔病原体的抗菌作用。这样的代理人可能会被 用于比较LP系统在正常人群中的效果与 在接受该制剂的人群中的影响。

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.