Henriksson R, Fröjd O, Gustafsson H, Johansson S, Yi-Qing C, Franzén L, Bjermer L
Department of Oncology, University Hospital, Umeå, Sweden.
Br J Cancer. 1994 Feb;69(2):320-6. doi: 10.1038/bjc.1994.58.
The detailed mechanisms which can explain the inherent radiosensitivity of salivary glands remain to be elucidated. Although DNA is the most plausible critical target for the lethal effects of irradiation, interactions with other constituents, such as cell membrane and neuropeptides, have been suggested to cause important physiological changes. Moreover, mast cells seem to be closely linked to radiation-induced pneumonitis. Therefore, in the present study the effects of fractionated irradiation on salivary glands have been assessed with special regard to the appearance of mast cells and its correlation with damage to gland parenchyma. Sprague-Dawley strain rats were unilaterally irradiated to the head and neck with the salivary glands within the radiation field. The irradiation was delivered once daily for 5 days to a total dose of 20, 35 and 45 Gy. The contralateral parotid and submandibular glands served as intra-animal controls and parallel analysis of glands was performed 2, 4, 10 or 180 days following the last radiation treatment. Morphological analysis revealed no obvious changes up to 10 days after the irradiation. At 180 days a radiation dose-dependent loss of gland parenchyma was seen, especially with regard to serious acinar cells in parotid gland and acinar cells and serous CGT (convoluted granular tubule) cells in the submandibular gland. These changes displayed a close correlation with a concomitant dose-dependent enhanced density of mast cells and staining for hyaluronic acid. This cell population seems to conform with the features of the connective tissue mast cell type. The parotid seems to be more sensitive to irradiation than the submandibular gland. Thus, the present results further strengthen the role of and the potential interaction of mast cells with radiation-induced tissue injury and alterations in normal tissue integrity.
能够解释唾液腺固有放射敏感性的详细机制仍有待阐明。虽然DNA是辐射致死效应最合理的关键靶点，但有人提出与其他成分（如细胞膜和神经肽）的相互作用会引起重要的生理变化。此外，肥大细胞似乎与放射性肺炎密切相关。因此，在本研究中，已特别针对肥大细胞的出现及其与腺实质损伤的相关性，评估了分次照射对唾液腺的影响。将Sprague-Dawley品系大鼠的头部和颈部进行单侧照射，唾液腺位于辐射野内。每天照射一次，共照射5天，总剂量分别为20、35和45 Gy。对侧腮腺和颌下腺作为动物体内对照，并在最后一次放射治疗后的2、4、10或180天对腺体进行平行分析。形态学分析显示，照射后10天内无明显变化。在180天时，可见腺实质出现辐射剂量依赖性丧失，尤其是腮腺中的严重腺泡细胞以及颌下腺中的腺泡细胞和浆液性CGT（盘曲颗粒小管）细胞。这些变化与肥大细胞密度和透明质酸染色的剂量依赖性增强密切相关。这群细胞似乎符合结缔组织肥大细胞类型的特征。腮腺似乎比颌下腺对辐射更敏感。因此，本研究结果进一步强化了肥大细胞在辐射诱导的组织损伤以及正常组织完整性改变中的作用和潜在相互作用。
