Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery · 2014
Injury in Minipig Parotid Glands following Fractionated Exposure to 30 Gy of Ionizing Radiation.
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Wang Ren-Sheng, Zhang Ting-Ting, Xu Zhuo-Hua, Hu Kai, Shi Yu, Long Sha, Yue Hai-Ying
Аннотация
OBJECTIVE: To explore the effects of 30 Gy of (60)Co γ-rays on apoptosis and reactive oxygen species (ROS) levels in minipig parotid cells as a possible mechanism for radiation-induced parotid injury.
STUDY DESIGN: Experimental study.
SETTING: Department of Radiotherapy, First Affiliated Hospital, Guangxi Medical University, Nanning, China.
SUBJECTS AND METHODS: Forty male minipigs were divided into control and irradiated groups. Terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling was used for detecting apoptosis in the parotid cells, immunohistochemistry, and western blots were used to test expression of the B-cell lymphoma 2 (Bcl-2) and BCL2-associated X (Bax) proteins, and reverse transcription polymerase chain reaction was used to analyze the expression of Bcl-2, Bax, p53, and caspase-3 messenger ribonucleic acid. An enzyme-linked immunosorbent assay was used to detect ROS levels in the parotid tissue.
RESULTS: At each time point, the apoptotic rates in the irradiated group were higher than those in the control group. Furthermore, the ROS and expression levels of Bax, p53, and caspase-3 messenger ribonucleic acid and proteins gradually increased and were higher than those in the control group. Conversely, the expression of Bcl-2 was decreased in the irradiated group (P < .05).
CONCLUSIONS: Ionizing radiation induces the production of ROS and promotes changes in the expression of several apoptotic proteins, which increases apoptosis and likely contributes to the mechanism of radiation-induced parotid injury.
STUDY DESIGN: Experimental study.
SETTING: Department of Radiotherapy, First Affiliated Hospital, Guangxi Medical University, Nanning, China.
SUBJECTS AND METHODS: Forty male minipigs were divided into control and irradiated groups. Terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling was used for detecting apoptosis in the parotid cells, immunohistochemistry, and western blots were used to test expression of the B-cell lymphoma 2 (Bcl-2) and BCL2-associated X (Bax) proteins, and reverse transcription polymerase chain reaction was used to analyze the expression of Bcl-2, Bax, p53, and caspase-3 messenger ribonucleic acid. An enzyme-linked immunosorbent assay was used to detect ROS levels in the parotid tissue.
RESULTS: At each time point, the apoptotic rates in the irradiated group were higher than those in the control group. Furthermore, the ROS and expression levels of Bax, p53, and caspase-3 messenger ribonucleic acid and proteins gradually increased and were higher than those in the control group. Conversely, the expression of Bcl-2 was decreased in the irradiated group (P < .05).
CONCLUSIONS: Ionizing radiation induces the production of ROS and promotes changes in the expression of several apoptotic proteins, which increases apoptosis and likely contributes to the mechanism of radiation-induced parotid injury.