Abstract: Mitoferrin is closely associated with mitochondrial function, which is the focus in Parkinson's disease (PD). To study the effect of mitoferrin on PD, this paper adopted model organism Drosophila melanogaster for experimentation. It was found that the life span and motor ability of wild Drosophila melanogaster were significantly affected by rotenone exposure, and the fluorescence intensity of reactive oxygen species (ROS) of Drosophila melanogaster brain increased, while the adenosine triphosphate (ATP) level decreased. However, the life span, motor ability, ROS accumulation and ATP level of Drosophila melanogaster with dopaminergic neuron mitoferrin overexpression (mitoferrin OE) under rotenone exposure were significantly rescued. The results show that the dopaminergic neuron mitoferrin OE may save the Drosophila melanogaster PD model caused by rotenone exposure by restoring the brain mitochondrial productivity and reducing the brain ROS accumulation. This study provides theoretical support for exploring the pathogeny and treatment of PD.
Keywords: mitoferrin; Parkinson's disease (PD); Drosophila melanogaster; adenosine triphosphate (ATP); reactive oxygen species (ROS)