Abstract

HYDROGEN SULFIDE AND ACUTE LUNG INJURY

Yuanlin Song* and Linlin Wang

ABSTRACT

Gaseous molecules continue to hold new promise in molecular medicine as experimental and clinical therapeutics. Along with nitric oxide (NO) and carbon monoxide (CO), hydrogen sulfide (H2S) also is a toxic inhalation hazard, and a common component of air pollution. H2S can be produced endogenously by two key enzymes cystathionine-𝛽-synthase (CBS) and cystathionine-𝛾-lyase (CSE). Now H2S is known as endogenous gaseous transmitter, involved in physiological and pathological processes of many diseases. ALI remains a leading cause for morbidity and mortality in critically ill patients. The lung injury may be resulted from pneumonia, aspiration, mechanical ventilation, trauma and high oxygen therapy and sepsis. The pathophysiology of ALI is characterized by disruption of the lung endothelial and alveolar epithelial barriers, translocation of protein-rich edema fluid into the alveolar, release of pro-inflammatory cytokines, and deposition of fibrin in the alveolar space. H2S has been implied to act as potential therapeutics in preclinical animal models of ALI including ventilator-induced lung injury, ischemia/reperfusion injury, oleic acid-induced ALI, LPS-induced injury and hyperoxia-induced injury, to name a few. The mechanisms are involved in the regulation of inflammation, apoptosis, oxidative stress, mitochondrial function and so on.

Keywords: acute lung injury; hydrogen sulfide; inflammation; oxidative stress; apoptosis; mitochondrial function.