Conclusion
Reactive oxygen and nitrogen intermediates, produced by the interaction of NO with partially reduced oxygen species, affect lung function and homeostasis in a variety of different ways. They act as signaling agents and play an essential role in pathogen killing. On the other hand, they may contribute to tissue injury by upregulating genes responsible for the production of inflammatory mediators and by directly nitrating and oxidizing proteins, events known to adversely affect critical functions. A significant challenge to defining their role in lung injury results from their short biological half-lives, and lack of sensitive detection techniques, and the difficulty in deciphering the relevance of the various substrate concentrations to a particular measured response. Thus, many questions relating to the chemical, physiological, pathobiological, and clinical consequences of ROS and RNS generation remain unanswered. Therapeutic strategies, such as enhanced anti-inflammatory and antioxidant therapies are in their infancy in the clinical arena. Hence, this discussion of what is known leads one to realize how much is not known with regard to the role of RNS/ROS in lung injury.
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Matalon, S., Davis, I.C., Lang, J.D. (2007). Involvement of Reactive Oxygen and Nitrogen Species in the Pathogenesis of Acute Lung Injury. In: Abraham, E., Singer, M. (eds) Mechanisms of Sepsis-Induced Organ Dysfunction and Recovery. Update in Intensive Care and Emergency Medicine, vol 44. Springer, Berlin, Heidelberg . https://doi.org/10.1007/3-540-30328-6_7
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