Misawa M, Arai H
Department of Pharmacology, School of Pharmacy, Hoshi University, Tokyo, Japan.
J Toxicol Environ Health. 1993 Apr;38(4):435-48. doi: 10.1080/15287399309531730.
Reactive oxygens are now considered to be important substances in promoting inflammatory process. Recently, airway inflammation has attracted attention closely linked to bronchial asthma. The present study was undertaken to examine whether hydrogen peroxide, one of the reactive oxygens, could produce airway inflammation. Airway inflammation was assessed by airway vascular permeability in terms of pontamine sky blue (PSB) exudation. Airway resistance was measured with a modified Konzett-Rössler method and was expressed as a change in ventilation overflow. Inhalation of hydrogen peroxide (0.01-1.0 M) markedly caused a PSB exudation in a concentration-dependent manner in all of the trachea, main bronchus, and lungs. The hydrogen peroxide-induced PSB exudation effect was attenuated was attenuated by pretreatment with catalase, although heat-inactivated catalase had no inhibitory effect. Deferoxamine, which inhibits conversion of hydrogen peroxide into hydroxyl radical, decreased the PSB exudation induced by hydrogen peroxide. On the other hand, inhalation of hydrogen peroxide (1.0 M) caused a significant and biphasic increase in ventilation overflow. This airway constriction was suppressed by pretreatment with inhaled catalase, but not by inhaled deferoxamine. These results indicate that hydrogen peroxide causes an intense airway inflammation; this inflammatory effect may be mediated not only by hydrogen peroxide itself but also by hydroxyl radical. Hydrogen peroxide and hydroxyl radical may thus play an important role in bronchial asthma and bronchitis through inducing airway inflammation.
活性氧现在被认为是促进炎症过程的重要物质。最近，气道炎症与支气管哮喘密切相关，已引起关注。本研究旨在探讨活性氧之一的过氧化氢是否会引发气道炎症。通过以丽春红天蓝（PSB）渗出量来评估气道血管通透性，以此衡量气道炎症。采用改良的Konzett-Rössler方法测量气道阻力，并将其表示为通气溢出的变化。吸入过氧化氢（0.01 - 1.0 M）在所有气管、主支气管和肺部均显著引起PSB渗出，且呈浓度依赖性。过氧化氢诱导的PSB渗出效应可被过氧化氢酶预处理所减弱，而热灭活的过氧化氢酶则无抑制作用。去铁胺可抑制过氧化氢转化为羟基自由基，它能降低过氧化氢诱导的PSB渗出。另一方面，吸入过氧化氢（1.0 M）导致通气溢出显著且呈双相增加。这种气道收缩可被吸入过氧化氢酶预处理所抑制，但不能被吸入去铁胺所抑制。这些结果表明，过氧化氢会引发强烈的气道炎症；这种炎症效应可能不仅由过氧化氢本身介导，还由羟基自由基介导。因此，过氧化氢和羟基自由基可能通过诱导气道炎症在支气管哮喘和支气管炎中发挥重要作用。
