Amelioration of gamma irradiation-induced salivary gland damage in mice using melatonin.

Salivary gland damage caused by ionizing radiation (IR) severely affects the patient quality of life and influences the efficacy of radiotherapy. Most current treatment modalities are palliative, so effective prevention of damage caused by IR is essential. Melatonin (MLT) is an antioxidant that has been reported to prevent IR-induced damage in a range of systems, including the hematopoietic system and gastrointestinal tract. In this study, we explored the effects of MLT on whole-neck irradiation (WNI)-induced salivary gland damage in mice. The results revealed that by protecting the channel protein AQP-5, MLT not only alleviates salivary gland dysfunction and maintains salivary flow rate, but also protects salivary gland structure and inhibits the WNI-induced reduction in mucin production and degree of fibrosis. Compared with WNI-treated mice, in those receiving MLT, we observed a modulation of oxidative stress in salivary glands via its effects on 8-OHdG and SOD2, as well as an inhibition of DNA damage and apoptosis. With respect to its radioprotective mechanism, we found that MLT may alleviate WNI-induced xerostomia partly by regulating RPL18A. In vitro, we demonstrated that MLT has radioprotective effects on salivary gland stem cells (SGSCs). In conclusion, our data this study indicate that MLT can effectively alleviate radiation-induced damage in salivary glands, thereby providing a new candidate for the prevention of WNI-induced xerostomia.

D-galactose protects the intestine from ionizing radiation-induced injury by altering the gut microbiome.

This article aims to investigate the protection of the intestine from ionizing radiation-induced injury by using D-galactose (D-gal) to alter the gut microbiome. In addition, this observation opens up further lines of research to further increase therapeutic potentials. Male C57BL/6 mice were exposed to 7.5 Gy of total body irradiation (TBI) or 13 Gy of total abdominal irradiation (TAI) in this study. After adjustment, D-gal was intraperitoneally injected into mice at a dose of 750 mg/kg/day. Survival rates, body weights, histological experiments and the level of the inflammatory factor IL-1ß were observed after TBI to investigate radiation injury in mice. Feces were collected from mice for 16S high-throughput sequencing after TAI. Furthermore, fecal microorganism transplantation (FMT) was performed to confirm the effect of D-gal on radiation injury recovery. Intraperitoneally administered D-gal significantly increased the survival of irradiated mice by altering the gut microbiota structure. Furthermore, the fecal microbiota transplanted from D-gal-treated mice protected against radiation injury and improved the survival rate of recipient mice. Taken together, D-gal accelerates gut recovery following radiation injury by promoting the growth of specific microorganisms, especially those in the class Erysipelotrichia. The study discovered that D-gal-induced changes in the microbiota protect against radiation-induced intestinal injury. Erysipelotrichia and its metabolites are a promising therapeutic option for post-radiation intestinal regeneration.