Salivary gland damage due to radiotherapy, leading to xerostomia and causing a great of suffering to patients, is a phenomenon known since the beginning of this century. The mechanism responsible for it has not been elucidated and no adequate treatment for patients is available. According to the mechanism suggested for the parotid irradiation-induced specific damage, the injurious agents resulting in delayed serous cell death, leading to specific parotid radiosensitivity, are transition, highly redox active metal ions, such as Fe and Cu, associated with secretion granules. These ions enhance the lethal effect that irradiation has on DNA, resulting in a reproductive delayed cell death. The immediate effects of metal-mediated enhancement of irradiation damage in cells may occur but does not seem to play a major role in the underlying mechanism. Indeed, in a series of recent experiments, it was succeeded in positively correlating an extended time point (two months) protection of parotid function with preirradiation degranulation and redox active metal ion mobilization out of the gland into the secreted saliva prior to irradiation. In contrast, a negative correlation in the submandibular gland, with no protection, no degranulation, no metal ion mobilization and no redox activity was demonstrated. The ability to protect the parotid function at two months with Zn-DFO, a specific transition metal ion mobilizer, from sensitive intracellular targets lends further credence to these studies.
Biomedical Reviews 1998; 9: 121-129.
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