Mandel L, Svoboda V
Mikrobiologický ústav CSAV, Praha.
Sb Ved Pr Lek Fak Karlovy Univerzity Hradci Kralove Suppl. 1991;34(4):477-503.
In the recent years, more attention is paid by radiobiologists to both prevention and therapy of a relatively less studied gastrointestinal postirradiation syndrome (GPS). Moreover, the increase in interest in GPS is motivated with the requirement as to obtain the decrease in action of ionizing radiation on the intestinal mucosa at making radiotherapy of abdominal or pelvic region. The GPS occurs consequently to the affected abdominal region or all the organism with ionizing radiation. Its approximal doses from 10 to 100 Gy (gamma) are critical for the survival of intestinal mucosa, especially that of jejunum and ileum. Under the threshold of a single and total dose from 6 to 10 Gy, the intestinal mucosa may usually regenerate, and the survival depends mainly on the preservation or restoration of hemopoietic activity of blood forming tissues. The main pathogenetic GPS factor resides in the afflication of stem cells of mucosal crypts. The intestinal epithelium stops to be fluently replaced after the irradiation. The motion arrests of epithelial cells from crypts to the apex of villi. The elderly cells undergoes degradation, and after several days the denudation of mucosa occurs with possible distortion of deeper layers of intestinal wall. The intestinal microflora is involved in the pathogenesis both directly and indirectly. Amongst the former events is ranged the invasion of distorted mucosa in compromised both local and systemic immunity. Indirectly, the intestinal microflora is GPS associated by stimulating mitotic activity in crypts, therefore more cells are in the radiosensitive phase. In germ-free animals there is a significant decrease in mitotic activity of crypts, and the migration time of epithelial cells from crypts to the apex villi is twice more prolongated, what induces possible restoration of active center after the irradiation. The GPS also results in disorder of metabolic processes which are conditioned with intestinal mucosa. Its typical manifestation resides in the wash-out of mucus, decreased resorption of nutrients and loss of water and minerals into the intestinal lumen. The GPS-related are another disorders of the organism, those of liver and kidney apparently induced due to the intoxication with catabolic products. The microflora has been stated to be involved in GPS by the experiments on germ-free animals. In the absence of microflora, the survival is greater in duration. After a total pigs irradiation with 10-30 Gy, more than two times survival prolongation occurs. The abdominal irradiation with 12 Gy results to the death of only conventional pigs, whereas those germ-free show a survival.(ABSTRACT TRUNCATED AT 400 WORDS)
近年来,放射生物学家越来越关注相对较少研究的胃肠道辐射后综合征(GPS)的预防和治疗。此外,对GPS兴趣的增加是出于在进行腹部或盆腔放疗时减少电离辐射对肠黏膜作用的要求。GPS是腹部区域或整个机体受到电离辐射后产生的。其近似剂量为10至100戈瑞(γ),对肠黏膜尤其是空肠和回肠黏膜的存活至关重要。在单次和总剂量低于6至10戈瑞的阈值时,肠黏膜通常可以再生,存活主要取决于造血组织造血活性的维持或恢复。GPS的主要致病因素在于黏膜隐窝干细胞的损伤。照射后肠上皮细胞不再能顺利更新。上皮细胞从隐窝向绒毛顶端的移动停止。衰老细胞发生降解,几天后黏膜剥脱,肠壁深层可能出现变形。肠道微生物群直接或间接参与发病机制。前者包括受损的局部和全身免疫中变形黏膜的侵袭。间接而言,则是肠道微生物群通过刺激隐窝中的有丝分裂活动与GPS相关,因此更多细胞处于放射敏感阶段。在无菌动物中,隐窝的有丝分裂活动显著降低,上皮细胞从隐窝到绒毛顶端的迁移时间延长两倍,这可能促使照射后活性中心的恢复。GPS还会导致由肠黏膜调节的代谢过程紊乱。其典型表现为黏液冲刷、营养物质吸收减少以及水和矿物质流失到肠腔。与GPS相关的还有机体的其他紊乱,明显是由于分解代谢产物中毒导致的肝脏和肾脏紊乱。通过对无菌动物的实验表明,微生物群参与了GPS。在没有微生物群的情况下,存活时间更长。用10 - 30戈瑞对猪进行全身照射后,存活时间延长两倍多。用12戈瑞进行腹部照射,仅使普通猪死亡,而无菌猪存活。(摘要截选至400字)