Respiratory distress is the leading cause of death in preterm newborns.
Current modes of treatment require assisted ventilation with high concentrations of oxygen which may lead to chronic pulmonary injury with increased morbidity and mortality. In newborns, cysteine deficiency may develop and lead to lower than adequate tissue GSH levels, which could impair ability to detoxify reactive oxygen species. In prematures, this may be causative in respiratory distress and in the progression of lung damage during hyperoxic exposure. Our research explores the role of GSH and ascorbate in the development of respiratory distress syndrome in premature neonates and their protective role in hyperoxic exposure mediated lung damage. Research on prematures with respiratory distress include measurement of lymphocyte, plasma, airway lining fluid GSH levels, and lung extraction of plasma GSH as potential markers for lung GSH status.