汞蒸气暴露诱导小鼠肺组织超氧化物歧化酶同工酶选择性诱导。

Isozyme selective induction of mouse pulmonary superoxide dismutase by the exposure to mercury vapor.

机构信息

Department of Environmental Medicine, University of Tsukuba, Tsukuba, Ibaraki 305, Japan.

出版信息

Environ Toxicol Pharmacol. 1996 Aug 15;2(1):35-7. doi: 10.1016/1382-6689(96)00025-7.

Abstract

Alterations in lung superoxide dismutase (SOD) isozymes after exposure of mice to mercury vapor were examined. Inhalation of mercury vapor (10 mg/m(3)) for 1 h by mice resulted in a higher accumulation of mercury in the kidney and lung compared to other organs, at 1 h after exposure. Under these conditions marked enhancement of protein content in bronchoalveolar fluid (BALF), attributed to lung injury, was observed. Exposure to mercury vapor caused a significant increase in the pulmonary Cu,Zn-SOD activity (1.32-fold at 48 h) whereas Mn-SOD activity was suppressed to 82% of the control level, suggesting different sensitivity to the metal inhalation. The selective induction of Cu,Zn-SOD protein (1.79-fold at 48 h) was confirmed by immunoblot analysis with polyclonal antibodies against these isozymes. These observations suggest that the selective induction of Cu,Zn-SOD at the translational level appears to occur as an initial defense against mercury-promoted oxidative stress.

摘要

研究了暴露于汞蒸气后小鼠肺中超氧化物歧化酶（SOD）同工酶的变化。吸入汞蒸气（10 mg/m³）1 小时后，与其他器官相比，暴露后 1 小时，肾脏和肺部的汞积累量更高。在这些条件下，观察到支气管肺泡灌洗液（BALF）中的蛋白质含量明显增加，这归因于肺损伤。暴露于汞蒸气导致肺铜锌 SOD 活性显著增加（48 小时时为 1.32 倍），而 Mn-SOD 活性抑制至对照水平的 82%，表明对金属吸入的敏感性不同。用针对这些同工酶的多克隆抗体进行免疫印迹分析证实了 Cu，Zn-SOD 蛋白的选择性诱导（48 小时时为 1.79 倍）。这些观察结果表明，在翻译水平上选择性诱导 Cu，Zn-SOD 似乎是作为对汞促进的氧化应激的初始防御而发生的。