Effect and Mechanism of PINK1/Parkin-Mediated Mitochondrial Autophagy in Rat Lung Injury Induced by Nano Lanthanum Oxide

Abstract

Nano lanthanum oxide particles (La2O3 NPs) are important nanoparticle materials which are widely used in photoelectric production, but their potential health hazards to the respiratory system are not clear. The purpose of this study was to explore the possible mechanism of lung injury induced by La2O3 NPs. In this study, 40 SPF male SD rats were randomly divided into low-, medium-, and high-dose groups and control groups, with 10 animals in each group. Rats were poisoned by tracheal injection. The low-, medium-, and high-dose groups were given La2O3 NPs suspension of 25, 50, and 100 mg/kg, respectively, and the control group was given an equal volume of high-temperature sterilized ultrapure water. The rats in each group were exposed once a week for 12 consecutive times. The gene transcription and protein expression levels of PINK1 and parkin in rat lung tissue were mainly detected. Compared with the control group, the gene transcription and protein expression levels of PINK1 and Parkin in the exposed group were significantly higher (p 2O3 NPs may activate PINK1/parkin-induced mitochondrial autophagy.

Keywords

• nanometer lanthanum oxide
• pulmonary
• mitochondrial autophagy injury
• PINK1/parkin