Akademik Veri Yönetim Sistemi
EUROPEAN JOURNAL OF THERAPEUTICS, 2025 (ESCI, TRDizin)
Objective: Ionizing radiation is widely used in cancer treatment but can cause damage to non-target tissues, including the pancreas. Amifostine is a cytoprotective agent shown to protect certain normal tissues from radiation injury. Given the structural and functional similarities between the pancreas and other exocrine glands such as the parotid, we hypothesized that amifostine could confer radioprotection to pancreatic islets. Method: Male rats were divided into three groups: control (no intervention), irradiation (whole-body abdominal exposure), and irradiation + amifostine (200 mg/ kg intraperitoneally, 30 min prior to irradiation). Pancreatic tissues were examined histologically using hematoxylin-eosin staining and immunohistochemically for insulin, glucagon, and somatostatin expression. Results: Irradiation induced significant histological damage in both endocrine and exocrine pancreas, characterized by cytoplasmic vacuolization and necrosis. Amifostine pretreatment did not prevent these alterations; the extent of histological injury in the irradiation + amifostine group was comparable to the irradiation group. Immunohistochemistry revealed decreased insulin and glucagon positivity in both irradiated groups compared to controls, whereas somatostatin expression was paradoxically increased. Conclusion: In this pilot model, amifostine failed to protect pancreatic islets from radiation-induced injury, suggesting organ-specific variability in its cytoprotective efficacy. These findings indicate that amifostine's benefit may depend on tissue-specific activation, pharmacokinetics, and radiation sensitivity, and that optimized, pancreastargeted protective strategies are needed.