O'Connell A C, Redman R S, Evans R L, Ambudkar I S
Gene Therapy and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, USA.
Radiat Res. 1999 Feb;151(2):150-8.
The mechanism(s) of radiation-induced salivary gland dysfunction is poorly understood. In the present study, we have assessed the secretory function (muscarinic agonist-stimulated saliva flow, intracellular calcium mobilization, Na+/K+/2Cl- cotransport activity) in rat submandibular glands 12 months postirradiation (single dose, 10 Gy). The morphological status of glands from control and irradiated rats was also determined. Pilocarpine-stimulated salivary flow was decreased by 67% at 12 months (but not at 3 months) after irradiation. This was associated with a 47% decrease in the wet weight of the irradiated glands. Histological and morphometric analysis demonstrated that acinar cells were smaller and occupied relatively less volume and convoluted granular tubules were smaller but occupied the same relative volume, while intercalated and striated ducts maintained their size but occupied a greater relative volume in submandibular glands from irradiated compared to control animals. In addition, no inflammation or fibrosis was observed in the irradiated tissues. Carbachol- or thapsigargin-stimulated mobilization of Ca2+ was similar in dispersed submandibular gland cells from control and irradiated animals. Further, [Ca2+]i imaging of individual ducts and acini from control and irradiated groups showed, for the first time, that mobilization of Ca2+ in either cell type was not altered by the radiation treatment. The carbachol-stimulated, bumetanide-sensitive component of the Na+/K+/ 2Cl- cotransport activity was also similar in submandibular gland cells from control and irradiated animals. These data demonstrate that a single dose of gamma radiation induces a progressive loss of submandibular gland tissue and function. This loss of salivary flow is not due to chronic inflammation or fibrosis of the gland or an alteration in the neurotransmitter signaling mechanism in the acinar or ductal cells. The radiation-induced decrease in fluid secretion appears to be related to a change in either the water-handling capacity of the acini or the number of acinar cells in the gland.
辐射诱导的唾液腺功能障碍机制尚不清楚。在本研究中,我们评估了大鼠下颌下腺在接受单次剂量10 Gy照射后12个月的分泌功能(毒蕈碱激动剂刺激的唾液分泌、细胞内钙动员、Na+/K+/2Cl-协同转运活性)。同时还确定了对照大鼠和受照射大鼠腺体的形态学状态。照射后12个月(而非3个月),毛果芸香碱刺激的唾液分泌减少了67%。这与受照射腺体湿重减少47%相关。组织学和形态计量学分析表明,腺泡细胞较小,所占体积相对较小,而蟠曲颗粒小管也较小,但所占相对体积相同,而闰管和纹状管大小保持不变,但在受照射大鼠的下颌下腺中所占相对体积比对照动物更大。此外,在受照射组织中未观察到炎症或纤维化。对照动物和受照射动物的分散下颌下腺细胞中,卡巴胆碱或毒胡萝卜素刺激的Ca2+动员相似。此外,对照和受照射组单个导管和腺泡的[Ca2+]i成像首次显示,两种细胞类型中的Ca2+动员均未因辐射处理而改变。对照动物和受照射动物的下颌下腺细胞中,卡巴胆碱刺激的、布美他尼敏感的Na+/K+/2Cl-协同转运活性成分也相似。这些数据表明,单次γ射线照射会导致下颌下腺组织和功能逐渐丧失。唾液分泌减少并非由于腺体的慢性炎症或纤维化,也不是由于腺泡或导管细胞中神经递质信号传导机制的改变。辐射诱导的液体分泌减少似乎与腺泡的水处理能力变化或腺体中腺泡细胞数量变化有关。