Nagler R M
Department of Oral and Maxillofacial Surgery, Oral Biochemistry Laboratory and Salivary Clinic, Rambam Medical Center, Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
In Vivo. 2003 Jul-Aug;17(4):369-75.
The purpose of this review is to suggest an updated description of early and late irradiation effects on salivary glands in rodents. Based on this description, the mechanism of the underlying xerostomia will be discussed.
To examine the assumption that the so-called "irradiation" effects on the parotid gland of the rat during the first two weeks are actually mucositic effects and, thus, are transient, both function and partitution-coefficient parameters of the salivary glands were examined in both irradiated and pair-fed but not irradiated rats.
Various studies were performed in which irradiated and non-irradiated rats were examined at varying intervals up to one year post-irradiation. Head and neck irradiation resulted not only in dysfunction and tissue loss of the salivary glands but also in a systemic effect expressed as profound body weight loss.
Based on the literature available and on our own studies, we believe that one can suggest an overall mechanism for the damage induced by irradiation to the salivary glands. Our results have shown a mutual delayed expression of irradiation-induced damage in both parotid and submandibular, more evident in the parotid gland.
We have suggested the following mechanism for the parotid irradiation-induced specific damage: The injurious agents resulting in delayed serous cell death leading to the specific parotid radiosensitivity are transition, highly redox-active metal ions, such as Fe and Cu, associated with secretion granules.
本综述的目的是对啮齿动物唾液腺早期和晚期辐射效应提出更新的描述。基于此描述,将讨论口干症潜在的机制。
为检验大鼠腮腺在前两周所谓的“辐射”效应实际上是黏膜炎性效应且因此是短暂性的这一假设,对接受辐射和配对饲养但未接受辐射的大鼠的唾液腺功能和分配系数参数进行了检测。
进行了多项研究,在辐射后长达一年的不同时间间隔对接受辐射和未接受辐射的大鼠进行检测。头颈部辐射不仅导致唾液腺功能障碍和组织损失,还导致一种表现为体重显著减轻的全身效应。
基于现有文献和我们自己的研究,我们认为可以提出辐射对唾液腺造成损伤的总体机制。我们的结果显示,腮腺和颌下腺辐射诱导损伤存在相互延迟表达,在腮腺中更明显。
我们提出了腮腺辐射诱导特异性损伤的以下机制:导致浆液性腺泡细胞延迟死亡从而导致腮腺特异性放射敏感性的损伤因子是与分泌颗粒相关的过渡态、高氧化还原活性金属离子,如铁和铜。