Mechanism of p47phox-induced increase of reactive oxygen species in peripheral blood mononuclear cells from premature infants on oxygen therapy.

OBJECTIVE

This study aimed to explore the mechanism of p47phox-induced increase of reactive oxygen species (ROS) in peripheral blood mononuclear cells (PBMCs) from premature infants after oxygen therapy, and determine a new target for oxidative stress injury alleviation in clinical setting.

METHODS

First, ROS levels as well as p47phox translocation and expression in PBMC samples were evaluated after treatment of premature infants with different concentrations of oxygen. Then, changes of all various parameters were detected after in vitro treatment of PBMCs with diphenyleneiodonium (DPI), apocynin, and high oxygen levels.

RESULTS

In premature infants, ROS levels increased significantly after treatment with oxygen, in a concentration-dependent manner (p < 0.05); meanwhile, p47phox translocation and expression were significantly enhanced (p < 0.05) as well. In agreement, PBMCs cultured in vitro showed increased ROS levels after treatment with high oxygen concentrations; p47phox translocation, and expression increased as well (p < 0.05). However, treatment with DPI or apocynin resulted in opposite effects.

CONCLUSION

Treatment with oxygen increases p47phox translocationand expression, which in turn induce ROS production. DPI and apocynin have the opposite effects.