Wells J E, Russell J B
Section of Microbiology, Cornell University, Ithaca, NY 14853, USA.
J Dairy Sci. 1996 Aug;79(8):1487-95. doi: 10.3168/jds.S0022-0302(96)76508-6.
Studies using 15N have indicated that as much as 50% of the microbial mass turns over before N passes to the lower gut, and this N recycling significantly decreases the availability of microbial protein. Protozoa digest bacteria and smaller protozoa, but bacterial protein can turn over even if protozoa are not present. Fibrobacter succinogenes cultures lyse even when they are growing, and the lysis rate is independent of growth rate. When extracellular sugar is depleted, F. succinogenes secretes an extracellular proteinase that inactivates the autolysins. This method of autolytic regulation decreases the turnover of stationary cells. Bacteriophage and anaeroplasma can cause lysogeny, but, as yet, there is little proof that these processes are important determinants of bacterial turnover in vivo. Dietary manipulations (e.g., salt feeding and particle size reduction) that increase liquid and solid dilution rates can increase bacterial flow by decreasing bacterial residence time and turnover. Some dead ruminal bacteria are able to maintain their cellular integrity, and the ratio of dead to live cells in ruminal fluid may be as great as 10:1. Bacterial survival appears to be at least partially explained by the method of sugar transport. When bacteria rely solely on mechanisms of ion-coupled sugar symport, an energized membrane is necessary for the reinitiation of growth. If group translocation (phosphotransferase system) is the mechanisms of transport, uptake can be driven by phosphoenolpyruvate, and an energized membrane and the storage of intracellular reserve materials are not an absolute criteria for survival. In some cases, N deprivation accelerates death. When Prevotella ruminicola was limited for N under conditions of excess energy, methylglyoxal production caused a rapid decrease in viability. The impact of bacterial death in the rumen is not clear-cut. If the rate of fermentation is zero-order with respect to cell concentration (substrate-limited), cell death would have little impact on digestion.
使用¹⁵N的研究表明，在氮传递到下消化道之前，高达50%的微生物量会周转，这种氮的再循环显著降低了微生物蛋白质的可利用性。原生动物消化细菌和较小的原生动物，但即使没有原生动物，细菌蛋白质也会周转。琥珀酸纤维杆菌培养物即使在生长时也会裂解，且裂解速率与生长速率无关。当细胞外糖耗尽时，琥珀酸纤维杆菌会分泌一种细胞外蛋白酶，使自溶素失活。这种自溶调节方法降低了静止细胞的周转。噬菌体和厌氧支原体可导致溶原性，但目前几乎没有证据表明这些过程是体内细菌周转的重要决定因素。增加液体和固体稀释率的饮食操作（如喂盐和减小颗粒大小）可通过减少细菌停留时间和周转来增加细菌流量。一些死亡的瘤胃细菌能够保持其细胞完整性，瘤胃液中死细胞与活细胞的比例可能高达10:1。细菌的存活似乎至少部分可以用糖的运输方式来解释。当细菌仅依赖离子偶联糖同向转运机制时，重新开始生长需要有能量的膜。如果基团转位（磷酸转移酶系统）是运输机制，摄取可以由磷酸烯醇丙酮酸驱动，有能量的膜和细胞内储备物质的储存不是存活的绝对标准。在某些情况下，氮缺乏会加速死亡。当反刍普雷沃氏菌在能量过剩的条件下氮受限，甲基乙二醛的产生会导致其活力迅速下降。瘤胃中细菌死亡的影响并不明确。如果发酵速率相对于细胞浓度是零级（底物受限），细胞死亡对消化的影响就很小。
