Source: Annual Congress 2010 - Acute respiratory failure
Disease area: Airway diseases, Respiratory critical care

Abstract

[Objective] The pulmonary toxicity of prolonged exposure to high concentration of oxygen during mechanical ventilation, which relates to an excess generation of reactive oxygen species (ROS), is well recognized. Since it is reported that hydrogen (H₂) specifically quenches harmful ROS, we expect H₂ to reduce the adverse effect of the oxygen exposure. The aim of the present study was to determine whether H₂ is capable of protecting alveolar epithelial cells against the exposure to ROS in vitro.
[Methods] Human alveolar epithelial cells (A549) were incubated with xanthine/xanthine oxidase (XOD) which generates extracellular superoxide anion or with menadione which enhances the generation of intracellular ROS. The living cells were counted using tetrazolium salt. Production of harmful ROS in the cells was evaluated using aminophenyl fluorescein which detects harmful ROS like hydroxyl radical, hypochlorite and peroxynitrite. Hydrogen concentration in CO₂ incubator (CO₂=5%, O₂=20%) was 2%, which is under the flammability limit (4%) of H₂ in air.
[Results] The number of the living cells incubated with XOD or menadione without H₂ significantly decreased in comparison to that with H₂. Increased ROS in the cells incubated with XOD or menadione was suppressed in the cells incubated with H₂, indicating that the effects of harmful ROS exogenously induced by superoxide anion or endogenously induced by menadione were suppressed by H₂.
[Conclusions] Hydrogen protects alveolar epithelial cells (A549) against injury induced by reactive oxygen species in vitro, indicating that the toxicity of oxygen will be possibly reduced by hydrogen administration.

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Citations should be made in the following way:
K. Kokubo, K. Yamashita, T. Shinbo, M. Hirose, H. Kobayashi (Sagamihara, Japan). Hydrogen protects alveolar epithelial cells (A549) against injury induced by reactive oxygen species in vitro. Eur Respir J 2010; 36: Suppl. 54, 2284

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