Reactive Oxygen Species and X-Ray Disrupted Spontaneous [Ca2+]i Oscillation in Alveolar Macrophages
Reactive Oxygen Species and X-Ray Disrupted Spontaneous [Ca2+]i Oscillation in Alveolar Macrophages
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DOI：
10.1667/rr3006.1
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发表时间：
2013-04-01
影响因子：
3.4
通讯作者：
Ma, Wan-Li
中科院分区：
文献类型：
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作者：
Chen, Hao;Ye, Hong;Ma, Wan-Li
辐射导致活性氧（ROS）快速爆发，这被认为是辐射损伤的主要原因之一。 ROS 先前已被证明可诱导胞质 Ca2+ ([Ca2+](i)) 的变化，包括 [Ca2+](i) 振荡。然而，人们对辐射在 [Ca2+](i) 振荡中的作用知之甚少。本研究的目的是确定 ROS 和 X 射线对 [Ca2+](i) 振荡的影响，以及它们在辐射引起的肺损伤中的作用。在不存在和存在不同剂量的过氧化氢（H2O2）的情况下培养肺泡巨噬细胞，或暴露于X射线照射下，使用或不使用氯化二亚苯基碘鎓（DPI，NADPH氧化酶抑制剂）或粉防己碱（TET，钙进入阻滞剂）预处理，并通过荧光Ca2+指示剂Fura-2检测胞质Ca2+浓度。采用40 Gy X射线在体内诱导大鼠放射性肺损伤，并采用DPI或TET预防放射性肺损伤。结果表明，正常情况下肺泡巨噬细胞存在自发[Ca2+](i)振荡，H2O2(100-500 μM)或2 Gy X射线处理可抑制自发[Ca2+](i)振荡并诱导[Ca2+](i)升高。 TET 消除了 H2O2 或 X 射线诱导的肺泡巨噬细胞 [Ca2+](i) 升高，并减轻了体内 X 射线诱导的大鼠肺泡炎。 DPI 可防止 X 射线诱导的肺泡巨噬细胞 [Ca2+](i) 振荡抑制，并预防 X 射线诱导的大鼠肺泡炎。综上所述，数据表明，[Ca2+](i) 振荡的破坏和通过 ROS 诱导 [Ca2+](i) 上升参与了辐射引起的肺损伤的机制。 (C) 2013 年放射线研究会
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 Xray 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 mu M) 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. (C) 2013 by Radiation Research Society