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• W2138561220 abstract "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." @default.
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• W2138561220 date "2013-04-01" @default.
• W2138561220 modified "2023-10-17" @default.
• W2138561220 title "Reactive Oxygen Species and X-Ray Disrupted Spontaneous [Ca²⁺]_iOscillation in Alveolar Macrophages" @default.
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• W2138561220 doi "https://doi.org/10.1667/rr3006.1" @default.
• W2138561220 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23421826" @default.
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