Oxygen sensitive pyruvate formate-lyase and its activating enzyme in oral microorganisms.

丙酮酸甲酸裂解酶(PFL)是链球菌在厌氧条件下产生甲酸、醋酸和乙醇的关键酶。在血链球菌细胞中，PFL在氧敏感、活性和耐氧性之间发生转化，而在变形链球菌中则不能。所有PFL在变形链球菌细胞中均保持活性。对这种转化差异的生物化学机制进行了探讨。NADPH是激活变形链球菌PFL的最有效的还原剂。相反，NADPH对血链球菌则没有那么有效。PFL活化酶需要Fe~(2+)~(2+)和Se~(2+)，PFL失活酶参与PFL的活性中心，PFL失活酶将活性转化为耐氧灭活。血链球菌的PFL失活酶活性高于变形链球菌，这可以用来解释PFL的胞内转化。微量丙酮酸和无机磷抑制PFL失活酶的活性，保持PFL的活性形态，而CoA则促进PFL失活。从目的上讲，这些监管机制可能是重要的。山梨醇在一定条件下对变形链球菌的葡萄糖或蔗糖代谢有抑制作用。山梨醇的加入导致了较高的NADH/NAD比值，并抑制了链球菌的糖代谢，因为PFL活性不足以维持氧化/还原平衡。山梨醇还能抑制牙菌斑中微生物的糖代谢。

Pyruvate formate-lyase (PFL) is a key enzyme of production of formic and acetic acid and ethanol by streptococci under anaerobic conditions. PFL was converted between oxygen-sensitive, active and oxygen tolerant, inactive forms in the cells of Streptococcus sanguis but not in the cells of Streptococcus mutans. All PFL was kept active in S.mutans cells. The biochmical mechanism of this difference in the interconversion was investigated. NADPH was the most efficient reducing agent for the activation of the inactive PFL of S.mutans. On the contrary, NADPH was not so efficient in S.sanguis. Fe^<2+> and selenium were required for PFL activating enzyme, and protein radial was involved in the active center of PFL.PFL inactivating enzyme, which converted active form to oxygen-tolerant inactive form, was found in streptococci. S.sanguis had higher activity of PFL inactivating enzyme than S.mutans.Intracellular conversion of PFL could be explained by these findings. Minute levels of pyruvate and inorganic phosphate inhibited the activity of PFL inactivating enzyme and kept active form of PFL.However, CoA enhanced PFL inactivation. These regulatory mechanism could be important teleologically. Glucose or sucrose metabolism was inhibited by sorbitol in S.mutans under certain conditions. The incorporation of sorbitol resulted in high NADH/NAD ratio and inhibited streptococcal sugar metabolism, since PFL activity was not enough to keep the oxidation/reduction balance. Sorbitol also inhibited sugar metabolism of microorganisms in dental plaque in situ.