A normobaric gas exposure animal chamber and its validation in hyperoxia exposure.

We are living in an environment full of gases, and any change in the concentration of a component of the air or contaminants (usually toxic) in the air may significantly threaten human health. Thus, to investigate the influence of gases in animal models it is helpful to elucidate the pathogenesis of gas-related injury. Although there are devices used for gas exposure in animals, there are still limitations in the establishment of these animal models, such as the change in gas concentration during the refreshing of water, food and litter, and the contamination of toxic gases released by animals. Herein, we freshly prepared a chamber for normobaric gas exposure. During the exposure in this chamber, the refreshing of water, food and litter does not require opening of the chamber. The chamber gases are continuously circulated and filtered, and the gas concentration remains very stable. To validate the feasibility of this chamber, rats were exposed to pure oxygen as an example. Results showed that rats with hyperoxia-induced lung injury simulated by pure oxygen exposure displayed the representative characteristics as observed in humans: shortness of breath, lung edema, alveolar septal rupture, infiltration of inflammatory cells, oxidative and inflammatory injury. This suggests that it is feasible to establish animal models using this chamber for the investigation of gas toxicity.

Role of iron in lung injury-induced by hyperoxia.

Iron is essential to life due to its unusual flexibility in serving as both an electron donor and acceptor. However, free iron can damage tissues by catalyzing the conversion of hydrogen peroxide to free-radical ions that attack lipids, proteins and DNA. Hyperoxia-induced lung injury (HILI) occurs when breathing elevated partial pressure of oxygen (usually > 0.5 atmospheres absolute) for extended periods. A few studies have shown that iron and proteins related to iron metabolism are closely related to HILI, and iron chelation may exert protective effects on HILI. As a rate-limiting enzyme in the degradation of heme, heme oxygenases (HOs) play a crucial role in the iron metabolism. Although some studies have been conducted to investigate the role of HOs in the pathogenesis of HILI, findings still conflict, and HOs of different isoforms may function differently in the pathogenesis of HILI. On the available findings, there might be a beneficial threshold of HO-1 expression in HILI. More studies are required to confirm the above findings and to provide evidence for the clinical treatment of HILI by iron chelation.