Radiation-Induced Microvascular Injury as a Mechanism of Salivary Gland Hypofunction and Potential Target for Radioprotectors

August 2016 in “ Radiation Research ”

Aviram Mizrachi, Ana P. Cotrim, Nora Katabi, James B. Mitchell, Marcel Verheij, Adriana Haimovitz‐Friedman

radiation therapy salivary gland damage xerostomia microvascular dysfunction bovine aortic endothelial cell apoptosis ceramide production reactive oxygen species scavengers microvessel density Tempol alopecia ROS scavengers

TLDR Radiation damages salivary glands by harming blood vessels, but antioxidants might help protect them.

Radiation therapy for head and neck squamous cell carcinoma (HNSCC) often caused salivary gland (SG) damage, leading to xerostomia due to microvascular dysfunction. This study investigated the mechanisms behind this damage, focusing on bovine aortic endothelial cell (BAEC) apoptosis and ceramide production after 5 Gy irradiation, and the effects of a 15 Gy dose on murine SG function. BAECs showed increased apoptosis and ceramide production, both mitigated by reactive oxygen species (ROS) scavengers. In mice, 15 Gy irradiation led to weight loss, alopecia, and reduced saliva production, with all but lysozyme levels improved by ROS scavengers. Reduced microvessel density in irradiated SGs was also alleviated by Tempol. The study concluded that SG hypofunction was largely due to microvascular dysfunction involving ceramide and ROS, suggesting ROS scavengers as potential radioprotectors for SG function in HNSCC patients.

View this study on europepmc.org →