Background: The worst long-term complication of head and neck cancer radiotherapy is osteoradionecrosis. The cellular and molecular mechanisms involved in osteoradionecrosis are caused by dysregulation of bone healing, such as deficient osteoblasts and osteoclasts, amplified by a cascade of cytokine activities via chronic oxidative stress, leading to abnormal reactive oxygen species (ROS). Metalloporphyrins (MnTE-2-PyP) have emerged as being especially promising due to their distinct antioxidant properties. The aim of this study was to investigate the role of MnTE-2-PyP in protection of osteoblastic and osteoclastic cells against radiation damage.
Material and method: Osteoblast (MC3T3-E1) and osteoclast (RAW264.7) cell lines were used. MnTE-2-PyP was added (10 μg/ml) into the cell cultures 1 h before irradiation. MC3T3-E1 and RAW cells were then exposed to gamma-ray irradiation at total doses of 0, 2, 4, 6, 8 and 10 Gy. Cell survival, Caspase3/7 apoptosis and oxidative burst analyses were performed 24 h post-irradiation to test the effect of MnTE-2-PyP with and without radiation on cells.
Result: For cell survival, MnTE-2-PyP significantly decreased radiation damage on MC3T3-E1 and RAW cells at all doses as well as 0 Gy control ( P < 0.01). On the contrary, caspase3/7 apoptosis levels were significantly decreased in irradiated cells treated with MnTE-2-PyP than their counterparts without MnTE-2-PyP ( P < 0.01). In addition, the oxidative burst activities which produce various highly ROS were significantly lowered in MnTE-2-PyP-treated cells at all radiation doses ( P < 0.01).
Conclusion: MnTE-2-PyP might protect normal bony tissues during radiotherapy via decreasing excessive levels of ROS and maintaining ROS homeostasis in vital cell organelles.
Conflict of interest: None declared.