Knowledge of the acute and late ionizing radiation exposure damage to the g
astrointestinal tract, particularly injury of the small intestine, is of gr
eat significance in radiotherapy, as is management of accidental radiation
exposure. Irradiation (X-ray, neutron, cobalt gamma) induces a series of ev
ents in this rapidly renewing tissue resulting in the well-known symptoms o
f the gastrointestinal (GI) radiation syndrome, such as GI haemorrhage, end
otoxemia, bacterial infection, anorexia, nausea, vomiting, diarrhoea, and l
oss of electrolytes and fluid. In spite of the significant advances that ha
ve occurred in research on underlying mechanisms over the last two decades,
the overall etiology and pathogenesis of the GI-syndrome still remains unc
lear. Currently, to our knowledge, these symptoms are probably due to a rap
id modification of the intestinal motility and to the structural alteration
of the intestinal mucosa (cell loss and altered crypt integrity). Several
evidences suggest that radiation-induced dysfunctions and structural change
s of this organ (either changes in subcellular, cellular, and histological
structure) are mediated by concerted and interrelated changes of a plethora
of various extracellular mediators and their intracellular messengers. The
aim of this review is to summarize our current knowledge about the pathomo
rphology and cell biology of the ionizing radiation response of the GI trac
t with a focus on the small intestine. (C) 2001 Elsevier Science Ltd. All l
ights reserved.