Reactive Oxygen Species and X-Ray Disrupted Spontaneous [Ca2+]i Oscillation in Alveolar Macrophages

• Published in: Radiation research 2013-04, Vol.179 (4), p.485-492
• Main Authors: Chen, Hao, Ye, Hong, Meng, Da-Quan, Cai, Peng-Cheng, Chen, Feng, Zhu, Li-Ping, Tang, Qiu, Long, Zhi-Xiong, Zhou, Qiong, Jin, Yang, Xin, Jian-Bao, Tao, Xiao-Nan, Ma, Wan-Li
• Format: Article
• Language: English
• Subjects: Animals; Benzylisoquinolines - pharmacology; Calcium Signaling - radiation effects; Cells, Cultured; Macrophages, Alveolar - metabolism; Macrophages, Alveolar - radiation effects; Male; NADPH Oxidases - antagonists & inhibitors; Onium Compounds - pharmacology; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species - metabolism; REGULAR ARTICLES; Space life sciences; X-Rays
• ISSN: 0033-7587; 1938-5404
• DOI: 10.1667/RR3006.1

Radiation leads to a rapid burst of reactive oxygen species (ROS), which is considered to be one of the major causes of radiation-induced injury. ROS have previously been shown to induce changes in cytosolic Ca2+ ([Ca2+]i) including [Ca2+]i oscillation. However, the role of radiation in [Ca2+]i oscillation is poorly understood. The purpose of this study was to identify the effect of ROS and X ray on [Ca2+]i oscillation, as well as their role in radiation-induced lung injury. Alveolar macrophages were cultured in the absence and presence of different doses of hydrogen peroxide (H2O2) or exposed to X-ray irradiation with or without pretreatment of diphenyleneiodonium chloride (DPI, an inhibitor of NADPH oxidases) or tetrandrine (TET, a calcium entry blocker) and cytosolic Ca2+ concentration was detected by fluorescent Ca2+ indicator Fura-2. Rat radiation lung injury was induced in vivo by using 40 Gy X ray and DPI or TET was used to prevent radiation-induced lung injury. The results showed that there was spontaneous [Ca2+]i oscillation in alveolar macrophages under normal conditions, and treatment of H2O2 (100–500 μM) or 2 Gy X ray inhibited the spontaneous [Ca2+]i oscillation and induced [Ca2+]i rise. TET abolished H2O2 or X ray induced [Ca2+]i rise in alveolar macrophages, and attenuated X ray- induced rat alveolitis in vivo. DPI prevented X-ray-induced inhibition of [Ca2+]i oscillation in alveolar macrophages and prevented X-ray-induced rat alveolitis. Taken together, the data suggest that the disruption of [Ca2+]i oscillation and induction of [Ca2+]i rise through ROS is involved in the mechanism of radiation-induced lung injury.